Mortality nearly halved with dual antiplatelet therapy in severe PAD

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WASHINGTON – Long-term dual-antiplatelet therapy may provide a mortality benefit over aspirin alone in patients with symptomatic peripheral artery disease.

In an observational study of 629 patients with claudication or critical limb ischemia, the 348 who were on dual antiplatelet therapy (DAPT) with aspirin plus clopidogrel had a 3-year all-cause mortality rate of 11%, compared with 21% for those on aspirin monotherapy, Dr. Ehrin J. Armstrong said at the annual meeting of the American College of Cardiology.

The group on DAPT also had a significantly lower 3-year rate of major adverse cardiovascular events: 20%, compared with 28% in the monotherapy group. However, this was driven by the reduced risk of mortality. Rates of nonfatal MI and stroke were similar in the two groups. So were rates of lower extremity bypass surgery and major amputations, according to Dr. Armstrong, a cardiologist at the University of California, Davis.

The group on DAPT had a significantly higher baseline prevalence of diabetes at the time of angiography: 54%, compared with 45% for patients on aspirin alone. The DAPT group also had a higher baseline prevalence of known coronary artery disease – 56% vs. 45% – and greater use of beta-blockers, by a margin of 55%, compared with 48%. In a multivariate regression analysis adjusted for these and other potential confounders, DAPT was associated with a 45% reduction in the risk of mortality and a 35% decrease in major adverse cardiovascular events.

The rate of the combined endpoint of death or major amputation was 18% in the DAPT group and 27% with aspirin monotherapy, for a highly significant 47% relative risk reduction.

Although a study such as this can’t be considered definitive, these data suggest DAPT is worth considering in patients with symptomatic peripheral artery disease, the cardiologist said.

He reported having no financial conflicts of interest.

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WASHINGTON – Long-term dual-antiplatelet therapy may provide a mortality benefit over aspirin alone in patients with symptomatic peripheral artery disease.

In an observational study of 629 patients with claudication or critical limb ischemia, the 348 who were on dual antiplatelet therapy (DAPT) with aspirin plus clopidogrel had a 3-year all-cause mortality rate of 11%, compared with 21% for those on aspirin monotherapy, Dr. Ehrin J. Armstrong said at the annual meeting of the American College of Cardiology.

The group on DAPT also had a significantly lower 3-year rate of major adverse cardiovascular events: 20%, compared with 28% in the monotherapy group. However, this was driven by the reduced risk of mortality. Rates of nonfatal MI and stroke were similar in the two groups. So were rates of lower extremity bypass surgery and major amputations, according to Dr. Armstrong, a cardiologist at the University of California, Davis.

The group on DAPT had a significantly higher baseline prevalence of diabetes at the time of angiography: 54%, compared with 45% for patients on aspirin alone. The DAPT group also had a higher baseline prevalence of known coronary artery disease – 56% vs. 45% – and greater use of beta-blockers, by a margin of 55%, compared with 48%. In a multivariate regression analysis adjusted for these and other potential confounders, DAPT was associated with a 45% reduction in the risk of mortality and a 35% decrease in major adverse cardiovascular events.

The rate of the combined endpoint of death or major amputation was 18% in the DAPT group and 27% with aspirin monotherapy, for a highly significant 47% relative risk reduction.

Although a study such as this can’t be considered definitive, these data suggest DAPT is worth considering in patients with symptomatic peripheral artery disease, the cardiologist said.

He reported having no financial conflicts of interest.

[email protected]

WASHINGTON – Long-term dual-antiplatelet therapy may provide a mortality benefit over aspirin alone in patients with symptomatic peripheral artery disease.

In an observational study of 629 patients with claudication or critical limb ischemia, the 348 who were on dual antiplatelet therapy (DAPT) with aspirin plus clopidogrel had a 3-year all-cause mortality rate of 11%, compared with 21% for those on aspirin monotherapy, Dr. Ehrin J. Armstrong said at the annual meeting of the American College of Cardiology.

The group on DAPT also had a significantly lower 3-year rate of major adverse cardiovascular events: 20%, compared with 28% in the monotherapy group. However, this was driven by the reduced risk of mortality. Rates of nonfatal MI and stroke were similar in the two groups. So were rates of lower extremity bypass surgery and major amputations, according to Dr. Armstrong, a cardiologist at the University of California, Davis.

The group on DAPT had a significantly higher baseline prevalence of diabetes at the time of angiography: 54%, compared with 45% for patients on aspirin alone. The DAPT group also had a higher baseline prevalence of known coronary artery disease – 56% vs. 45% – and greater use of beta-blockers, by a margin of 55%, compared with 48%. In a multivariate regression analysis adjusted for these and other potential confounders, DAPT was associated with a 45% reduction in the risk of mortality and a 35% decrease in major adverse cardiovascular events.

The rate of the combined endpoint of death or major amputation was 18% in the DAPT group and 27% with aspirin monotherapy, for a highly significant 47% relative risk reduction.

Although a study such as this can’t be considered definitive, these data suggest DAPT is worth considering in patients with symptomatic peripheral artery disease, the cardiologist said.

He reported having no financial conflicts of interest.

[email protected]

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Major finding: Patients with severe peripheral artery disease who were on dual antiplatelet therapy had an adjusted 45% reduction in the 3-year risk of all-cause mortality compared with those on aspirin monotherapy.

Data source: A retrospective, single-center study of 348 patients on DAPT with aspirin and clopidogrel and 281 on aspirin alone, all with PAD marked by claudication or critical limb ischemia.

Disclosures: This study was conducted free of commercial support. The presenter reported having no financial conflicts.

Discrepancies in dyschromia

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Dyschromias are one of the most common skin concerns among women and persons of color. In the April issue of Journal of Drugs in Dermatology, Dr. S.J. Kang and associates conducted an excellent study to determine whether racial or ethnic groups are treated differently for dyschromia.

The investigators searched the National Ambulatory Medical Care Survey (NAMCS) database for visits including the diagnosis of dyschromia (ICD-9 codes 709.00 or 709.09) during an 18-year period (1993-2010). They found 24.7 million visits for dyschromia and 5,531,000 patients with a sole diagnosis of dyschromia. Of those with a sole diagnosis of dyschromia, 76% were seen by a dermatologist, and more than half were female. Seventy-five percent were white, 11% African American, 7% Asian/Pacific Islander, and 9% Hispanic, although Asians demonstrated the highest number of visits per 100,000 persons.

In this review, hydroquinone monotherapy was the most commonly prescribed medication by dermatologists. Combination therapy with hydroquinone plus a retinoid and corticosteroid was utilized for women 10 times more than for men. African American patients were less likely to be prescribed combination therapy or receive procedures (such as cryotherapy, chemical peels or lasers). Additionally, sunscreens were recommended less often to black and Asian patients, compared with white patients.

While the underlying reason for dyschromia plays a role in the type of treatment given, overall combination therapies are often more effective than therapy with hydroquinone alone. This study demonstrates that combination therapy may be under-utilized in patients of color.

In my practice, I find that unless the patient’s skin is completely hydroquinone-naive, combination therapy with hydroquinone, retinoid, and corticosteroid is often a first-line treatment that may achieve faster results. Sun protection is a vital component in the treatment of dyschromia, and it is recommended for every patient, regardless of race or ethnicity. Nonhydroquinone topical agents containing ingredients such as kojic acid, arbutin, licorice, niacinamide, resveratrol, and superficial chemical peels are also used in all ethnic groups. In my Asian, Hispanic, and African American or darker-skinned patients, I do use caution with deeper peels and lasers and often perform a test spot first if this type of therapy is considered.

Dr. Wesley practices dermatology in Beverly Hills, Calif.

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Dyschromias are one of the most common skin concerns among women and persons of color. In the April issue of Journal of Drugs in Dermatology, Dr. S.J. Kang and associates conducted an excellent study to determine whether racial or ethnic groups are treated differently for dyschromia.

The investigators searched the National Ambulatory Medical Care Survey (NAMCS) database for visits including the diagnosis of dyschromia (ICD-9 codes 709.00 or 709.09) during an 18-year period (1993-2010). They found 24.7 million visits for dyschromia and 5,531,000 patients with a sole diagnosis of dyschromia. Of those with a sole diagnosis of dyschromia, 76% were seen by a dermatologist, and more than half were female. Seventy-five percent were white, 11% African American, 7% Asian/Pacific Islander, and 9% Hispanic, although Asians demonstrated the highest number of visits per 100,000 persons.

In this review, hydroquinone monotherapy was the most commonly prescribed medication by dermatologists. Combination therapy with hydroquinone plus a retinoid and corticosteroid was utilized for women 10 times more than for men. African American patients were less likely to be prescribed combination therapy or receive procedures (such as cryotherapy, chemical peels or lasers). Additionally, sunscreens were recommended less often to black and Asian patients, compared with white patients.

While the underlying reason for dyschromia plays a role in the type of treatment given, overall combination therapies are often more effective than therapy with hydroquinone alone. This study demonstrates that combination therapy may be under-utilized in patients of color.

