The Journal of Community and Supportive Oncology

Many oncologists remember the storied history of homoharringtonine (HHT) and wonder whatever happened to it. HHT showed initial promise for myeloid leukemias, particularly for chronic myelogenous leukemia (CML) where it seemed to induce more cytogenetic remissions than did interferon alpha.1 Unfortunately for HHT investigators, but fortunately for everybody else, these studies coincided with those being done with imatinib. The phenomenal introduction of imatinib contributed to the shelving of HHT in the mid to late 1990s.2 As is often the case, though, imatinib is not perfect. Some patients with CML develop resistance and approximately half of these do so through the acquisition of binding site mutations. One mutation in particular, T315I, rendered patients with CML resistant to all available tyrosine kinase inhibitors (TKI). In the meantime, a semisynthetic version of HHT, omacetaxine mepesuccinate, was developed. With the help of partners in industry, investigators at MD Anderson Cancer Center initiated new studies of omacetaxine in TKI resistant CML patients. Among 62 CML patients with a T315I mutation, complete hematologic response was achieved in 77% with median response duration of 9.1 months.3 Further, cytogenetic response was also achieved in a portion of patients, complete in 16%. These data prompted application for approval by the Food and Drug Administration, but were rejected for lack of a standardized test for T315I mutations. The additional data presented in the Community Translations article on page 194 formed the basis of a second application, this time for an indication in patients with CML resistant to 2 or more TKIs.

Many oncologists remember the storied history of homoharringtonine (HHT) and wonder whatever happened to it. HHT showed initial promise for myeloid leukemias, particularly for chronic myelogenous leukemia (CML) where it seemed to induce more cytogenetic remissions than did interferon alpha.1 Unfortunately for HHT investigators, but fortunately for everybody else, these studies coincided with those being done with imatinib. The phenomenal introduction of imatinib contributed to the shelving of HHT in the mid to late 1990s.2 As is often the case, though, imatinib is not perfect. Some patients with CML develop resistance and approximately half of these do so through the acquisition of binding site mutations. One mutation in particular, T315I, rendered patients with CML resistant to all available tyrosine kinase inhibitors (TKI). In the meantime, a semisynthetic version of HHT, omacetaxine mepesuccinate, was developed. With the help of partners in industry, investigators at MD Anderson Cancer Center initiated new studies of omacetaxine in TKI resistant CML patients. Among 62 CML patients with a T315I mutation, complete hematologic response was achieved in 77% with median response duration of 9.1 months.3 Further, cytogenetic response was also achieved in a portion of patients, complete in 16%. These data prompted application for approval by the Food and Drug Administration, but were rejected for lack of a standardized test for T315I mutations. The additional data presented in the Community Translations article on page 194 formed the basis of a second application, this time for an indication in patients with CML resistant to 2 or more TKIs.

Many oncologists remember the storied history of homoharringtonine (HHT) and wonder whatever happened to it. HHT showed initial promise for myeloid leukemias, particularly for chronic myelogenous leukemia (CML) where it seemed to induce more cytogenetic remissions than did interferon alpha.1 Unfortunately for HHT investigators, but fortunately for everybody else, these studies coincided with those being done with imatinib. The phenomenal introduction of imatinib contributed to the shelving of HHT in the mid to late 1990s.2 As is often the case, though, imatinib is not perfect. Some patients with CML develop resistance and approximately half of these do so through the acquisition of binding site mutations. One mutation in particular, T315I, rendered patients with CML resistant to all available tyrosine kinase inhibitors (TKI). In the meantime, a semisynthetic version of HHT, omacetaxine mepesuccinate, was developed. With the help of partners in industry, investigators at MD Anderson Cancer Center initiated new studies of omacetaxine in TKI resistant CML patients. Among 62 CML patients with a T315I mutation, complete hematologic response was achieved in 77% with median response duration of 9.1 months.3 Further, cytogenetic response was also achieved in a portion of patients, complete in 16%. These data prompted application for approval by the Food and Drug Administration, but were rejected for lack of a standardized test for T315I mutations. The additional data presented in the Community Translations article on page 194 formed the basis of a second application, this time for an indication in patients with CML resistant to 2 or more TKIs.

With this issue of COMMUNITY ONCOLOGY, memories of this year’s annual meeting of the American Society of Clinical Oncology in Chicago are starting to fade, but we are still trying to make sense of the wealth of data that was presented there. I found a number of the presentations particularly noteworthy and some of the findings likely to have an impact on how we practice. The aTTom trial1 by a group of British researchers was presented at the plenary session and dovetailed nicely with the ATLAS trial² findings that were presented at last year’s San Antonio Breast Cancer Symposium. Both trials examined 5 and 10 years of adjuvant tamoxifen in women with early stage, hormone-positive breast cancer, and findings from both trials showed reductions in recurrence, breast cancer mortality, and overall mortality in women who remained on tamoxifen to year 10. Two presentations examined frequency of scanning in Hodgkin and non-Hodgkin lymphoma and both groups of researchers concluded what many of us have often suspected – that we overscan, and that clinical surveillance is an adequate strategy for detecting recurrence. One study showed that most diffuse large B-cell lymphoma relapses were found by detection of symptoms during a physical exam, lab abnormalities, or even the patients themselves, and that routine surveillance scans did not add much to the detection of relapse.³ Findings from a second study showed that routine surveillance did not result in any survival advantage in patients with classical Hodgkin lymphoma who had achieved complete remission.⁴

