SYDNEY - Australia declared on Monday the AIDS epidemic is no longer a public health issue there, a month after the United Nations adopted an ambitious target to eliminate the threat globally by 2030.

The government-backed Australian Federation of AIDS Organisations (AFAO) and top scientists said the number of people being diagnosed with AIDS in Australia was now so small it was no longer reported.

AIDS cases in Australia peaked in 1994, at 953 cases, according to the Kirby Institute for infection and immunity in society.

Since then, following the introduction of antiretroviral treatment, that prevent AIDS developing in people who are infected with the HIV virus, and awareness campaigns, AIDS diagnoses have declined sharply.

"Australia is incredibly fortunate to be in the position and its because of farsighted government policy," said Darryl O'Donnell, chief executive AFAO.

"We had community organizations of gay men, sex workers and drug users doing outreach campaigns that were extraordinarily effective," O'Donnell said.

A spokeswoman for the Federal Department of Health said while it was tremendous that AIDS was "not the automatic death sentence that it once was," approximately 1,100 cases of HIV are detected each year.

"We must not let down our guard."

Worldwide there are 36.7 million people living with HIV, according to the World Health Organisation, with 180,000 people dying from AIDS-related illness in the Asia-Pacific region last year.

The United Nations agreed a new declaration on ending the AIDS epidemic at a meeting in New York last month.

The UNAIDS Fast-Track approach to ending the AIDS epidemic has a set of time-bound targets, including reducing the number of people newly infected with HIV from 2.1 million in 2015 to fewer than 500,000 in 2020, reducing the number of people dying from AIDS-related illnesses from 1.1 million in 2015 to fewer than 500,000 in 2020 and eliminating HIV-related discrimination.

Andrew Grulich, head of the HIV Epidemiology and Prevention Program at the Kirby Institute, said other countries could learn from Australia.

"The thing that has characterized Australia is a partnership between all sectors involved," he said. "Community, research and the government - and having bipartisan political support."

SYDNEY - Australia declared on Monday the AIDS epidemic is no longer a public health issue there, a month after the United Nations adopted an ambitious target to eliminate the threat globally by 2030.

The government-backed Australian Federation of AIDS Organisations (AFAO) and top scientists said the number of people being diagnosed with AIDS in Australia was now so small it was no longer reported.

AIDS cases in Australia peaked in 1994, at 953 cases, according to the Kirby Institute for infection and immunity in society.

Since then, following the introduction of antiretroviral treatment, that prevent AIDS developing in people who are infected with the HIV virus, and awareness campaigns, AIDS diagnoses have declined sharply.

"Australia is incredibly fortunate to be in the position and its because of farsighted government policy," said Darryl O'Donnell, chief executive AFAO.

"We had community organizations of gay men, sex workers and drug users doing outreach campaigns that were extraordinarily effective," O'Donnell said.

A spokeswoman for the Federal Department of Health said while it was tremendous that AIDS was "not the automatic death sentence that it once was," approximately 1,100 cases of HIV are detected each year.

"We must not let down our guard."

Worldwide there are 36.7 million people living with HIV, according to the World Health Organisation, with 180,000 people dying from AIDS-related illness in the Asia-Pacific region last year.

The United Nations agreed a new declaration on ending the AIDS epidemic at a meeting in New York last month.

The UNAIDS Fast-Track approach to ending the AIDS epidemic has a set of time-bound targets, including reducing the number of people newly infected with HIV from 2.1 million in 2015 to fewer than 500,000 in 2020, reducing the number of people dying from AIDS-related illnesses from 1.1 million in 2015 to fewer than 500,000 in 2020 and eliminating HIV-related discrimination.

Andrew Grulich, head of the HIV Epidemiology and Prevention Program at the Kirby Institute, said other countries could learn from Australia.

"The thing that has characterized Australia is a partnership between all sectors involved," he said. "Community, research and the government - and having bipartisan political support."

SYDNEY - Australia declared on Monday the AIDS epidemic is no longer a public health issue there, a month after the United Nations adopted an ambitious target to eliminate the threat globally by 2030.

The government-backed Australian Federation of AIDS Organisations (AFAO) and top scientists said the number of people being diagnosed with AIDS in Australia was now so small it was no longer reported.

AIDS cases in Australia peaked in 1994, at 953 cases, according to the Kirby Institute for infection and immunity in society.

Since then, following the introduction of antiretroviral treatment, that prevent AIDS developing in people who are infected with the HIV virus, and awareness campaigns, AIDS diagnoses have declined sharply.

"Australia is incredibly fortunate to be in the position and its because of farsighted government policy," said Darryl O'Donnell, chief executive AFAO.

"We had community organizations of gay men, sex workers and drug users doing outreach campaigns that were extraordinarily effective," O'Donnell said.

A spokeswoman for the Federal Department of Health said while it was tremendous that AIDS was "not the automatic death sentence that it once was," approximately 1,100 cases of HIV are detected each year.

"We must not let down our guard."

Worldwide there are 36.7 million people living with HIV, according to the World Health Organisation, with 180,000 people dying from AIDS-related illness in the Asia-Pacific region last year.

The United Nations agreed a new declaration on ending the AIDS epidemic at a meeting in New York last month.