In my practice, I find that unless the patient’s skin is completely hydroquinone-naive, combination therapy with hydroquinone, retinoid, and corticosteroid is often a first-line treatment that may achieve faster results. Sun protection is a vital component in the treatment of dyschromia, and it is recommended for every patient, regardless of race or ethnicity. Nonhydroquinone topical agents containing ingredients such as kojic acid, arbutin, licorice, niacinamide, resveratrol, and superficial chemical peels are also used in all ethnic groups. In my Asian, Hispanic, and African American or darker-skinned patients, I do use caution with deeper peels and lasers and often perform a test spot first if this type of therapy is considered.

Dr. Wesley practices dermatology in Beverly Hills, Calif.

Dyschromias are one of the most common skin concerns among women and persons of color. In the April issue of Journal of Drugs in Dermatology, Dr. S.J. Kang and associates conducted an excellent study to determine whether racial or ethnic groups are treated differently for dyschromia.

The investigators searched the National Ambulatory Medical Care Survey (NAMCS) database for visits including the diagnosis of dyschromia (ICD-9 codes 709.00 or 709.09) during an 18-year period (1993-2010). They found 24.7 million visits for dyschromia and 5,531,000 patients with a sole diagnosis of dyschromia. Of those with a sole diagnosis of dyschromia, 76% were seen by a dermatologist, and more than half were female. Seventy-five percent were white, 11% African American, 7% Asian/Pacific Islander, and 9% Hispanic, although Asians demonstrated the highest number of visits per 100,000 persons.

In this review, hydroquinone monotherapy was the most commonly prescribed medication by dermatologists. Combination therapy with hydroquinone plus a retinoid and corticosteroid was utilized for women 10 times more than for men. African American patients were less likely to be prescribed combination therapy or receive procedures (such as cryotherapy, chemical peels or lasers). Additionally, sunscreens were recommended less often to black and Asian patients, compared with white patients.

While the underlying reason for dyschromia plays a role in the type of treatment given, overall combination therapies are often more effective than therapy with hydroquinone alone. This study demonstrates that combination therapy may be under-utilized in patients of color.

In my practice, I find that unless the patient’s skin is completely hydroquinone-naive, combination therapy with hydroquinone, retinoid, and corticosteroid is often a first-line treatment that may achieve faster results. Sun protection is a vital component in the treatment of dyschromia, and it is recommended for every patient, regardless of race or ethnicity. Nonhydroquinone topical agents containing ingredients such as kojic acid, arbutin, licorice, niacinamide, resveratrol, and superficial chemical peels are also used in all ethnic groups. In my Asian, Hispanic, and African American or darker-skinned patients, I do use caution with deeper peels and lasers and often perform a test spot first if this type of therapy is considered.

Dr. Wesley practices dermatology in Beverly Hills, Calif.

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Leukemic breast tumors may cause resistance in AML, ALL

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SAN DIEGO—One woman’s curiosity and self-described “aggressive” approach to research have led to some unexpected discoveries about acute leukemias.

Isabel Cunningham, MD, of Columbia University in New York, has found evidence to suggest that treatment resistance in leukemia patients may sometimes result from an interaction between leukemic cells and the breast.

She discovered that leukemic cells in extramedullary niches can adopt a tumor phenotype similar to breast cancer.

And many genes are similarly upregulated in leukemic and epithelial breast tumors.

Her research indicates that a new approach to resistant leukemias that incorporates the principles of solid-tumor treatment—scans to identify any tumors and surgery to remove them—could decrease marrow relapse and death.

Dr Cunningham and her colleagues presented these findings in a poster at the AACR Annual Meeting 2014 (abstract 3996*).

“Chemotherapy resistance is our main problem in treating leukemia,” Dr Cunningham said. “It’s been known for a long time that, occasionally, leukemia forms tumors in an organ, but there’s never been a unified approach to treatment, except for leukemia that occurs in the testis and the meninges.”

Dr Cunningham had encountered many patients with resistant leukemia throughout her career, but her research actually began with a patient she had never met. A case study of a leukemia patient with a breast tumor sparked Dr Cunningham’s interest, and she emailed the study’s author to find out what ultimately became of the patient.

The response she received peaked her curiosity further. So she began seeking more of these cases, contacting authors, and collecting information on this phenomenon.

“I took this on as sort of a hobby,” Dr Cunningham said. “I never had any idea where this was going to lead.”

Eventually, she had amassed information on 235 cases—163 patients with acute myeloid leukemia (AML) and 72 with acute lymphoblastic leukemia (ALL)—who ranged from 1 year to 75 years of age. And an analysis of these cases led to some surprising discoveries.

Clinical findings

Dr Cunningham found these leukemic breast tumors can occur before, during, or after marrow leukemia. And, clinically, they resemble breast cancer. Most tumors were palpable, and some were detected only on routine mammograms.

There were single or multiple nodules that may have involved the entire breast. Sixty percent of cases were unilateral on presentation, but, often, the other breast became involved. Seventy percent of cases exhibited axillary lymphadenopathy that was ipsilateral.

Most tumors grew rapidly, to as large as 12 cm. The tumor behavior was similar in AML and ALL. And the tumors had a metastatic pattern similar to lobular breast cancer—spreading to the contralateral breast, the abdomen or pelvis, the meninges, and culminating in death.

However, some patients did survive. Four percent of patients who were treated only with chemotherapy were alive at 4 years. Twenty-five percent of patients had their tumors excised prior to chemotherapy and were alive anywhere from 3 years to more than 26 years after treatment.

Histology and gene expression

To build upon these findings, Dr Cunningham set her sights on patient samples. She was able to obtain paraffin blocks of leukemic breast tumors from 25 patients and perform immunohistochemical staining.

“It became clear that the leukemic tumors—which are marked by leukemic markers and not breast cancer markers—look, histologically, like breast cancer, specifically, lobular breast cancer,” Dr Cunningham said. “An additional pathologic finding was a specific type of desmoplastic fibrosis seen in all 25 contributed biopsies.”

Dr Cunningham also performed gene expression studies on 3 of the tumors (2 ALL and 1 AML), which were collected 8 months to 22 months after diagnosis, while marrows were in remission. The analyses revealed that a number of genes are significantly upregulated in both leukemic breast tumors and breast cancer.

 

 

These include genes involved in adhesion and interactions with the extracellular matrix (ADAM8, COMP, and CDH22), genes involved in the ubiquitin-proteasome pathway (UBE2S, USP32, MDM2, and UBE2C), genes encoding for kinases (MAP4K1, PIM1, and NEK2), and genes involved in RAS signaling (RANBP1 and RAB10).

Conclusions and next steps

“It seems that there’s some kind of crosstalk between the organ microenvironment and leukemic cells that make the leukemic cells have the phenotype of breast cancer,” Dr Cunningham said. “And it may well be that relapse sometimes results from the presence of an undiagnosed collection of these cells.”

Therefore, Dr Cunningham suggests performing scans in treatment-resistant leukemia patients. If a patient relapses, and particularly if lactic dehydrogenase levels are increased, a scan might be in order.

“If we can recognize these tumors and cut them out, the patient could be cured, because we’re successful at treating the bone marrow,” Dr Cunningham said. “We’ve had very good bone marrow drugs for 50 years.”

For her part, Dr Cunningham is delving further into this phenomenon. She is now conducting gene expression studies on the rest of the 25 leukemic breast tumor samples and comparing these tumors to breast cancer to identify the most significant dysregulated genes in both entities. The long-term goal is to find a way to predict which patients will develop leukemic breast tumors.

*Information in the abstract differs from that presented at the meeting.

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SAN DIEGO—One woman’s curiosity and self-described “aggressive” approach to research have led to some unexpected discoveries about acute leukemias.

Isabel Cunningham, MD, of Columbia University in New York, has found evidence to suggest that treatment resistance in leukemia patients may sometimes result from an interaction between leukemic cells and the breast.

She discovered that leukemic cells in extramedullary niches can adopt a tumor phenotype similar to breast cancer.

And many genes are similarly upregulated in leukemic and epithelial breast tumors.

Her research indicates that a new approach to resistant leukemias that incorporates the principles of solid-tumor treatment—scans to identify any tumors and surgery to remove them—could decrease marrow relapse and death.

Dr Cunningham and her colleagues presented these findings in a poster at the AACR Annual Meeting 2014 (abstract 3996*).

“Chemotherapy resistance is our main problem in treating leukemia,” Dr Cunningham said. “It’s been known for a long time that, occasionally, leukemia forms tumors in an organ, but there’s never been a unified approach to treatment, except for leukemia that occurs in the testis and the meninges.”

Dr Cunningham had encountered many patients with resistant leukemia throughout her career, but her research actually began with a patient she had never met. A case study of a leukemia patient with a breast tumor sparked Dr Cunningham’s interest, and she emailed the study’s author to find out what ultimately became of the patient.

The response she received peaked her curiosity further. So she began seeking more of these cases, contacting authors, and collecting information on this phenomenon.

“I took this on as sort of a hobby,” Dr Cunningham said. “I never had any idea where this was going to lead.”

Eventually, she had amassed information on 235 cases—163 patients with acute myeloid leukemia (AML) and 72 with acute lymphoblastic leukemia (ALL)—who ranged from 1 year to 75 years of age. And an analysis of these cases led to some surprising discoveries.

Clinical findings

Dr Cunningham found these leukemic breast tumors can occur before, during, or after marrow leukemia. And, clinically, they resemble breast cancer. Most tumors were palpable, and some were detected only on routine mammograms.

There were single or multiple nodules that may have involved the entire breast. Sixty percent of cases were unilateral on presentation, but, often, the other breast became involved. Seventy percent of cases exhibited axillary lymphadenopathy that was ipsilateral.

