The Journal of Community and Supportive Oncology

Enthusiasm continues in the medical community anxious for effective agents for men with metastatic castration-resistant prostate cancer (mCRPC). Most prostate cancer patients who develop metastatic disease are initially treated with readily available luteinizing hormone-releasing hormone (LHRH) agonists or antagonists, with or without an anti-androgen. The rationale here is to decrease androgen levels and/or block androgen receptor (AR) binding. In patients whose disease becomes refractory to this front-line hormonal deprivation, the molecular mechanisms involved in androgen independence include androgen receptor gene amplification, AR mutations that allow stimulation by a variety of weak androgens, and AR activation by autocrine production of androgens from tumor cells. Patients with metastatic castration-resistant prostate cancer (mCRPC) who biochemically recur after androgendeprivation therapy with significant prostate-specific antigen (PSA) elevations and/or who develop radiographic or symptomatic metastases are then usually considered for cytotoxic chemotherapy. The only approved initial cytotoxic chemotherapeutic agent that has demonstrated improved survival for patients with mCRPC is docetaxel. For patients who fail docetaxel, cabazitaxel with prednisone is an approved second-line treatment. Similarly, another approved second-line treatment (albeit, hormonal) for patients who have failed docetaxel therapy is abiraterone acetate, which attacks the adrenal and extragonadal synthesis of androgen. The magnitude of this effect was not appreciated until it was recognized that the androgen receptor and ligand-dependent androgen receptor signaling remain active and upregulated in men with castrate levels of testosterone ( 50 ng/dL).1 Recognition of the importance of the signaling of the androgen receptor and its seemingly independent behavior in a milieu of little or no androgen is now appreciated.

Enthusiasm continues in the medical community anxious for effective agents for men with metastatic castration-resistant prostate cancer (mCRPC). Most prostate cancer patients who develop metastatic disease are initially treated with readily available luteinizing hormone-releasing hormone (LHRH) agonists or antagonists, with or without an anti-androgen. The rationale here is to decrease androgen levels and/or block androgen receptor (AR) binding. In patients whose disease becomes refractory to this front-line hormonal deprivation, the molecular mechanisms involved in androgen independence include androgen receptor gene amplification, AR mutations that allow stimulation by a variety of weak androgens, and AR activation by autocrine production of androgens from tumor cells. Patients with metastatic castration-resistant prostate cancer (mCRPC) who biochemically recur after androgendeprivation therapy with significant prostate-specific antigen (PSA) elevations and/or who develop radiographic or symptomatic metastases are then usually considered for cytotoxic chemotherapy. The only approved initial cytotoxic chemotherapeutic agent that has demonstrated improved survival for patients with mCRPC is docetaxel. For patients who fail docetaxel, cabazitaxel with prednisone is an approved second-line treatment. Similarly, another approved second-line treatment (albeit, hormonal) for patients who have failed docetaxel therapy is abiraterone acetate, which attacks the adrenal and extragonadal synthesis of androgen. The magnitude of this effect was not appreciated until it was recognized that the androgen receptor and ligand-dependent androgen receptor signaling remain active and upregulated in men with castrate levels of testosterone ( 50 ng/dL).1 Recognition of the importance of the signaling of the androgen receptor and its seemingly independent behavior in a milieu of little or no androgen is now appreciated.

Enthusiasm continues in the medical community anxious for effective agents for men with metastatic castration-resistant prostate cancer (mCRPC). Most prostate cancer patients who develop metastatic disease are initially treated with readily available luteinizing hormone-releasing hormone (LHRH) agonists or antagonists, with or without an anti-androgen. The rationale here is to decrease androgen levels and/or block androgen receptor (AR) binding. In patients whose disease becomes refractory to this front-line hormonal deprivation, the molecular mechanisms involved in androgen independence include androgen receptor gene amplification, AR mutations that allow stimulation by a variety of weak androgens, and AR activation by autocrine production of androgens from tumor cells. Patients with metastatic castration-resistant prostate cancer (mCRPC) who biochemically recur after androgendeprivation therapy with significant prostate-specific antigen (PSA) elevations and/or who develop radiographic or symptomatic metastases are then usually considered for cytotoxic chemotherapy. The only approved initial cytotoxic chemotherapeutic agent that has demonstrated improved survival for patients with mCRPC is docetaxel. For patients who fail docetaxel, cabazitaxel with prednisone is an approved second-line treatment. Similarly, another approved second-line treatment (albeit, hormonal) for patients who have failed docetaxel therapy is abiraterone acetate, which attacks the adrenal and extragonadal synthesis of androgen. The magnitude of this effect was not appreciated until it was recognized that the androgen receptor and ligand-dependent androgen receptor signaling remain active and upregulated in men with castrate levels of testosterone ( 50 ng/dL).1 Recognition of the importance of the signaling of the androgen receptor and its seemingly independent behavior in a milieu of little or no androgen is now appreciated.