The UNAIDS Fast-Track approach to ending the AIDS epidemic has a set of time-bound targets, including reducing the number of people newly infected with HIV from 2.1 million in 2015 to fewer than 500,000 in 2020, reducing the number of people dying from AIDS-related illnesses from 1.1 million in 2015 to fewer than 500,000 in 2020 and eliminating HIV-related discrimination.

Andrew Grulich, head of the HIV Epidemiology and Prevention Program at the Kirby Institute, said other countries could learn from Australia.

"The thing that has characterized Australia is a partnership between all sectors involved," he said. "Community, research and the government - and having bipartisan political support."

A comparison of psoriasis-like eruptions in Kawasaki disease (KD) with classic psoriasis shows a distinct phenotype with greater remission, report Ellen S. Haddock, AB, MBA and coauthors from the School of Medicine at the University of California, San Diego.

Investigators performed a retrospective study of 11 KD cases with a psoriasiform eruption matched by gender, age, and ethnicity with psoriasis-only and KD-only controls. Genotyping was performed in 10 cases for a deletion of two late cornified envelope genes associated with pediatric-onset psoriasis.

KD-associated eruptions were similar to classic psoriasis in presentation, but with less frequent diaper area involvement, more crust, more serious exudate, and significantly higher remission (91% vs. 23%; P less than .001), the authors noted.

The findings indicate that despite similarities to classic psoriasis, “this appears to be a distinct phenotype with significantly greater propensity for remission,” the authors concluded.

Read the full article in the Journal of the American Academy of Dermatology.

A comparison of psoriasis-like eruptions in Kawasaki disease (KD) with classic psoriasis shows a distinct phenotype with greater remission, report Ellen S. Haddock, AB, MBA and coauthors from the School of Medicine at the University of California, San Diego.

Investigators performed a retrospective study of 11 KD cases with a psoriasiform eruption matched by gender, age, and ethnicity with psoriasis-only and KD-only controls. Genotyping was performed in 10 cases for a deletion of two late cornified envelope genes associated with pediatric-onset psoriasis.

KD-associated eruptions were similar to classic psoriasis in presentation, but with less frequent diaper area involvement, more crust, more serious exudate, and significantly higher remission (91% vs. 23%; P less than .001), the authors noted.

The findings indicate that despite similarities to classic psoriasis, “this appears to be a distinct phenotype with significantly greater propensity for remission,” the authors concluded.

Read the full article in the Journal of the American Academy of Dermatology.

A comparison of psoriasis-like eruptions in Kawasaki disease (KD) with classic psoriasis shows a distinct phenotype with greater remission, report Ellen S. Haddock, AB, MBA and coauthors from the School of Medicine at the University of California, San Diego.

Investigators performed a retrospective study of 11 KD cases with a psoriasiform eruption matched by gender, age, and ethnicity with psoriasis-only and KD-only controls. Genotyping was performed in 10 cases for a deletion of two late cornified envelope genes associated with pediatric-onset psoriasis.

KD-associated eruptions were similar to classic psoriasis in presentation, but with less frequent diaper area involvement, more crust, more serious exudate, and significantly higher remission (91% vs. 23%; P less than .001), the authors noted.

The findings indicate that despite similarities to classic psoriasis, “this appears to be a distinct phenotype with significantly greater propensity for remission,” the authors concluded.

Read the full article in the Journal of the American Academy of Dermatology.

Click here to download the PDF.

Click here to download the PDF.

Click here to download the PDF.

We appreciate Dr. Nasrallah referencing our work to assert that “most SGAs are similar to FGAs.” (Current Psychiatry, Comments & Controversies, October 2013, p. 39-40; http://bit.ly/177QOy6). What we actually found in our 2003¹ and 2011² meta-analyses was that “some antipsychotics are more efficacious than others,” and the first-generation antipsychotic vs second-generation antipsychotic distinction is not very useful clinically.³ These findings have repeatedly been replicated.³

John M. Davis, MD
Professor
Department of Psychiatry
University of Illinois at Chicago
Chicago, Illinois

Ira D. Glick, MD
Professor Emeritus of Psychiatry and Behavioral Sciences
Department of Psychiatry
Stanford University School of Medicine
Stanford, California

We appreciate Dr. Nasrallah referencing our work to assert that “most SGAs are similar to FGAs.” (Current Psychiatry, Comments & Controversies, October 2013, p. 39-40; http://bit.ly/177QOy6). What we actually found in our 2003¹ and 2011² meta-analyses was that “some antipsychotics are more efficacious than others,” and the first-generation antipsychotic vs second-generation antipsychotic distinction is not very useful clinically.³ These findings have repeatedly been replicated.³

John M. Davis, MD
Professor
Department of Psychiatry
University of Illinois at Chicago
Chicago, Illinois

Ira D. Glick, MD
Professor Emeritus of Psychiatry and Behavioral Sciences
Department of Psychiatry
Stanford University School of Medicine
Stanford, California

We appreciate Dr. Nasrallah referencing our work to assert that “most SGAs are similar to FGAs.” (Current Psychiatry, Comments & Controversies, October 2013, p. 39-40; http://bit.ly/177QOy6). What we actually found in our 2003¹ and 2011² meta-analyses was that “some antipsychotics are more efficacious than others,” and the first-generation antipsychotic vs second-generation antipsychotic distinction is not very useful clinically.³ These findings have repeatedly been replicated.³

John M. Davis, MD
Professor
Department of Psychiatry
University of Illinois at Chicago
Chicago, Illinois

Ira D. Glick, MD
Professor Emeritus of Psychiatry and Behavioral Sciences
Department of Psychiatry
Stanford University School of Medicine
Stanford, California

Thinking of joining an online physician collaboration network but don't know where to start?