Most tumors grew rapidly, to as large as 12 cm. The tumor behavior was similar in AML and ALL. And the tumors had a metastatic pattern similar to lobular breast cancer—spreading to the contralateral breast, the abdomen or pelvis, the meninges, and culminating in death.

However, some patients did survive. Four percent of patients who were treated only with chemotherapy were alive at 4 years. Twenty-five percent of patients had their tumors excised prior to chemotherapy and were alive anywhere from 3 years to more than 26 years after treatment.

Histology and gene expression

To build upon these findings, Dr Cunningham set her sights on patient samples. She was able to obtain paraffin blocks of leukemic breast tumors from 25 patients and perform immunohistochemical staining.

“It became clear that the leukemic tumors—which are marked by leukemic markers and not breast cancer markers—look, histologically, like breast cancer, specifically, lobular breast cancer,” Dr Cunningham said. “An additional pathologic finding was a specific type of desmoplastic fibrosis seen in all 25 contributed biopsies.”

Dr Cunningham also performed gene expression studies on 3 of the tumors (2 ALL and 1 AML), which were collected 8 months to 22 months after diagnosis, while marrows were in remission. The analyses revealed that a number of genes are significantly upregulated in both leukemic breast tumors and breast cancer.

 

 

These include genes involved in adhesion and interactions with the extracellular matrix (ADAM8, COMP, and CDH22), genes involved in the ubiquitin-proteasome pathway (UBE2S, USP32, MDM2, and UBE2C), genes encoding for kinases (MAP4K1, PIM1, and NEK2), and genes involved in RAS signaling (RANBP1 and RAB10).

Conclusions and next steps

“It seems that there’s some kind of crosstalk between the organ microenvironment and leukemic cells that make the leukemic cells have the phenotype of breast cancer,” Dr Cunningham said. “And it may well be that relapse sometimes results from the presence of an undiagnosed collection of these cells.”

Therefore, Dr Cunningham suggests performing scans in treatment-resistant leukemia patients. If a patient relapses, and particularly if lactic dehydrogenase levels are increased, a scan might be in order.

“If we can recognize these tumors and cut them out, the patient could be cured, because we’re successful at treating the bone marrow,” Dr Cunningham said. “We’ve had very good bone marrow drugs for 50 years.”

For her part, Dr Cunningham is delving further into this phenomenon. She is now conducting gene expression studies on the rest of the 25 leukemic breast tumor samples and comparing these tumors to breast cancer to identify the most significant dysregulated genes in both entities. The long-term goal is to find a way to predict which patients will develop leukemic breast tumors.

*Information in the abstract differs from that presented at the meeting.

SAN DIEGO—One woman’s curiosity and self-described “aggressive” approach to research have led to some unexpected discoveries about acute leukemias.

Isabel Cunningham, MD, of Columbia University in New York, has found evidence to suggest that treatment resistance in leukemia patients may sometimes result from an interaction between leukemic cells and the breast.

She discovered that leukemic cells in extramedullary niches can adopt a tumor phenotype similar to breast cancer.

And many genes are similarly upregulated in leukemic and epithelial breast tumors.

Her research indicates that a new approach to resistant leukemias that incorporates the principles of solid-tumor treatment—scans to identify any tumors and surgery to remove them—could decrease marrow relapse and death.

Dr Cunningham and her colleagues presented these findings in a poster at the AACR Annual Meeting 2014 (abstract 3996*).

“Chemotherapy resistance is our main problem in treating leukemia,” Dr Cunningham said. “It’s been known for a long time that, occasionally, leukemia forms tumors in an organ, but there’s never been a unified approach to treatment, except for leukemia that occurs in the testis and the meninges.”

Dr Cunningham had encountered many patients with resistant leukemia throughout her career, but her research actually began with a patient she had never met. A case study of a leukemia patient with a breast tumor sparked Dr Cunningham’s interest, and she emailed the study’s author to find out what ultimately became of the patient.

The response she received peaked her curiosity further. So she began seeking more of these cases, contacting authors, and collecting information on this phenomenon.

“I took this on as sort of a hobby,” Dr Cunningham said. “I never had any idea where this was going to lead.”

Eventually, she had amassed information on 235 cases—163 patients with acute myeloid leukemia (AML) and 72 with acute lymphoblastic leukemia (ALL)—who ranged from 1 year to 75 years of age. And an analysis of these cases led to some surprising discoveries.

Clinical findings

Dr Cunningham found these leukemic breast tumors can occur before, during, or after marrow leukemia. And, clinically, they resemble breast cancer. Most tumors were palpable, and some were detected only on routine mammograms.

There were single or multiple nodules that may have involved the entire breast. Sixty percent of cases were unilateral on presentation, but, often, the other breast became involved. Seventy percent of cases exhibited axillary lymphadenopathy that was ipsilateral.

Most tumors grew rapidly, to as large as 12 cm. The tumor behavior was similar in AML and ALL. And the tumors had a metastatic pattern similar to lobular breast cancer—spreading to the contralateral breast, the abdomen or pelvis, the meninges, and culminating in death.

However, some patients did survive. Four percent of patients who were treated only with chemotherapy were alive at 4 years. Twenty-five percent of patients had their tumors excised prior to chemotherapy and were alive anywhere from 3 years to more than 26 years after treatment.

Histology and gene expression

To build upon these findings, Dr Cunningham set her sights on patient samples. She was able to obtain paraffin blocks of leukemic breast tumors from 25 patients and perform immunohistochemical staining.

“It became clear that the leukemic tumors—which are marked by leukemic markers and not breast cancer markers—look, histologically, like breast cancer, specifically, lobular breast cancer,” Dr Cunningham said. “An additional pathologic finding was a specific type of desmoplastic fibrosis seen in all 25 contributed biopsies.”

Dr Cunningham also performed gene expression studies on 3 of the tumors (2 ALL and 1 AML), which were collected 8 months to 22 months after diagnosis, while marrows were in remission. The analyses revealed that a number of genes are significantly upregulated in both leukemic breast tumors and breast cancer.

 

 

These include genes involved in adhesion and interactions with the extracellular matrix (ADAM8, COMP, and CDH22), genes involved in the ubiquitin-proteasome pathway (UBE2S, USP32, MDM2, and UBE2C), genes encoding for kinases (MAP4K1, PIM1, and NEK2), and genes involved in RAS signaling (RANBP1 and RAB10).

Conclusions and next steps

“It seems that there’s some kind of crosstalk between the organ microenvironment and leukemic cells that make the leukemic cells have the phenotype of breast cancer,” Dr Cunningham said. “And it may well be that relapse sometimes results from the presence of an undiagnosed collection of these cells.”

Therefore, Dr Cunningham suggests performing scans in treatment-resistant leukemia patients. If a patient relapses, and particularly if lactic dehydrogenase levels are increased, a scan might be in order.

“If we can recognize these tumors and cut them out, the patient could be cured, because we’re successful at treating the bone marrow,” Dr Cunningham said. “We’ve had very good bone marrow drugs for 50 years.”

For her part, Dr Cunningham is delving further into this phenomenon. She is now conducting gene expression studies on the rest of the 25 leukemic breast tumor samples and comparing these tumors to breast cancer to identify the most significant dysregulated genes in both entities. The long-term goal is to find a way to predict which patients will develop leukemic breast tumors.

*Information in the abstract differs from that presented at the meeting.

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Embedded miRNA, not its host, drives AML, group says

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AML cells

Credit: Lance Liotta

A small gene embedded in a larger gene appears to be the driving force behind acute myeloid leukemia (AML) development, according to research published in Science Signaling.

The smaller gene, microRNA-3151 (miR-3151), is embedded in intron 1 of the larger gene, BAALC.

As both genes have been associated with poor prognosis in AML, researchers wanted to determine the degree to which each of the genes contributes to AML.

“We discovered that the smaller microRNA gene, and not the larger host gene, is the major oncogenic driver of the 2 molecules in AML,” said principal investigator Albert de la Chapelle, MD, PhD, of The Ohio State University Comprehensive Cancer Center (OSUCCC) in Columbus.

“When both genes are highly expressed, it means a bad prognosis for patients, but our experiments indicate that it is high expression of miR-3151 that really matters. Overexpression of BAALC alone had only limited cancer-causing activity.”

Dr de la Chapelle and his colleagues used AML cells derived from patients, AML cell lines, and an animal model of the disease to investigate the role of miR-3151 and BAALC in older patients with cytogenetically normal AML.

The team found that miR-3151 promotes leukemia development by targeting the tumor suppressor TP53 and 7 other genes in the TP53 pathway.

“When miR-3151 blocks TP53 in the tumor cells, it enables the cells to survive, divide, and grow faster,” said study author Clara D. Bloomfield, MD, of OSUCCC.

Experiments also showed that overexpressing miR-3151 promotes AML cell growth. BAALC overexpression enhances that effect, but blocking miR-3151 or overexpressing TP53 reverses it.

In mice, miR-3151 alone and in combination with BAALC promoted leukemia development.

Finally, the researchers discovered that miR-3151 overexpression can be inhibited by the proteasome inhibitor bortezomib, which suggests a possible therapy for miR-3151 overexpression.

“About one-third of the several hundred known human microRNAs are encoded in host genes,” said study author Ann-Kathrin Eisfeld, MD, of OSUCCC.