The effects of sequestration-related cuts on oncology practices have kicked in. In early April, Sarah Kliff, a blogger at The Washington Post, reported that cancer clinics had already started turning away Medicare patients because the funding cuts would make it impossible for them to continue treating their chemotherapy patients and avoid financial ruin.1 In early May, a month after the April 1 cuts took effect, we already had 2 separate survey reports, one from the American Society of Clinical Oncology (ASCO), the other from the Community Oncology Alliance (COA), that showed that the 2% cut in Medicare reimbursement had caused oncology practices “to make signifi- cant shifts in how they do business and care for patients.”2 ASCO surveyed 500 of its members (41% in suburban settings; 41%, in urban; 16%, in rural). In all, 80% of respondents said sequestration was affecting their practices, and about 75% said they were having trouble paying for chemotherapy drugs. Half of the respondents said they could care only for patients who had other sources of income independent of Medicare, 14% had stopped seeing Medicare patients, and half said they were sending their Medicare patients to outpatient infusion centers for their chemotherapy. ASCO president Sandra Swain expressed concern that some patients’ care was being disrupted and compromised, which could be detrimental to the clinical outcomes and emotional well-being of these fragile individuals, and she warned in a statement that the society’s initial findings “may just be the tip of the iceberg.”³ The fact that a quarter of respondents reported that they were planning to close satellite clinics should also raise concerns about the impact such closures might have on research and participation in clinical trials.

The effects of sequestration-related cuts on oncology practices have kicked in. In early April, Sarah Kliff, a blogger at The Washington Post, reported that cancer clinics had already started turning away Medicare patients because the funding cuts would make it impossible for them to continue treating their chemotherapy patients and avoid financial ruin.1 In early May, a month after the April 1 cuts took effect, we already had 2 separate survey reports, one from the American Society of Clinical Oncology (ASCO), the other from the Community Oncology Alliance (COA), that showed that the 2% cut in Medicare reimbursement had caused oncology practices “to make signifi- cant shifts in how they do business and care for patients.”2 ASCO surveyed 500 of its members (41% in suburban settings; 41%, in urban; 16%, in rural). In all, 80% of respondents said sequestration was affecting their practices, and about 75% said they were having trouble paying for chemotherapy drugs. Half of the respondents said they could care only for patients who had other sources of income independent of Medicare, 14% had stopped seeing Medicare patients, and half said they were sending their Medicare patients to outpatient infusion centers for their chemotherapy. ASCO president Sandra Swain expressed concern that some patients’ care was being disrupted and compromised, which could be detrimental to the clinical outcomes and emotional well-being of these fragile individuals, and she warned in a statement that the society’s initial findings “may just be the tip of the iceberg.”³ The fact that a quarter of respondents reported that they were planning to close satellite clinics should also raise concerns about the impact such closures might have on research and participation in clinical trials.

The effects of sequestration-related cuts on oncology practices have kicked in. In early April, Sarah Kliff, a blogger at The Washington Post, reported that cancer clinics had already started turning away Medicare patients because the funding cuts would make it impossible for them to continue treating their chemotherapy patients and avoid financial ruin.1 In early May, a month after the April 1 cuts took effect, we already had 2 separate survey reports, one from the American Society of Clinical Oncology (ASCO), the other from the Community Oncology Alliance (COA), that showed that the 2% cut in Medicare reimbursement had caused oncology practices “to make signifi- cant shifts in how they do business and care for patients.”2 ASCO surveyed 500 of its members (41% in suburban settings; 41%, in urban; 16%, in rural). In all, 80% of respondents said sequestration was affecting their practices, and about 75% said they were having trouble paying for chemotherapy drugs. Half of the respondents said they could care only for patients who had other sources of income independent of Medicare, 14% had stopped seeing Medicare patients, and half said they were sending their Medicare patients to outpatient infusion centers for their chemotherapy. ASCO president Sandra Swain expressed concern that some patients’ care was being disrupted and compromised, which could be detrimental to the clinical outcomes and emotional well-being of these fragile individuals, and she warned in a statement that the society’s initial findings “may just be the tip of the iceberg.”³ The fact that a quarter of respondents reported that they were planning to close satellite clinics should also raise concerns about the impact such closures might have on research and participation in clinical trials.

It is well known that clinicians experience distress and grief in response to their patients’ suffering. Oncologists and palliative care specialists are no exception since they commonly experience patient loss and are often affected by unprocessed grief. These emotions can compromise clinicians’ personal well-being, since unexamined emotions may lead to burnout, moral distress, compassion fatigue, and poor clinical decisions which adversely affect patient care. One approach to mitigate this harm is selfcare, defined as a cadre of activities performed independently by an individual to promote and maintain personal well-being throughout life.

This article emphasizes the importance of having a self-care and self-awareness plan when caring for patients with life-limiting cancer and discusses validated methods to increase self-care, enhance self-awareness and improve patient care.

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

It is well known that clinicians experience distress and grief in response to their patients’ suffering. Oncologists and palliative care specialists are no exception since they commonly experience patient loss and are often affected by unprocessed grief. These emotions can compromise clinicians’ personal well-being, since unexamined emotions may lead to burnout, moral distress, compassion fatigue, and poor clinical decisions which adversely affect patient care. One approach to mitigate this harm is selfcare, defined as a cadre of activities performed independently by an individual to promote and maintain personal well-being throughout life.

This article emphasizes the importance of having a self-care and self-awareness plan when caring for patients with life-limiting cancer and discusses validated methods to increase self-care, enhance self-awareness and improve patient care.

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

It is well known that clinicians experience distress and grief in response to their patients’ suffering. Oncologists and palliative care specialists are no exception since they commonly experience patient loss and are often affected by unprocessed grief. These emotions can compromise clinicians’ personal well-being, since unexamined emotions may lead to burnout, moral distress, compassion fatigue, and poor clinical decisions which adversely affect patient care. One approach to mitigate this harm is selfcare, defined as a cadre of activities performed independently by an individual to promote and maintain personal well-being throughout life.

This article emphasizes the importance of having a self-care and self-awareness plan when caring for patients with life-limiting cancer and discusses validated methods to increase self-care, enhance self-awareness and improve patient care.

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