Here is a list of large physician online communities and listservs to help you connect, communicate, and network with your colleagues.

Sermo: This online community of physicians has over 200,000 members in 68 specialties. It is a place where physicians can securely post questions, insights, and observations for discussion.

Medscape Physician Connect: This is another online private community of physicians that has over 170,000 members.

Doximity: This online networking site is similar to LinkedIn, except that is is only for physicians. Users create a profile to connect with colleagues and to access the "nation’s most complete physician directory," according to their website.

DermRounds: This online networking site is the Facebook of dermatology. Users can pose questions, share videos and images, learn about upcoming CME conferences, and more.

RxDerm-L: This listserv group is open to dermatologists and dermatology residents only. To subscribe, send an email to [email protected], and in the body of the message write "subscribe rxderm-L" followed by your name.

ACADERM-L: This listserv group is open to teaching dermatolgists, or dermatologists serving in an administraction for a dermatology program. To subscribe, send an email to [email protected], and in the body of the message write "subscribe acaderm-L" followed by your name.

AMA Listservs: The AMA offers multiple listservs, including ones for residents and fellows and young physicians.

Thinking of joining an online physician collaboration network but don't know where to start?

Here is a list of large physician online communities and listservs to help you connect, communicate, and network with your colleagues.

Sermo: This online community of physicians has over 200,000 members in 68 specialties. It is a place where physicians can securely post questions, insights, and observations for discussion.

Medscape Physician Connect: This is another online private community of physicians that has over 170,000 members.

Doximity: This online networking site is similar to LinkedIn, except that is is only for physicians. Users create a profile to connect with colleagues and to access the "nation’s most complete physician directory," according to their website.

DermRounds: This online networking site is the Facebook of dermatology. Users can pose questions, share videos and images, learn about upcoming CME conferences, and more.

RxDerm-L: This listserv group is open to dermatologists and dermatology residents only. To subscribe, send an email to [email protected], and in the body of the message write "subscribe rxderm-L" followed by your name.

ACADERM-L: This listserv group is open to teaching dermatolgists, or dermatologists serving in an administraction for a dermatology program. To subscribe, send an email to [email protected], and in the body of the message write "subscribe acaderm-L" followed by your name.

AMA Listservs: The AMA offers multiple listservs, including ones for residents and fellows and young physicians.

Thinking of joining an online physician collaboration network but don't know where to start?

Here is a list of large physician online communities and listservs to help you connect, communicate, and network with your colleagues.

Sermo: This online community of physicians has over 200,000 members in 68 specialties. It is a place where physicians can securely post questions, insights, and observations for discussion.

Medscape Physician Connect: This is another online private community of physicians that has over 170,000 members.

Doximity: This online networking site is similar to LinkedIn, except that is is only for physicians. Users create a profile to connect with colleagues and to access the "nation’s most complete physician directory," according to their website.

DermRounds: This online networking site is the Facebook of dermatology. Users can pose questions, share videos and images, learn about upcoming CME conferences, and more.

RxDerm-L: This listserv group is open to dermatologists and dermatology residents only. To subscribe, send an email to [email protected], and in the body of the message write "subscribe rxderm-L" followed by your name.

ACADERM-L: This listserv group is open to teaching dermatolgists, or dermatologists serving in an administraction for a dermatology program. To subscribe, send an email to [email protected], and in the body of the message write "subscribe acaderm-L" followed by your name.

AMA Listservs: The AMA offers multiple listservs, including ones for residents and fellows and young physicians.

According to a CDC study, 59% of physicians use social media networks. 

Do you use social media networking? If so, share your favorite places to network in the poll below, or leave a note for your colleagues in the comments field.

According to a CDC study, 59% of physicians use social media networks. 

Do you use social media networking? If so, share your favorite places to network in the poll below, or leave a note for your colleagues in the comments field.

According to a CDC study, 59% of physicians use social media networks. 

Do you use social media networking? If so, share your favorite places to network in the poll below, or leave a note for your colleagues in the comments field.

MIAMI – Patients with psoriatic arthritis had a higher prevalence and greater extent of coronary artery plaque in a pilot study comparison with healthy control patients that may point to increased risk independent of traditional cardiovascular risk factors.

In the study, coronary artery plaque as assessed by cardiac computed tomography angiography (CCTA) occurred in 39 (78%) of 50 patients with psoriatic arthritis, a significantly higher rate than that observed for healthy controls (11 of 25, 44%).

©vizualis/thinkstockphotos.com

Investigators not only measured plaque volume, but also assessed the type of plaque: calcified, noncalcified, or mixed. Mixed plaque predominated. This could be important because “noncalcified and mixed carry higher risk for rupture and later cardiovascular events,” Agnes Szentpetery, MD, a research fellow at St. Vincent’s University Hospital in Dublin, said at the annual meeting of the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis.