“We know very little about how microRNAs located within introns are regulated and how they interact with their host genes. These findings provide an important example of that interaction.”

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AML cells

Credit: Lance Liotta

A small gene embedded in a larger gene appears to be the driving force behind acute myeloid leukemia (AML) development, according to research published in Science Signaling.

The smaller gene, microRNA-3151 (miR-3151), is embedded in intron 1 of the larger gene, BAALC.

As both genes have been associated with poor prognosis in AML, researchers wanted to determine the degree to which each of the genes contributes to AML.

“We discovered that the smaller microRNA gene, and not the larger host gene, is the major oncogenic driver of the 2 molecules in AML,” said principal investigator Albert de la Chapelle, MD, PhD, of The Ohio State University Comprehensive Cancer Center (OSUCCC) in Columbus.

“When both genes are highly expressed, it means a bad prognosis for patients, but our experiments indicate that it is high expression of miR-3151 that really matters. Overexpression of BAALC alone had only limited cancer-causing activity.”

Dr de la Chapelle and his colleagues used AML cells derived from patients, AML cell lines, and an animal model of the disease to investigate the role of miR-3151 and BAALC in older patients with cytogenetically normal AML.

The team found that miR-3151 promotes leukemia development by targeting the tumor suppressor TP53 and 7 other genes in the TP53 pathway.

“When miR-3151 blocks TP53 in the tumor cells, it enables the cells to survive, divide, and grow faster,” said study author Clara D. Bloomfield, MD, of OSUCCC.

Experiments also showed that overexpressing miR-3151 promotes AML cell growth. BAALC overexpression enhances that effect, but blocking miR-3151 or overexpressing TP53 reverses it.

In mice, miR-3151 alone and in combination with BAALC promoted leukemia development.

Finally, the researchers discovered that miR-3151 overexpression can be inhibited by the proteasome inhibitor bortezomib, which suggests a possible therapy for miR-3151 overexpression.

“About one-third of the several hundred known human microRNAs are encoded in host genes,” said study author Ann-Kathrin Eisfeld, MD, of OSUCCC.

“We know very little about how microRNAs located within introns are regulated and how they interact with their host genes. These findings provide an important example of that interaction.”

AML cells

Credit: Lance Liotta

A small gene embedded in a larger gene appears to be the driving force behind acute myeloid leukemia (AML) development, according to research published in Science Signaling.

The smaller gene, microRNA-3151 (miR-3151), is embedded in intron 1 of the larger gene, BAALC.

As both genes have been associated with poor prognosis in AML, researchers wanted to determine the degree to which each of the genes contributes to AML.

“We discovered that the smaller microRNA gene, and not the larger host gene, is the major oncogenic driver of the 2 molecules in AML,” said principal investigator Albert de la Chapelle, MD, PhD, of The Ohio State University Comprehensive Cancer Center (OSUCCC) in Columbus.

“When both genes are highly expressed, it means a bad prognosis for patients, but our experiments indicate that it is high expression of miR-3151 that really matters. Overexpression of BAALC alone had only limited cancer-causing activity.”

Dr de la Chapelle and his colleagues used AML cells derived from patients, AML cell lines, and an animal model of the disease to investigate the role of miR-3151 and BAALC in older patients with cytogenetically normal AML.

The team found that miR-3151 promotes leukemia development by targeting the tumor suppressor TP53 and 7 other genes in the TP53 pathway.

“When miR-3151 blocks TP53 in the tumor cells, it enables the cells to survive, divide, and grow faster,” said study author Clara D. Bloomfield, MD, of OSUCCC.

Experiments also showed that overexpressing miR-3151 promotes AML cell growth. BAALC overexpression enhances that effect, but blocking miR-3151 or overexpressing TP53 reverses it.

In mice, miR-3151 alone and in combination with BAALC promoted leukemia development.

Finally, the researchers discovered that miR-3151 overexpression can be inhibited by the proteasome inhibitor bortezomib, which suggests a possible therapy for miR-3151 overexpression.

“About one-third of the several hundred known human microRNAs are encoded in host genes,” said study author Ann-Kathrin Eisfeld, MD, of OSUCCC.

“We know very little about how microRNAs located within introns are regulated and how they interact with their host genes. These findings provide an important example of that interaction.”

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FDA proposes new program for medical devices

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Researcher tests how a medical

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Credit: FDA

The US Food and Drug Administration (FDA) is proposing a new program to provide patients with earlier access to high-risk medical devices intended to treat or diagnose serious conditions whose medical needs are unmet by current technology.

The proposed program is called Expedited Access Premarket Approval Application for Unmet Medical Needs for Life Threatening or Irreversibly Debilitating Diseases or Conditions (shortened to EAP).

The goal of EAP is to reduce the time for premarket review of a device and the time associated with product development.

EAP allows for earlier and more interactive engagement with FDA staff, including the involvement of senior management and a plan for collecting the scientific and clinical data to support approval. The FDA says these features should help provide patients with earlier access to safe and effective medical devices.

To be eligible for participation in the program, a medical device must:

• Be intended to treat or diagnose a life-threatening or irreversibly-debilitating disease or condition

• Have an acceptable data development plan that has been approved by the FDA

• Represent 1 of the following:

1. No approved alternative treatment/diagnostic exists

2. A breakthrough technology that provides a clinically meaningful advantage over existing technology

3. Offers a significant, clinically meaningful advantage over existing approved alternatives

4. Availability is in the patient’s best interest.

In addition to the EAP, the FDA published a separate draft guidance that outlines the agency’s current policy on when data can be collected after product approval and what actions are available to the FDA if approval conditions, such as postmarket data collection, are not met.

Included in the guidance is advice on the use of surrogate or independent markers to support approval, similar to the data points used for accelerated approval of prescription drugs.

The FDA is seeking public comment on both documents:

Expedited Access for Premarket Approval Medical Devices Intended for Unmet Medical Need for Life Threatening or Irreversibly Debilitating Diseases or Conditions - Draft Guidance for Industry and FDA Staff

Balancing Premarket and Postmarket Data Collection for Devices Subject to Premarket Approval - Draft Guidance for Industry and FDA Staff.

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device responds to stress

Credit: FDA

The US Food and Drug Administration (FDA) is proposing a new program to provide patients with earlier access to high-risk medical devices intended to treat or diagnose serious conditions whose medical needs are unmet by current technology.

The proposed program is called Expedited Access Premarket Approval Application for Unmet Medical Needs for Life Threatening or Irreversibly Debilitating Diseases or Conditions (shortened to EAP).

The goal of EAP is to reduce the time for premarket review of a device and the time associated with product development.

EAP allows for earlier and more interactive engagement with FDA staff, including the involvement of senior management and a plan for collecting the scientific and clinical data to support approval. The FDA says these features should help provide patients with earlier access to safe and effective medical devices.

To be eligible for participation in the program, a medical device must:

• Be intended to treat or diagnose a life-threatening or irreversibly-debilitating disease or condition

• Have an acceptable data development plan that has been approved by the FDA

• Represent 1 of the following:

1. No approved alternative treatment/diagnostic exists

2. A breakthrough technology that provides a clinically meaningful advantage over existing technology

3. Offers a significant, clinically meaningful advantage over existing approved alternatives

4. Availability is in the patient’s best interest.

In addition to the EAP, the FDA published a separate draft guidance that outlines the agency’s current policy on when data can be collected after product approval and what actions are available to the FDA if approval conditions, such as postmarket data collection, are not met.

Included in the guidance is advice on the use of surrogate or independent markers to support approval, similar to the data points used for accelerated approval of prescription drugs.

The FDA is seeking public comment on both documents:

Expedited Access for Premarket Approval Medical Devices Intended for Unmet Medical Need for Life Threatening or Irreversibly Debilitating Diseases or Conditions - Draft Guidance for Industry and FDA Staff

Balancing Premarket and Postmarket Data Collection for Devices Subject to Premarket Approval - Draft Guidance for Industry and FDA Staff.

Researcher tests how a medical

device responds to stress

Credit: FDA

The US Food and Drug Administration (FDA) is proposing a new program to provide patients with earlier access to high-risk medical devices intended to treat or diagnose serious conditions whose medical needs are unmet by current technology.

The proposed program is called Expedited Access Premarket Approval Application for Unmet Medical Needs for Life Threatening or Irreversibly Debilitating Diseases or Conditions (shortened to EAP).

The goal of EAP is to reduce the time for premarket review of a device and the time associated with product development.

EAP allows for earlier and more interactive engagement with FDA staff, including the involvement of senior management and a plan for collecting the scientific and clinical data to support approval. The FDA says these features should help provide patients with earlier access to safe and effective medical devices.

To be eligible for participation in the program, a medical device must:

• Be intended to treat or diagnose a life-threatening or irreversibly-debilitating disease or condition

• Have an acceptable data development plan that has been approved by the FDA

• Represent 1 of the following:

1. No approved alternative treatment/diagnostic exists

2. A breakthrough technology that provides a clinically meaningful advantage over existing technology

3. Offers a significant, clinically meaningful advantage over existing approved alternatives

4. Availability is in the patient’s best interest.

In addition to the EAP, the FDA published a separate draft guidance that outlines the agency’s current policy on when data can be collected after product approval and what actions are available to the FDA if approval conditions, such as postmarket data collection, are not met.

Included in the guidance is advice on the use of surrogate or independent markers to support approval, similar to the data points used for accelerated approval of prescription drugs.

The FDA is seeking public comment on both documents:

Expedited Access for Premarket Approval Medical Devices Intended for Unmet Medical Need for Life Threatening or Irreversibly Debilitating Diseases or Conditions - Draft Guidance for Industry and FDA Staff

Balancing Premarket and Postmarket Data Collection for Devices Subject to Premarket Approval - Draft Guidance for Industry and FDA Staff.

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Protein helps HSP90 inhibitors fight cancers

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Drug release in a cancer cell

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Researchers have discovered how a molecule called CUL5 helps HSP90 inhibitors kill cancer cells, according to a study published in Proceedings of the National Academy of Sciences.

The team found that CUL5 is required for the degradation of proteins that promote cancer cell proliferation, and CUL5 works in opposition to HSP90.

When cancer cells are treated with HSP90 inhibitors, CUL5 immediately steps in to help dispose of the proliferation-promoting proteins.

Based on these findings, the researchers speculate that some patients may be resistant to HSP90 inhibitors if their cancer cells have lower amounts of CUL5. And conversely, the drugs may work better in patients with higher CUL5 levels.

Paul Workman, PhD, of The Institute of Cancer Research in London, UK, and his colleagues conducted this research in cell lines of melanoma, as well as colon, breast, and lung cancers.

They first tested the HSP90 inhibitor 17-AAG in HT29 cells and found that CUL5 is involved in the drug-induced degradation of several protein kinase clients of HSP90.

Then, the researchers assessed the effects of silencing CUL5 and discovered that it delays the abrogation of protein signaling caused by an HSP90 inhibitor.

Furthermore, silencing CUL5 reduced cellular sensitivity to 3 different HSP90 inhibitors across the 4 different cancer types studied, which, as the researchers pointed out, are driven by different protein kinases.

So the team believes this research could apply to a number of different cancers. HSP90 inhibitors have proven effective against a range of malignancies, including leukemias, lymphomas, and multiple myeloma.

“We’ve known for some time that drugs that block HSP90 have great potential as treatments for cancers . . . , and we had an initial clue that the protein CUL5 may be involved in some way in how these drugs work,” Dr Workman said.

“Our new research shows that CUL5 is not only vital in the response of cancer cells to HSP90 inhibitors but also reveals surprising insights into precisely how it works by acting at several different levels. What also surprised us was that CUL5 gets rid of many more of the cancer-causing proteins than we’d previously imagined and that it’s effective across several types of tumor.”

“This suggests that a test for CUL5 in patients could help us tell whether they might respond to HSP90-blocking drugs, as well as pointing to new targets to develop more effective drugs.”

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Topics

Drug release in a cancer cell

Credit: PNAS

Researchers have discovered how a molecule called CUL5 helps HSP90 inhibitors kill cancer cells, according to a study published in Proceedings of the National Academy of Sciences.

The team found that CUL5 is required for the degradation of proteins that promote cancer cell proliferation, and CUL5 works in opposition to HSP90.

When cancer cells are treated with HSP90 inhibitors, CUL5 immediately steps in to help dispose of the proliferation-promoting proteins.

Based on these findings, the researchers speculate that some patients may be resistant to HSP90 inhibitors if their cancer cells have lower amounts of CUL5. And conversely, the drugs may work better in patients with higher CUL5 levels.

Paul Workman, PhD, of The Institute of Cancer Research in London, UK, and his colleagues conducted this research in cell lines of melanoma, as well as colon, breast, and lung cancers.

They first tested the HSP90 inhibitor 17-AAG in HT29 cells and found that CUL5 is involved in the drug-induced degradation of several protein kinase clients of HSP90.

Then, the researchers assessed the effects of silencing CUL5 and discovered that it delays the abrogation of protein signaling caused by an HSP90 inhibitor.

Furthermore, silencing CUL5 reduced cellular sensitivity to 3 different HSP90 inhibitors across the 4 different cancer types studied, which, as the researchers pointed out, are driven by different protein kinases.

So the team believes this research could apply to a number of different cancers. HSP90 inhibitors have proven effective against a range of malignancies, including leukemias, lymphomas, and multiple myeloma.

“We’ve known for some time that drugs that block HSP90 have great potential as treatments for cancers . . . , and we had an initial clue that the protein CUL5 may be involved in some way in how these drugs work,” Dr Workman said.

“Our new research shows that CUL5 is not only vital in the response of cancer cells to HSP90 inhibitors but also reveals surprising insights into precisely how it works by acting at several different levels. What also surprised us was that CUL5 gets rid of many more of the cancer-causing proteins than we’d previously imagined and that it’s effective across several types of tumor.”

“This suggests that a test for CUL5 in patients could help us tell whether they might respond to HSP90-blocking drugs, as well as pointing to new targets to develop more effective drugs.”

Drug release in a cancer cell

Credit: PNAS

Researchers have discovered how a molecule called CUL5 helps HSP90 inhibitors kill cancer cells, according to a study published in Proceedings of the National Academy of Sciences.

The team found that CUL5 is required for the degradation of proteins that promote cancer cell proliferation, and CUL5 works in opposition to HSP90.

When cancer cells are treated with HSP90 inhibitors, CUL5 immediately steps in to help dispose of the proliferation-promoting proteins.

Based on these findings, the researchers speculate that some patients may be resistant to HSP90 inhibitors if their cancer cells have lower amounts of CUL5. And conversely, the drugs may work better in patients with higher CUL5 levels.

Paul Workman, PhD, of The Institute of Cancer Research in London, UK, and his colleagues conducted this research in cell lines of melanoma, as well as colon, breast, and lung cancers.

They first tested the HSP90 inhibitor 17-AAG in HT29 cells and found that CUL5 is involved in the drug-induced degradation of several protein kinase clients of HSP90.

Then, the researchers assessed the effects of silencing CUL5 and discovered that it delays the abrogation of protein signaling caused by an HSP90 inhibitor.

Furthermore, silencing CUL5 reduced cellular sensitivity to 3 different HSP90 inhibitors across the 4 different cancer types studied, which, as the researchers pointed out, are driven by different protein kinases.

So the team believes this research could apply to a number of different cancers. HSP90 inhibitors have proven effective against a range of malignancies, including leukemias, lymphomas, and multiple myeloma.

“We’ve known for some time that drugs that block HSP90 have great potential as treatments for cancers . . . , and we had an initial clue that the protein CUL5 may be involved in some way in how these drugs work,” Dr Workman said.

“Our new research shows that CUL5 is not only vital in the response of cancer cells to HSP90 inhibitors but also reveals surprising insights into precisely how it works by acting at several different levels. What also surprised us was that CUL5 gets rid of many more of the cancer-causing proteins than we’d previously imagined and that it’s effective across several types of tumor.”

“This suggests that a test for CUL5 in patients could help us tell whether they might respond to HSP90-blocking drugs, as well as pointing to new targets to develop more effective drugs.”

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Keep an eye on the HPV p16 protein in head and neck cancer

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At the 2014 Multidisciplinary Head and Neck Cancer Symposium in Scottsdale, Arizona, experts presented their findings on novel therapies and surgical and radiotherapeutic techniques with a view to improving outcomes, refining supportive care, and easing toxicity. Neil Osterweil reported from the symposium, which was sponsored by the American Society for Radiation Oncology, the American Society of Clinical Oncology, and the American Head & Neck Society...

 

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At the 2014 Multidisciplinary Head and Neck Cancer Symposium in Scottsdale, Arizona, experts presented their findings on novel therapies and surgical and radiotherapeutic techniques with a view to improving outcomes, refining supportive care, and easing toxicity. Neil Osterweil reported from the symposium, which was sponsored by the American Society for Radiation Oncology, the American Society of Clinical Oncology, and the American Head & Neck Society...

 

Click on the PDF icon at the top of this introduction to read the full article.

 

At the 2014 Multidisciplinary Head and Neck Cancer Symposium in Scottsdale, Arizona, experts presented their findings on novel therapies and surgical and radiotherapeutic techniques with a view to improving outcomes, refining supportive care, and easing toxicity. Neil Osterweil reported from the symposium, which was sponsored by the American Society for Radiation Oncology, the American Society of Clinical Oncology, and the American Head & Neck Society...

 

Click on the PDF icon at the top of this introduction to read the full article.

 

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The late effects of cancer and cancer treatment: a rapid review

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The late effects of cancer and cancer treatment: a rapid review
This paper aims to synthesize literature about the definition, prevalence, onset and treatments associated with late effects. A rapid review was conducted using Google Scholar to identify reviews related to the late effects of adult-onset cancers. Papers were included if they provided a definition of late effects and/or presented a review of late effects as a result of adult-onset cancers in patients aged 18 years or older. Reviews related to nonmelanoma skin cancer were excluded. Reviews focusing on late effects in survivors of childhood-onset cancers (younger than 18 years) were ineligible for inclusion in the review. A total of 16 reviews were identified. Between 0% and 100% of survivors experienced a range of physical, psychological and social late effects.
 