She and her colleagues also found more clinically significant stenosis among the 50 participants with psoriatic arthritis, compared with 25 healthy controls matched for age, sex, smoking status, and presence of metabolic syndrome. “This pilot study is the first to assess coronary plaques in asymptomatic patients with psoriatic arthritis with CCTA,” Dr. Szentpetery said.

Total plaque volume was higher in the psoriatic arthritis group versus controls, and higher in the left main artery for psoriatic arthritis patients, both with and without metabolic syndrome.

The study points to increased risk independent of traditional cardiovascular risk factors. For example, CCTA revealed no difference in plaque volume between patients with and without metabolic disease. In addition, a previous study suggests “the burden of carotid artery plaques is higher in patients with psoriatic arthritis compared to those with psoriasis alone,” Dr. Szentpetery said, citing a cross-sectional study comparing 125 people with psoriasis to 114 others with psoriatic arthritis (Ann Rheum Dis. 2013 May;72[5]:715-20).

Perhaps not surprisingly, inflammation could be driving the association between psoriatic and cardiovascular disease risk. Other investigators suggest chronic, low-grade inflammation leads to atherosclerosis through a maladaptive immune response and altered lipid metabolism, for example (Nat Med. 2011 Nov;17[11]:1410-22).

In the current study, the patients with psoriatic arthritis had well-established disease, occurring for a mean duration of 19 years. Mean age was 58 years, and 54% were men. Approximately 60% were taking disease-modifying antirheumatic drugs, two-thirds were taking biologics, and about one-third were on combination treatment. Controls were similar demographically with a mean age of 57 years, and 52% were men.

Interestingly, Psoriasis Area and Severity Index (PASI) scores did not correlate with increased risk. During discussion after the presentation of the study, a researcher unaffiliated with the study offered an answer. “It could be their skin disease was controlled by the biologics. You had 67% on biologics,” said Nehal Mehta, MD, Clinical Research Scholar in the section of inflammation and cardiometabolic disease at the National Heart, Lung, and Blood Institute. “We at the NIH see a strong correlation between PASI and coronary artery disease risk.”

“We know methotrexate and anti-TNF agents can have a protective effect on atherosclerosis, but we did not look at this specifically,” Dr. Szentpetery said. Overall, PASI scores were relatively low in the study population, she added, which “may explain why we did not see the correlation with PASI scores.”

Dr. Szentpetery and Dr. Mehta had no relevant financial disclosures.

MIAMI – Patients with psoriatic arthritis had a higher prevalence and greater extent of coronary artery plaque in a pilot study comparison with healthy control patients that may point to increased risk independent of traditional cardiovascular risk factors.

In the study, coronary artery plaque as assessed by cardiac computed tomography angiography (CCTA) occurred in 39 (78%) of 50 patients with psoriatic arthritis, a significantly higher rate than that observed for healthy controls (11 of 25, 44%).

©vizualis/thinkstockphotos.com

Investigators not only measured plaque volume, but also assessed the type of plaque: calcified, noncalcified, or mixed. Mixed plaque predominated. This could be important because “noncalcified and mixed carry higher risk for rupture and later cardiovascular events,” Agnes Szentpetery, MD, a research fellow at St. Vincent’s University Hospital in Dublin, said at the annual meeting of the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis.

She and her colleagues also found more clinically significant stenosis among the 50 participants with psoriatic arthritis, compared with 25 healthy controls matched for age, sex, smoking status, and presence of metabolic syndrome. “This pilot study is the first to assess coronary plaques in asymptomatic patients with psoriatic arthritis with CCTA,” Dr. Szentpetery said.

Total plaque volume was higher in the psoriatic arthritis group versus controls, and higher in the left main artery for psoriatic arthritis patients, both with and without metabolic syndrome.

The study points to increased risk independent of traditional cardiovascular risk factors. For example, CCTA revealed no difference in plaque volume between patients with and without metabolic disease. In addition, a previous study suggests “the burden of carotid artery plaques is higher in patients with psoriatic arthritis compared to those with psoriasis alone,” Dr. Szentpetery said, citing a cross-sectional study comparing 125 people with psoriasis to 114 others with psoriatic arthritis (Ann Rheum Dis. 2013 May;72[5]:715-20).

Perhaps not surprisingly, inflammation could be driving the association between psoriatic and cardiovascular disease risk. Other investigators suggest chronic, low-grade inflammation leads to atherosclerosis through a maladaptive immune response and altered lipid metabolism, for example (Nat Med. 2011 Nov;17[11]:1410-22).

In the current study, the patients with psoriatic arthritis had well-established disease, occurring for a mean duration of 19 years. Mean age was 58 years, and 54% were men. Approximately 60% were taking disease-modifying antirheumatic drugs, two-thirds were taking biologics, and about one-third were on combination treatment. Controls were similar demographically with a mean age of 57 years, and 52% were men.

Interestingly, Psoriasis Area and Severity Index (PASI) scores did not correlate with increased risk. During discussion after the presentation of the study, a researcher unaffiliated with the study offered an answer. “It could be their skin disease was controlled by the biologics. You had 67% on biologics,” said Nehal Mehta, MD, Clinical Research Scholar in the section of inflammation and cardiometabolic disease at the National Heart, Lung, and Blood Institute. “We at the NIH see a strong correlation between PASI and coronary artery disease risk.”

“We know methotrexate and anti-TNF agents can have a protective effect on atherosclerosis, but we did not look at this specifically,” Dr. Szentpetery said. Overall, PASI scores were relatively low in the study population, she added, which “may explain why we did not see the correlation with PASI scores.”

Dr. Szentpetery and Dr. Mehta had no relevant financial disclosures.

MIAMI – Patients with psoriatic arthritis had a higher prevalence and greater extent of coronary artery plaque in a pilot study comparison with healthy control patients that may point to increased risk independent of traditional cardiovascular risk factors.

In the study, coronary artery plaque as assessed by cardiac computed tomography angiography (CCTA) occurred in 39 (78%) of 50 patients with psoriatic arthritis, a significantly higher rate than that observed for healthy controls (11 of 25, 44%).

©vizualis/thinkstockphotos.com

Investigators not only measured plaque volume, but also assessed the type of plaque: calcified, noncalcified, or mixed. Mixed plaque predominated. This could be important because “noncalcified and mixed carry higher risk for rupture and later cardiovascular events,” Agnes Szentpetery, MD, a research fellow at St. Vincent’s University Hospital in Dublin, said at the annual meeting of the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis.

She and her colleagues also found more clinically significant stenosis among the 50 participants with psoriatic arthritis, compared with 25 healthy controls matched for age, sex, smoking status, and presence of metabolic syndrome. “This pilot study is the first to assess coronary plaques in asymptomatic patients with psoriatic arthritis with CCTA,” Dr. Szentpetery said.

Total plaque volume was higher in the psoriatic arthritis group versus controls, and higher in the left main artery for psoriatic arthritis patients, both with and without metabolic syndrome.

The study points to increased risk independent of traditional cardiovascular risk factors. For example, CCTA revealed no difference in plaque volume between patients with and without metabolic disease. In addition, a previous study suggests “the burden of carotid artery plaques is higher in patients with psoriatic arthritis compared to those with psoriasis alone,” Dr. Szentpetery said, citing a cross-sectional study comparing 125 people with psoriasis to 114 others with psoriatic arthritis (Ann Rheum Dis. 2013 May;72[5]:715-20).

Perhaps not surprisingly, inflammation could be driving the association between psoriatic and cardiovascular disease risk. Other investigators suggest chronic, low-grade inflammation leads to atherosclerosis through a maladaptive immune response and altered lipid metabolism, for example (Nat Med. 2011 Nov;17[11]:1410-22).

In the current study, the patients with psoriatic arthritis had well-established disease, occurring for a mean duration of 19 years. Mean age was 58 years, and 54% were men. Approximately 60% were taking disease-modifying antirheumatic drugs, two-thirds were taking biologics, and about one-third were on combination treatment. Controls were similar demographically with a mean age of 57 years, and 52% were men.

Interestingly, Psoriasis Area and Severity Index (PASI) scores did not correlate with increased risk. During discussion after the presentation of the study, a researcher unaffiliated with the study offered an answer. “It could be their skin disease was controlled by the biologics. You had 67% on biologics,” said Nehal Mehta, MD, Clinical Research Scholar in the section of inflammation and cardiometabolic disease at the National Heart, Lung, and Blood Institute. “We at the NIH see a strong correlation between PASI and coronary artery disease risk.”

“We know methotrexate and anti-TNF agents can have a protective effect on atherosclerosis, but we did not look at this specifically,” Dr. Szentpetery said. Overall, PASI scores were relatively low in the study population, she added, which “may explain why we did not see the correlation with PASI scores.”

Dr. Szentpetery and Dr. Mehta had no relevant financial disclosures.

Micrograph showing LSCs

Image by Robert Paulson

New research suggests leukemia stem cells (LSCs) can “hide” in gonadal adipose tissue (GAT) and transform the tissue so they can survive treatment.

Experiments in a mouse model of chronic myeloid leukemia (CML) showed that LSCs are enriched in GAT.

While there, the LSCs create a microenvironment that supports leukemic growth and resistance to treatment, and expression of the fatty acid transporter CD36 makes LSCs particularly resistant.

Craig Jordan, PhD, of University of Colorado in Aurora, and his colleagues conducted this research and detailed their findings in Cell Stem Cell.

The researchers began by examining cancer cells found in GAT from mice with blast crisis CML. Rather than containing the expected mix of regular leukemia cells and LSCs, the tissue was enriched for LSCs.

And these GAT-resident LSCs used a different energy source than LSCs in the bone marrow microenvironment. The GAT-resident LSCs powered their survival and growth with fatty acids, manufacturing energy by the process of fatty acid oxidization.

In fact, the GAT-resident LSCs actively signaled fat to undergo lipolysis, which released fatty acids into the microenvironment.

“The basic biology was fascinating,” Dr Jordan said. “The tumor adapted the local environment to suit itself.”

Dr Jordan and his colleagues also found that CD36 played a role. CD36+ LSCs were enriched in GAT, were more likely to migrate to GAT than to bone marrow, and were protected from treatment by GAT.