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This paper aims to synthesize literature about the definition, prevalence, onset and treatments associated with late effects. A rapid review was conducted using Google Scholar to identify reviews related to the late effects of adult-onset cancers. Papers were included if they provided a definition of late effects and/or presented a review of late effects as a result of adult-onset cancers in patients aged 18 years or older. Reviews related to nonmelanoma skin cancer were excluded. Reviews focusing on late effects in survivors of childhood-onset cancers (younger than 18 years) were ineligible for inclusion in the review. A total of 16 reviews were identified. Between 0% and 100% of survivors experienced a range of physical, psychological and social late effects.
 

Click on the PDF icon at the top of this introduction to read the full article.

 

This paper aims to synthesize literature about the definition, prevalence, onset and treatments associated with late effects. A rapid review was conducted using Google Scholar to identify reviews related to the late effects of adult-onset cancers. Papers were included if they provided a definition of late effects and/or presented a review of late effects as a result of adult-onset cancers in patients aged 18 years or older. Reviews related to nonmelanoma skin cancer were excluded. Reviews focusing on late effects in survivors of childhood-onset cancers (younger than 18 years) were ineligible for inclusion in the review. A total of 16 reviews were identified. Between 0% and 100% of survivors experienced a range of physical, psychological and social late effects.
 

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Pinterest as a marketing tool

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My wife and I recently (and successfully) had our kitchen and bathrooms remodeled. It wouldn’t have been possible without Pinterest.

For the uninitiated, Pinterest is a wildly popular social media site that allows users to find, share, and organize images called "pins." Pinterest launched in September 2010, and today it has more than 70 million active users. It’s one of the fastest-growing social media sites in history, and it ranks as one of the Top 50 most-visited websites in the United States.

In a previous column about Pinterest, I mentioned several reasons why it’s important for your medical practice. More than 80% of Pinterest users are female, and, according to the U.S. Department of Labor, women make 80% of health care decisions for their families. Therefore, Pinterest could be a persuasive marketing tool for physicians looking to expand their practices. Pinterest also can be an effective platform to share patient stories, to introduce your practice and staff to the public, and to show before and after images of medical procedures.

New research from Vision Critical, the world’s leading provider of Insight Communities, discovered a surprising new finding about Pinterest (published in the July-August 2013 issue of Harvard Business Review).

The researchers examined "showrooming," a phenomenon whereby shoppers visit actual stores to examine merchandise before purchasing it online. They say the threat is so intense to brick-and-mortar stores that at least one merchant has begun charging people to browse in his store! Their research, however, shows much less of a threat. Of the 3,000 social media users they surveyed, only 26% reported "regularly engaging in showrooming."

What they found more surprising was that 41% of respondents said that practice "reverse showrooming;" that is, they browse online first then purchase the product in a store. That’s exactly what my wife did when choosing and purchasing our new furniture, lighting fixtures, wallpaper, paint, and more.

This led me to contemplate how "reverse showrooming" might help a physician market his or her medical practice. First, understand that Pinterest relies on aspirational messaging. Marketers use images that tap into our desires, wants, and dreams. Pinterest typically represents our idealized selves – the fashion-forward woman, the perfect garden wedding, the sublime oceanfront hotel room. Pinterest is about the version of you that you want to become. The you with flawless skin, lustrous hair, and smooth thighs.

Pinterest can be a powerful marketing tool for dermatologists, particularly cosmetic dermatologists. Consider the Pinterest customer base: Data show that 83% of Pinterest users are female and 45% are aged 35-54 years. Consumers turn to Pinterest largely for fashion and beauty, DIY projects, home design, inspiration, education, humor, and product recommendations. In fact, Pinterest has become the No. 1 traffic driver to websites of women’s lifestyle magazines.

You can use Pinterest to drive traffic to your office website, where people can book appointments or buy products online. Although no formal data exist for physician referrals from Pinterest, the study showed that the social-to-sale purchasing power was 17% for hair and beauty products and women’s and men’s apparel.

How can Pinterest help you market your practice and encourage "pinners" to "reverse showroom" into your office? Let’s use the example of a cosmetic surgeon who is seeking to expand her patient base and promote her organic skincare product line.

Pinterest users are more likely to purchase items that are easy to find. So, if they’re looking for an organic sunscreen, and they click through the Pinterest image the doctor posted and land on her website where they can buy it, then they’ll be more apt to do so. Research shows that the likelihood of a purchase increases by an additional 34% when there are existing reviews and recommendations for the product, and 30% when there are product details provided.

Pins don’t have to be strictly medical; consider more purely social boards that relate to your specialty, such as the following examples:

Family practice doctors could use Pinterest for wellness promotion, with boards for spreading happiness, healthy recipes, and habits of healthy families. Oncologists could use Pinterest to share inspirational patient testimonials, best foods for chemotherapy patients, and support for caregivers. Ob.gyns could use Pinterest as an outreach tool for expectant and new moms with boards for breast-feeding tutorials, fashionable maternity clothing, and cool baby gear.

Pinterest has proven to deliver value to businesses. With the above recommendations, you can quickly and cost-effectively add this platform to your marketing and patient relationship efforts.

Dr. Jeffrey Benabio is a partner physician in the department of dermatology of the Southern California Permanente Group in San Diego and a volunteer clinical assistant professor at the University of California, San Diego. Dr. Benabio is @Dermdoc on Twitter.

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My wife and I recently (and successfully) had our kitchen and bathrooms remodeled. It wouldn’t have been possible without Pinterest.

For the uninitiated, Pinterest is a wildly popular social media site that allows users to find, share, and organize images called "pins." Pinterest launched in September 2010, and today it has more than 70 million active users. It’s one of the fastest-growing social media sites in history, and it ranks as one of the Top 50 most-visited websites in the United States.

In a previous column about Pinterest, I mentioned several reasons why it’s important for your medical practice. More than 80% of Pinterest users are female, and, according to the U.S. Department of Labor, women make 80% of health care decisions for their families. Therefore, Pinterest could be a persuasive marketing tool for physicians looking to expand their practices. Pinterest also can be an effective platform to share patient stories, to introduce your practice and staff to the public, and to show before and after images of medical procedures.

New research from Vision Critical, the world’s leading provider of Insight Communities, discovered a surprising new finding about Pinterest (published in the July-August 2013 issue of Harvard Business Review).

The researchers examined "showrooming," a phenomenon whereby shoppers visit actual stores to examine merchandise before purchasing it online. They say the threat is so intense to brick-and-mortar stores that at least one merchant has begun charging people to browse in his store! Their research, however, shows much less of a threat. Of the 3,000 social media users they surveyed, only 26% reported "regularly engaging in showrooming."

What they found more surprising was that 41% of respondents said that practice "reverse showrooming;" that is, they browse online first then purchase the product in a store. That’s exactly what my wife did when choosing and purchasing our new furniture, lighting fixtures, wallpaper, paint, and more.

This led me to contemplate how "reverse showrooming" might help a physician market his or her medical practice. First, understand that Pinterest relies on aspirational messaging. Marketers use images that tap into our desires, wants, and dreams. Pinterest typically represents our idealized selves – the fashion-forward woman, the perfect garden wedding, the sublime oceanfront hotel room. Pinterest is about the version of you that you want to become. The you with flawless skin, lustrous hair, and smooth thighs.

Pinterest can be a powerful marketing tool for dermatologists, particularly cosmetic dermatologists. Consider the Pinterest customer base: Data show that 83% of Pinterest users are female and 45% are aged 35-54 years. Consumers turn to Pinterest largely for fashion and beauty, DIY projects, home design, inspiration, education, humor, and product recommendations. In fact, Pinterest has become the No. 1 traffic driver to websites of women’s lifestyle magazines.

You can use Pinterest to drive traffic to your office website, where people can book appointments or buy products online. Although no formal data exist for physician referrals from Pinterest, the study showed that the social-to-sale purchasing power was 17% for hair and beauty products and women’s and men’s apparel.

How can Pinterest help you market your practice and encourage "pinners" to "reverse showroom" into your office? Let’s use the example of a cosmetic surgeon who is seeking to expand her patient base and promote her organic skincare product line.

Pinterest users are more likely to purchase items that are easy to find. So, if they’re looking for an organic sunscreen, and they click through the Pinterest image the doctor posted and land on her website where they can buy it, then they’ll be more apt to do so. Research shows that the likelihood of a purchase increases by an additional 34% when there are existing reviews and recommendations for the product, and 30% when there are product details provided.

Pins don’t have to be strictly medical; consider more purely social boards that relate to your specialty, such as the following examples:

Family practice doctors could use Pinterest for wellness promotion, with boards for spreading happiness, healthy recipes, and habits of healthy families. Oncologists could use Pinterest to share inspirational patient testimonials, best foods for chemotherapy patients, and support for caregivers. Ob.gyns could use Pinterest as an outreach tool for expectant and new moms with boards for breast-feeding tutorials, fashionable maternity clothing, and cool baby gear.

Pinterest has proven to deliver value to businesses. With the above recommendations, you can quickly and cost-effectively add this platform to your marketing and patient relationship efforts.

Dr. Jeffrey Benabio is a partner physician in the department of dermatology of the Southern California Permanente Group in San Diego and a volunteer clinical assistant professor at the University of California, San Diego. Dr. Benabio is @Dermdoc on Twitter.

My wife and I recently (and successfully) had our kitchen and bathrooms remodeled. It wouldn’t have been possible without Pinterest.