The researchers tested the effects of several drugs (cytarabine, doxorubicin, etoposide, SN-38, irinotecan, and dasatinib) on CD36+ LSCs, CD36- LSCs, and bulk leukemia cells ex vivo.

Both CD36+ and CD36- LSCs were more resistant to treatment than bulk leukemia cells, but CD36+ LSCs were preferentially drug-resistant.

The researchers observed similar results in leukemic mice and found evidence to suggest that CD36 plays a similar role in patients with blast crisis CML and those with acute myeloid leukemia.

Micrograph showing LSCs

Image by Robert Paulson

New research suggests leukemia stem cells (LSCs) can “hide” in gonadal adipose tissue (GAT) and transform the tissue so they can survive treatment.

Experiments in a mouse model of chronic myeloid leukemia (CML) showed that LSCs are enriched in GAT.

While there, the LSCs create a microenvironment that supports leukemic growth and resistance to treatment, and expression of the fatty acid transporter CD36 makes LSCs particularly resistant.

Craig Jordan, PhD, of University of Colorado in Aurora, and his colleagues conducted this research and detailed their findings in Cell Stem Cell.

The researchers began by examining cancer cells found in GAT from mice with blast crisis CML. Rather than containing the expected mix of regular leukemia cells and LSCs, the tissue was enriched for LSCs.

And these GAT-resident LSCs used a different energy source than LSCs in the bone marrow microenvironment. The GAT-resident LSCs powered their survival and growth with fatty acids, manufacturing energy by the process of fatty acid oxidization.

In fact, the GAT-resident LSCs actively signaled fat to undergo lipolysis, which released fatty acids into the microenvironment.

“The basic biology was fascinating,” Dr Jordan said. “The tumor adapted the local environment to suit itself.”

Dr Jordan and his colleagues also found that CD36 played a role. CD36+ LSCs were enriched in GAT, were more likely to migrate to GAT than to bone marrow, and were protected from treatment by GAT.

The researchers tested the effects of several drugs (cytarabine, doxorubicin, etoposide, SN-38, irinotecan, and dasatinib) on CD36+ LSCs, CD36- LSCs, and bulk leukemia cells ex vivo.

Both CD36+ and CD36- LSCs were more resistant to treatment than bulk leukemia cells, but CD36+ LSCs were preferentially drug-resistant.

The researchers observed similar results in leukemic mice and found evidence to suggest that CD36 plays a similar role in patients with blast crisis CML and those with acute myeloid leukemia.

Micrograph showing LSCs

Image by Robert Paulson

New research suggests leukemia stem cells (LSCs) can “hide” in gonadal adipose tissue (GAT) and transform the tissue so they can survive treatment.

Experiments in a mouse model of chronic myeloid leukemia (CML) showed that LSCs are enriched in GAT.

While there, the LSCs create a microenvironment that supports leukemic growth and resistance to treatment, and expression of the fatty acid transporter CD36 makes LSCs particularly resistant.

Craig Jordan, PhD, of University of Colorado in Aurora, and his colleagues conducted this research and detailed their findings in Cell Stem Cell.

The researchers began by examining cancer cells found in GAT from mice with blast crisis CML. Rather than containing the expected mix of regular leukemia cells and LSCs, the tissue was enriched for LSCs.

And these GAT-resident LSCs used a different energy source than LSCs in the bone marrow microenvironment. The GAT-resident LSCs powered their survival and growth with fatty acids, manufacturing energy by the process of fatty acid oxidization.

In fact, the GAT-resident LSCs actively signaled fat to undergo lipolysis, which released fatty acids into the microenvironment.

“The basic biology was fascinating,” Dr Jordan said. “The tumor adapted the local environment to suit itself.”

Dr Jordan and his colleagues also found that CD36 played a role. CD36+ LSCs were enriched in GAT, were more likely to migrate to GAT than to bone marrow, and were protected from treatment by GAT.

The researchers tested the effects of several drugs (cytarabine, doxorubicin, etoposide, SN-38, irinotecan, and dasatinib) on CD36+ LSCs, CD36- LSCs, and bulk leukemia cells ex vivo.

Both CD36+ and CD36- LSCs were more resistant to treatment than bulk leukemia cells, but CD36+ LSCs were preferentially drug-resistant.

The researchers observed similar results in leukemic mice and found evidence to suggest that CD36 plays a similar role in patients with blast crisis CML and those with acute myeloid leukemia.

Ibrutinib (Imbruvica)

Photo courtesy of Janssen

Health Canada has approved the Bruton’s tyrosine kinase inhibitor ibrutinib (Imbruvica®) as a first-line treatment for patients with active chronic lymphocytic leukemia (CLL).

This is the fourth approval for ibrutinib in Canada. The drug is now approved for use in all CLL patients, patients with Waldenström’s macroglobulinemia, and patients with relapsed or refractory mantle cell lymphoma (conditional approval).

Ibrutinib is jointly developed and commercialized by Pharmacyclics LLC, an AbbVie company, and Janssen Biotech, Inc.

The latest approval of ibrutinib is based on results from the phase 3 RESONATE-2 trial

(PCYC-1115), which were presented at the 2015 ASH Annual Meeting and

simultaneously published in NEJM.

RESONATE-2 enrolled 269 treatment-naïve patients with CLL or small lymphocytic lymphoma who were 65 or older.

Patients were randomized to receive ibrutinib (n=136) at 420 mg once a day until progression or unacceptable toxicity, or chlorambucil (n=133) on days 1 and 15 of each 28-day cycle for up to 12 cycles. The starting dose for chlorambucil in cycle 1 was 0.5 mg/kg and was increased based on tolerability in cycle 2 by increments of 0.1 mg/kg to a maximum of 0.8 mg/kg.

The primary endpoint of the study was progression-free survival (PFS), as assessed by an independent review committee (IRC) according to the International Workshop on Chronic Lymphocytic Leukemia (iWCLL) 2008 criteria, with modification for treatment-related lymphocytosis.

Key secondary endpoints included overall response rate (based on the same iWCLL criteria), overall survival (OS), and safety.

Ibrutinib significantly prolonged PFS, as determined by the IRC, reducing the risk of progression or death by 84% compared to chlorambucil. The hazard ratio was 0.16 (P<0.001). The median PFS was not reached in the ibrutinib arm but was 18.9 months for the chlorambucil arm.

Ibrutinib significantly prolonged OS as well, although the median OS was not reached in either treatment arm. The OS rate at 24 months was 98% with ibrutinib and 85% with chlorambucil. The relative risk of death with ibrutinib was 84% lower than that with chlorambucil. The hazard ratio was 0.16 (P=0.001).

Ibrutinib was associated with a significantly higher IRC-assessed overall response rate compared to chlorambucil—82% and 35%, respectively (P<0.0001). Five

patients (4%) in the ibrutinib arm achieved a complete response, as did 2 patients (2%) in the chlorambucil arm.

The median duration of treatment was 17.4 months in the ibrutinib arm and 7.1 months in the chlorambucil arm.

The most common adverse events of any grade—in the ibrutinib and chlorambucil arms, respectively—were diarrhea (42% and 17%), fatigue (30% and 38%), cough (22% and 15%), nausea (22% and 39%), peripheral edema (19% and 9%), dry eye (17% and 5%), arthralgia (16% and 7%), neutropenia (16% and 23%), and vomiting (13% and 20%).

Adverse events of grade 3 or higher—in the ibrutinib and chlorambucil arms, respectively—were neutropenia (10% and 18%), anemia (6% and 8%), hypertension (4% and 0%), pneumonia (4% and 2%), diarrhea (4% and 0%), maculopapular rash (3% and 2%), decreased platelet count (3% and 1%), abdominal pain (3% and 1%), hyponatremia (3% and 0%), thrombocytopenia (2% and 6%), febrile neutropenia (2% and 2%), upper respiratory tract infection (2% and 2%), pleural effusion (2% and 1%), cellulitis (2% and 0%), fatigue (1% and 5%), syncope (1% and 2%), and hemolytic anemia (0% and 2%).

Ibrutinib (Imbruvica)

Photo courtesy of Janssen

Health Canada has approved the Bruton’s tyrosine kinase inhibitor ibrutinib (Imbruvica®) as a first-line treatment for patients with active chronic lymphocytic leukemia (CLL).

This is the fourth approval for ibrutinib in Canada. The drug is now approved for use in all CLL patients, patients with Waldenström’s macroglobulinemia, and patients with relapsed or refractory mantle cell lymphoma (conditional approval).

Ibrutinib is jointly developed and commercialized by Pharmacyclics LLC, an AbbVie company, and Janssen Biotech, Inc.

The latest approval of ibrutinib is based on results from the phase 3 RESONATE-2 trial

(PCYC-1115), which were presented at the 2015 ASH Annual Meeting and

simultaneously published in NEJM.

RESONATE-2 enrolled 269 treatment-naïve patients with CLL or small lymphocytic lymphoma who were 65 or older.

Patients were randomized to receive ibrutinib (n=136) at 420 mg once a day until progression or unacceptable toxicity, or chlorambucil (n=133) on days 1 and 15 of each 28-day cycle for up to 12 cycles. The starting dose for chlorambucil in cycle 1 was 0.5 mg/kg and was increased based on tolerability in cycle 2 by increments of 0.1 mg/kg to a maximum of 0.8 mg/kg.

The primary endpoint of the study was progression-free survival (PFS), as assessed by an independent review committee (IRC) according to the International Workshop on Chronic Lymphocytic Leukemia (iWCLL) 2008 criteria, with modification for treatment-related lymphocytosis.

Key secondary endpoints included overall response rate (based on the same iWCLL criteria), overall survival (OS), and safety.

Ibrutinib significantly prolonged PFS, as determined by the IRC, reducing the risk of progression or death by 84% compared to chlorambucil. The hazard ratio was 0.16 (P<0.001). The median PFS was not reached in the ibrutinib arm but was 18.9 months for the chlorambucil arm.

Ibrutinib significantly prolonged OS as well, although the median OS was not reached in either treatment arm. The OS rate at 24 months was 98% with ibrutinib and 85% with chlorambucil. The relative risk of death with ibrutinib was 84% lower than that with chlorambucil. The hazard ratio was 0.16 (P=0.001).