For the uninitiated, Pinterest is a wildly popular social media site that allows users to find, share, and organize images called "pins." Pinterest launched in September 2010, and today it has more than 70 million active users. It’s one of the fastest-growing social media sites in history, and it ranks as one of the Top 50 most-visited websites in the United States.

In a previous column about Pinterest, I mentioned several reasons why it’s important for your medical practice. More than 80% of Pinterest users are female, and, according to the U.S. Department of Labor, women make 80% of health care decisions for their families. Therefore, Pinterest could be a persuasive marketing tool for physicians looking to expand their practices. Pinterest also can be an effective platform to share patient stories, to introduce your practice and staff to the public, and to show before and after images of medical procedures.

New research from Vision Critical, the world’s leading provider of Insight Communities, discovered a surprising new finding about Pinterest (published in the July-August 2013 issue of Harvard Business Review).

The researchers examined "showrooming," a phenomenon whereby shoppers visit actual stores to examine merchandise before purchasing it online. They say the threat is so intense to brick-and-mortar stores that at least one merchant has begun charging people to browse in his store! Their research, however, shows much less of a threat. Of the 3,000 social media users they surveyed, only 26% reported "regularly engaging in showrooming."

What they found more surprising was that 41% of respondents said that practice "reverse showrooming;" that is, they browse online first then purchase the product in a store. That’s exactly what my wife did when choosing and purchasing our new furniture, lighting fixtures, wallpaper, paint, and more.

This led me to contemplate how "reverse showrooming" might help a physician market his or her medical practice. First, understand that Pinterest relies on aspirational messaging. Marketers use images that tap into our desires, wants, and dreams. Pinterest typically represents our idealized selves – the fashion-forward woman, the perfect garden wedding, the sublime oceanfront hotel room. Pinterest is about the version of you that you want to become. The you with flawless skin, lustrous hair, and smooth thighs.

Pinterest can be a powerful marketing tool for dermatologists, particularly cosmetic dermatologists. Consider the Pinterest customer base: Data show that 83% of Pinterest users are female and 45% are aged 35-54 years. Consumers turn to Pinterest largely for fashion and beauty, DIY projects, home design, inspiration, education, humor, and product recommendations. In fact, Pinterest has become the No. 1 traffic driver to websites of women’s lifestyle magazines.

You can use Pinterest to drive traffic to your office website, where people can book appointments or buy products online. Although no formal data exist for physician referrals from Pinterest, the study showed that the social-to-sale purchasing power was 17% for hair and beauty products and women’s and men’s apparel.

How can Pinterest help you market your practice and encourage "pinners" to "reverse showroom" into your office? Let’s use the example of a cosmetic surgeon who is seeking to expand her patient base and promote her organic skincare product line.

Pinterest users are more likely to purchase items that are easy to find. So, if they’re looking for an organic sunscreen, and they click through the Pinterest image the doctor posted and land on her website where they can buy it, then they’ll be more apt to do so. Research shows that the likelihood of a purchase increases by an additional 34% when there are existing reviews and recommendations for the product, and 30% when there are product details provided.

Pins don’t have to be strictly medical; consider more purely social boards that relate to your specialty, such as the following examples:

Family practice doctors could use Pinterest for wellness promotion, with boards for spreading happiness, healthy recipes, and habits of healthy families. Oncologists could use Pinterest to share inspirational patient testimonials, best foods for chemotherapy patients, and support for caregivers. Ob.gyns could use Pinterest as an outreach tool for expectant and new moms with boards for breast-feeding tutorials, fashionable maternity clothing, and cool baby gear.

Pinterest has proven to deliver value to businesses. With the above recommendations, you can quickly and cost-effectively add this platform to your marketing and patient relationship efforts.

Dr. Jeffrey Benabio is a partner physician in the department of dermatology of the Southern California Permanente Group in San Diego and a volunteer clinical assistant professor at the University of California, San Diego. Dr. Benabio is @Dermdoc on Twitter.

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Obstetrician-gynecologists play a unique role in screening women for various malignancies, including breast, colon, and cervical carcinoma. Although less common, genetic syndromes also can affect the female reproductive tract; therefore, knowledge of the screening guidelines for the most common genetic syndromes – hereditary breast and ovarian cancer syndrome, hereditary nonpolyposis colorectal cancer syndrome, and Cowden syndrome – is important.

Hereditary breast and ovarian cancer syndrome

Caused by autosomal-dominant deletions in the BRCA1/2 genes, the lifetime risk of ovarian cancer in patients with a BRCA1 and BRCA2 mutation is 39%-46% and 12%-20%, respectively. Although not proven to improve detection or survival, the American College of Obstetricians and Gynecologists (ACOG) and National Comprehensive Cancer Network (NCCN) guidelines recommend that women with BRCA1/2 mutations should undergo screening with transvaginal ultrasonography and CA125 every 6 months beginning between ages 30-35 years or 5-10 years prior to the age of the youngest affected family member. For patients who have not completed childbearing, a recent meta-analysis showed that use of oral contraceptives was associated with a decreased risk of ovarian cancer in patients with BRCA1/2 (J. Clin. Oncol. 2013;31:4188-98). Once childbearing has been completed or at the age of 40 years, a risk-reducing bilateral salpingo-oophorectomy (BSO) should be strongly considered (Gynecol. Oncol. 2009;113:6-11; Obstet. Gynecol. 2011;117:742-6).

In addition, patients with BRCA 1/2 mutations carry a 65%-74% lifetime risk of developing breast cancer (Gynecol. Oncol. 2009;113:6-11).ACOG recommends that these women begin screening for breast cancer at the age of 25 years through semiannual self-breast exams as well as annual mammography and breast MRI or sooner if a family member’s cancer was diagnosed prior to this age. Chemoprevention with tamoxifen also has been shown to reduce the risk of breast cancer in patients with BRCA2 disease, but is less effective for BRCA1 patients. Prophylactic mastectomy has the ability to reduce a woman’s risk of developing breast cancer by 90%-95%.

Hereditary nonpolyposis colorectal cancer syndrome

Another autosomal-dominant disorder, hereditary nonpolyposis colorectal cancer (HNPCC) syndrome arises as a result of a genetic defect in DNA mismatch repair mechanisms. Colon cancer is the most common malignancy associated with this syndrome, with a 70% risk by the age of 70 years (JAMA 2006;296:1507-17). Other associated cancers include those of the urinary tract, hepatobiliary tract, small intestine, skin, and brain, but strong supportive data are lacking. Beginning at age 20-25 years (or 10 years before the age of the youngest family member to develop colon cancer), a colonoscopy is recommended every 1-2 years. Annual urinalysis with cytology is advocated by some as a screening test for urinary tract cancers.

Patients with HNPCC have up to a 60% lifetime risk of endometrial cancer and a 10% risk of ovarian cancer (Int. J. Cancer 1999;81:214-8; Hum. Mol. Gene. 1997;6:105-10). The American Cancer Society recommends an endometrial biopsy and transvaginal ultrasonography annually between 30-35 years of age (JAMA 2006;296:1507-17). Schmeler et al. compared outcomes among 315 women with mismatch repair defects, 61 of whom underwent risk-reducing hysterectomy and BSO. With an average follow-up of greater than 7 years, none of the patients who underwent surgery developed cancer, while 33% of those who did not have surgery developed endometrial cancer and 5.5% developed ovarian cancer (N. Engl. J. Med. 2006;354:261-9). Because of these data, risk-reducing surgery at the age of 35 should be considered.

Cowden Syndrome

Cowden Syndrome, caused by an autosomal-dominant mutation in the PTEN gene, is associated with an up to 10% lifetime risk of endometrial cancer and a 50% risk of breast cancer (Obstet. Gynecol. Clin. N. Am. 2010;37:109-33). The NCCN notes that data are limited, but discussion of endometrial cancer symptoms should be encouraged (NCCN Guidelines Version 4, 2013). Annual endometrial sampling and ultrasound should be considered in woman aged 35-40 years or 10 years earlier than the youngest affected family member (Obstet. Gynecol. Clin. N. Am. 2010;37:109-33). Screening for breast cancer should include annual mammography and breast MRI starting between age 30-35 years or earlier depending on family history, per the NCCN guidelines.

It is important to note that additional genetic syndromes can have repercussions on the female genital tract, including the Li-Fraumeni (ovarian cancer), the Peutz-Jeghers (sex cord–stromal tumors of the ovary, granulosa cell tumors), and the Ollier (granulosa cell tumors) syndromes; unfortunately, screening guidelines for these rare syndromes have not been well studied (JAMA 2006;296:1507-17).

Dr. Schuler is a gynecologic oncologist at Good Samaritan Hospital in Cincinnati. Dr. Gehrig is professor and director of gynecologic oncology at the University of North Carolina at Chapel Hill. Dr. Gehrig and Dr. Schuler said they had no relevant financial disclosures.

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Obstetrician-gynecologists play a unique role in screening women for various malignancies, including breast, colon, and cervical carcinoma. Although less common, genetic syndromes also can affect the female reproductive tract; therefore, knowledge of the screening guidelines for the most common genetic syndromes – hereditary breast and ovarian cancer syndrome, hereditary nonpolyposis colorectal cancer syndrome, and Cowden syndrome – is important.