Ibrutinib was associated with a significantly higher IRC-assessed overall response rate compared to chlorambucil—82% and 35%, respectively (P<0.0001). Five

patients (4%) in the ibrutinib arm achieved a complete response, as did 2 patients (2%) in the chlorambucil arm.

The median duration of treatment was 17.4 months in the ibrutinib arm and 7.1 months in the chlorambucil arm.

The most common adverse events of any grade—in the ibrutinib and chlorambucil arms, respectively—were diarrhea (42% and 17%), fatigue (30% and 38%), cough (22% and 15%), nausea (22% and 39%), peripheral edema (19% and 9%), dry eye (17% and 5%), arthralgia (16% and 7%), neutropenia (16% and 23%), and vomiting (13% and 20%).

Adverse events of grade 3 or higher—in the ibrutinib and chlorambucil arms, respectively—were neutropenia (10% and 18%), anemia (6% and 8%), hypertension (4% and 0%), pneumonia (4% and 2%), diarrhea (4% and 0%), maculopapular rash (3% and 2%), decreased platelet count (3% and 1%), abdominal pain (3% and 1%), hyponatremia (3% and 0%), thrombocytopenia (2% and 6%), febrile neutropenia (2% and 2%), upper respiratory tract infection (2% and 2%), pleural effusion (2% and 1%), cellulitis (2% and 0%), fatigue (1% and 5%), syncope (1% and 2%), and hemolytic anemia (0% and 2%).

Ibrutinib (Imbruvica)

Photo courtesy of Janssen

Health Canada has approved the Bruton’s tyrosine kinase inhibitor ibrutinib (Imbruvica®) as a first-line treatment for patients with active chronic lymphocytic leukemia (CLL).

This is the fourth approval for ibrutinib in Canada. The drug is now approved for use in all CLL patients, patients with Waldenström’s macroglobulinemia, and patients with relapsed or refractory mantle cell lymphoma (conditional approval).

Ibrutinib is jointly developed and commercialized by Pharmacyclics LLC, an AbbVie company, and Janssen Biotech, Inc.

The latest approval of ibrutinib is based on results from the phase 3 RESONATE-2 trial

(PCYC-1115), which were presented at the 2015 ASH Annual Meeting and

simultaneously published in NEJM.

RESONATE-2 enrolled 269 treatment-naïve patients with CLL or small lymphocytic lymphoma who were 65 or older.

Patients were randomized to receive ibrutinib (n=136) at 420 mg once a day until progression or unacceptable toxicity, or chlorambucil (n=133) on days 1 and 15 of each 28-day cycle for up to 12 cycles. The starting dose for chlorambucil in cycle 1 was 0.5 mg/kg and was increased based on tolerability in cycle 2 by increments of 0.1 mg/kg to a maximum of 0.8 mg/kg.

The primary endpoint of the study was progression-free survival (PFS), as assessed by an independent review committee (IRC) according to the International Workshop on Chronic Lymphocytic Leukemia (iWCLL) 2008 criteria, with modification for treatment-related lymphocytosis.

Key secondary endpoints included overall response rate (based on the same iWCLL criteria), overall survival (OS), and safety.

Ibrutinib significantly prolonged PFS, as determined by the IRC, reducing the risk of progression or death by 84% compared to chlorambucil. The hazard ratio was 0.16 (P<0.001). The median PFS was not reached in the ibrutinib arm but was 18.9 months for the chlorambucil arm.

Ibrutinib significantly prolonged OS as well, although the median OS was not reached in either treatment arm. The OS rate at 24 months was 98% with ibrutinib and 85% with chlorambucil. The relative risk of death with ibrutinib was 84% lower than that with chlorambucil. The hazard ratio was 0.16 (P=0.001).

Ibrutinib was associated with a significantly higher IRC-assessed overall response rate compared to chlorambucil—82% and 35%, respectively (P<0.0001). Five

patients (4%) in the ibrutinib arm achieved a complete response, as did 2 patients (2%) in the chlorambucil arm.

The median duration of treatment was 17.4 months in the ibrutinib arm and 7.1 months in the chlorambucil arm.

The most common adverse events of any grade—in the ibrutinib and chlorambucil arms, respectively—were diarrhea (42% and 17%), fatigue (30% and 38%), cough (22% and 15%), nausea (22% and 39%), peripheral edema (19% and 9%), dry eye (17% and 5%), arthralgia (16% and 7%), neutropenia (16% and 23%), and vomiting (13% and 20%).

Adverse events of grade 3 or higher—in the ibrutinib and chlorambucil arms, respectively—were neutropenia (10% and 18%), anemia (6% and 8%), hypertension (4% and 0%), pneumonia (4% and 2%), diarrhea (4% and 0%), maculopapular rash (3% and 2%), decreased platelet count (3% and 1%), abdominal pain (3% and 1%), hyponatremia (3% and 0%), thrombocytopenia (2% and 6%), febrile neutropenia (2% and 2%), upper respiratory tract infection (2% and 2%), pleural effusion (2% and 1%), cellulitis (2% and 0%), fatigue (1% and 5%), syncope (1% and 2%), and hemolytic anemia (0% and 2%).