Hereditary breast and ovarian cancer syndrome

Caused by autosomal-dominant deletions in the BRCA1/2 genes, the lifetime risk of ovarian cancer in patients with a BRCA1 and BRCA2 mutation is 39%-46% and 12%-20%, respectively. Although not proven to improve detection or survival, the American College of Obstetricians and Gynecologists (ACOG) and National Comprehensive Cancer Network (NCCN) guidelines recommend that women with BRCA1/2 mutations should undergo screening with transvaginal ultrasonography and CA125 every 6 months beginning between ages 30-35 years or 5-10 years prior to the age of the youngest affected family member. For patients who have not completed childbearing, a recent meta-analysis showed that use of oral contraceptives was associated with a decreased risk of ovarian cancer in patients with BRCA1/2 (J. Clin. Oncol. 2013;31:4188-98). Once childbearing has been completed or at the age of 40 years, a risk-reducing bilateral salpingo-oophorectomy (BSO) should be strongly considered (Gynecol. Oncol. 2009;113:6-11; Obstet. Gynecol. 2011;117:742-6).

In addition, patients with BRCA 1/2 mutations carry a 65%-74% lifetime risk of developing breast cancer (Gynecol. Oncol. 2009;113:6-11).ACOG recommends that these women begin screening for breast cancer at the age of 25 years through semiannual self-breast exams as well as annual mammography and breast MRI or sooner if a family member’s cancer was diagnosed prior to this age. Chemoprevention with tamoxifen also has been shown to reduce the risk of breast cancer in patients with BRCA2 disease, but is less effective for BRCA1 patients. Prophylactic mastectomy has the ability to reduce a woman’s risk of developing breast cancer by 90%-95%.

Hereditary nonpolyposis colorectal cancer syndrome

Another autosomal-dominant disorder, hereditary nonpolyposis colorectal cancer (HNPCC) syndrome arises as a result of a genetic defect in DNA mismatch repair mechanisms. Colon cancer is the most common malignancy associated with this syndrome, with a 70% risk by the age of 70 years (JAMA 2006;296:1507-17). Other associated cancers include those of the urinary tract, hepatobiliary tract, small intestine, skin, and brain, but strong supportive data are lacking. Beginning at age 20-25 years (or 10 years before the age of the youngest family member to develop colon cancer), a colonoscopy is recommended every 1-2 years. Annual urinalysis with cytology is advocated by some as a screening test for urinary tract cancers.

Patients with HNPCC have up to a 60% lifetime risk of endometrial cancer and a 10% risk of ovarian cancer (Int. J. Cancer 1999;81:214-8; Hum. Mol. Gene. 1997;6:105-10). The American Cancer Society recommends an endometrial biopsy and transvaginal ultrasonography annually between 30-35 years of age (JAMA 2006;296:1507-17). Schmeler et al. compared outcomes among 315 women with mismatch repair defects, 61 of whom underwent risk-reducing hysterectomy and BSO. With an average follow-up of greater than 7 years, none of the patients who underwent surgery developed cancer, while 33% of those who did not have surgery developed endometrial cancer and 5.5% developed ovarian cancer (N. Engl. J. Med. 2006;354:261-9). Because of these data, risk-reducing surgery at the age of 35 should be considered.

Cowden Syndrome

Cowden Syndrome, caused by an autosomal-dominant mutation in the PTEN gene, is associated with an up to 10% lifetime risk of endometrial cancer and a 50% risk of breast cancer (Obstet. Gynecol. Clin. N. Am. 2010;37:109-33). The NCCN notes that data are limited, but discussion of endometrial cancer symptoms should be encouraged (NCCN Guidelines Version 4, 2013). Annual endometrial sampling and ultrasound should be considered in woman aged 35-40 years or 10 years earlier than the youngest affected family member (Obstet. Gynecol. Clin. N. Am. 2010;37:109-33). Screening for breast cancer should include annual mammography and breast MRI starting between age 30-35 years or earlier depending on family history, per the NCCN guidelines.

It is important to note that additional genetic syndromes can have repercussions on the female genital tract, including the Li-Fraumeni (ovarian cancer), the Peutz-Jeghers (sex cord–stromal tumors of the ovary, granulosa cell tumors), and the Ollier (granulosa cell tumors) syndromes; unfortunately, screening guidelines for these rare syndromes have not been well studied (JAMA 2006;296:1507-17).

Dr. Schuler is a gynecologic oncologist at Good Samaritan Hospital in Cincinnati. Dr. Gehrig is professor and director of gynecologic oncology at the University of North Carolina at Chapel Hill. Dr. Gehrig and Dr. Schuler said they had no relevant financial disclosures.

Obstetrician-gynecologists play a unique role in screening women for various malignancies, including breast, colon, and cervical carcinoma. Although less common, genetic syndromes also can affect the female reproductive tract; therefore, knowledge of the screening guidelines for the most common genetic syndromes – hereditary breast and ovarian cancer syndrome, hereditary nonpolyposis colorectal cancer syndrome, and Cowden syndrome – is important.

Hereditary breast and ovarian cancer syndrome

Caused by autosomal-dominant deletions in the BRCA1/2 genes, the lifetime risk of ovarian cancer in patients with a BRCA1 and BRCA2 mutation is 39%-46% and 12%-20%, respectively. Although not proven to improve detection or survival, the American College of Obstetricians and Gynecologists (ACOG) and National Comprehensive Cancer Network (NCCN) guidelines recommend that women with BRCA1/2 mutations should undergo screening with transvaginal ultrasonography and CA125 every 6 months beginning between ages 30-35 years or 5-10 years prior to the age of the youngest affected family member. For patients who have not completed childbearing, a recent meta-analysis showed that use of oral contraceptives was associated with a decreased risk of ovarian cancer in patients with BRCA1/2 (J. Clin. Oncol. 2013;31:4188-98). Once childbearing has been completed or at the age of 40 years, a risk-reducing bilateral salpingo-oophorectomy (BSO) should be strongly considered (Gynecol. Oncol. 2009;113:6-11; Obstet. Gynecol. 2011;117:742-6).

In addition, patients with BRCA 1/2 mutations carry a 65%-74% lifetime risk of developing breast cancer (Gynecol. Oncol. 2009;113:6-11).ACOG recommends that these women begin screening for breast cancer at the age of 25 years through semiannual self-breast exams as well as annual mammography and breast MRI or sooner if a family member’s cancer was diagnosed prior to this age. Chemoprevention with tamoxifen also has been shown to reduce the risk of breast cancer in patients with BRCA2 disease, but is less effective for BRCA1 patients. Prophylactic mastectomy has the ability to reduce a woman’s risk of developing breast cancer by 90%-95%.

Hereditary nonpolyposis colorectal cancer syndrome

Another autosomal-dominant disorder, hereditary nonpolyposis colorectal cancer (HNPCC) syndrome arises as a result of a genetic defect in DNA mismatch repair mechanisms. Colon cancer is the most common malignancy associated with this syndrome, with a 70% risk by the age of 70 years (JAMA 2006;296:1507-17). Other associated cancers include those of the urinary tract, hepatobiliary tract, small intestine, skin, and brain, but strong supportive data are lacking. Beginning at age 20-25 years (or 10 years before the age of the youngest family member to develop colon cancer), a colonoscopy is recommended every 1-2 years. Annual urinalysis with cytology is advocated by some as a screening test for urinary tract cancers.

Patients with HNPCC have up to a 60% lifetime risk of endometrial cancer and a 10% risk of ovarian cancer (Int. J. Cancer 1999;81:214-8; Hum. Mol. Gene. 1997;6:105-10). The American Cancer Society recommends an endometrial biopsy and transvaginal ultrasonography annually between 30-35 years of age (JAMA 2006;296:1507-17). Schmeler et al. compared outcomes among 315 women with mismatch repair defects, 61 of whom underwent risk-reducing hysterectomy and BSO. With an average follow-up of greater than 7 years, none of the patients who underwent surgery developed cancer, while 33% of those who did not have surgery developed endometrial cancer and 5.5% developed ovarian cancer (N. Engl. J. Med. 2006;354:261-9). Because of these data, risk-reducing surgery at the age of 35 should be considered.

Cowden Syndrome

Cowden Syndrome, caused by an autosomal-dominant mutation in the PTEN gene, is associated with an up to 10% lifetime risk of endometrial cancer and a 50% risk of breast cancer (Obstet. Gynecol. Clin. N. Am. 2010;37:109-33). The NCCN notes that data are limited, but discussion of endometrial cancer symptoms should be encouraged (NCCN Guidelines Version 4, 2013). Annual endometrial sampling and ultrasound should be considered in woman aged 35-40 years or 10 years earlier than the youngest affected family member (Obstet. Gynecol. Clin. N. Am. 2010;37:109-33). Screening for breast cancer should include annual mammography and breast MRI starting between age 30-35 years or earlier depending on family history, per the NCCN guidelines.

It is important to note that additional genetic syndromes can have repercussions on the female genital tract, including the Li-Fraumeni (ovarian cancer), the Peutz-Jeghers (sex cord–stromal tumors of the ovary, granulosa cell tumors), and the Ollier (granulosa cell tumors) syndromes; unfortunately, screening guidelines for these rare syndromes have not been well studied (JAMA 2006;296:1507-17).

Dr. Schuler is a gynecologic oncologist at Good Samaritan Hospital in Cincinnati. Dr. Gehrig is professor and director of gynecologic oncology at the University of North Carolina at Chapel Hill. Dr. Gehrig and Dr. Schuler said they had no relevant financial disclosures.

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