With this issue of COMMUNITY ONCOLOGY, memories of this year’s annual meeting of the American Society of Clinical Oncology in Chicago are starting to fade, but we are still trying to make sense of the wealth of data that was presented there. I found a number of the presentations particularly noteworthy and some of the findings likely to have an impact on how we practice. The aTTom trial1 by a group of British researchers was presented at the plenary session and dovetailed nicely with the ATLAS trial² findings that were presented at last year’s San Antonio Breast Cancer Symposium. Both trials examined 5 and 10 years of adjuvant tamoxifen in women with early stage, hormone-positive breast cancer, and findings from both trials showed reductions in recurrence, breast cancer mortality, and overall mortality in women who remained on tamoxifen to year 10. Two presentations examined frequency of scanning in Hodgkin and non-Hodgkin lymphoma and both groups of researchers concluded what many of us have often suspected – that we overscan, and that clinical surveillance is an adequate strategy for detecting recurrence. One study showed that most diffuse large B-cell lymphoma relapses were found by detection of symptoms during a physical exam, lab abnormalities, or even the patients themselves, and that routine surveillance scans did not add much to the detection of relapse.³ Findings from a second study showed that routine surveillance did not result in any survival advantage in patients with classical Hodgkin lymphoma who had achieved complete remission.⁴

With this issue of COMMUNITY ONCOLOGY, memories of this year’s annual meeting of the American Society of Clinical Oncology in Chicago are starting to fade, but we are still trying to make sense of the wealth of data that was presented there. I found a number of the presentations particularly noteworthy and some of the findings likely to have an impact on how we practice. The aTTom trial1 by a group of British researchers was presented at the plenary session and dovetailed nicely with the ATLAS trial² findings that were presented at last year’s San Antonio Breast Cancer Symposium. Both trials examined 5 and 10 years of adjuvant tamoxifen in women with early stage, hormone-positive breast cancer, and findings from both trials showed reductions in recurrence, breast cancer mortality, and overall mortality in women who remained on tamoxifen to year 10. Two presentations examined frequency of scanning in Hodgkin and non-Hodgkin lymphoma and both groups of researchers concluded what many of us have often suspected – that we overscan, and that clinical surveillance is an adequate strategy for detecting recurrence. One study showed that most diffuse large B-cell lymphoma relapses were found by detection of symptoms during a physical exam, lab abnormalities, or even the patients themselves, and that routine surveillance scans did not add much to the detection of relapse.³ Findings from a second study showed that routine surveillance did not result in any survival advantage in patients with classical Hodgkin lymphoma who had achieved complete remission.⁴

Many professional entities endorse the need to deliver cancer genetics risk assessment (CGRA) services through a multidisciplinary team that includes trained genetics professionals. However, market forces, a lack of regulation of genetic testing, patent laws, cost barriers, and a limited workforce in genetics have resulted in an increasing number of community practitioners who order and interpret genetic testing. In addition, varying state-level laws and licensure requirements for genetic counselors may contribute to the nonuniform delivery of CGRA services across the United States. Those who perform genetic testing without having adequate training or expertise may incur liability risks. Moreover, the patient might not enjoy the maximum benefit of testing at the hands of an inadequately trained individual. In the setting of a limited number of professional who are trained in CGRA and a dearth of education and training resources, it is a challenge to integrate genetic testing services into clinical care. With advances in genomics and the implementation of personalized medicine, the problem will only be magnified, and it is critical that there are more opportunities for high quality education and training in clinical cancer genetics free of commercial bias. Successful strategies for delivering comprehensive CGRA services include academic-community partnerships that focus on collaboration with nongenetics providers or the inclusion of a genetics professional in the community setting as part of multidisciplinary patient care. These approaches can leverage the expertise of genetics professionals while allowing patients to remain in their community and enjoy better access to resources for long-term follow-up care.

*Click on the link to the left for a PDF of the full article.

Many professional entities endorse the need to deliver cancer genetics risk assessment (CGRA) services through a multidisciplinary team that includes trained genetics professionals. However, market forces, a lack of regulation of genetic testing, patent laws, cost barriers, and a limited workforce in genetics have resulted in an increasing number of community practitioners who order and interpret genetic testing. In addition, varying state-level laws and licensure requirements for genetic counselors may contribute to the nonuniform delivery of CGRA services across the United States. Those who perform genetic testing without having adequate training or expertise may incur liability risks. Moreover, the patient might not enjoy the maximum benefit of testing at the hands of an inadequately trained individual. In the setting of a limited number of professional who are trained in CGRA and a dearth of education and training resources, it is a challenge to integrate genetic testing services into clinical care. With advances in genomics and the implementation of personalized medicine, the problem will only be magnified, and it is critical that there are more opportunities for high quality education and training in clinical cancer genetics free of commercial bias. Successful strategies for delivering comprehensive CGRA services include academic-community partnerships that focus on collaboration with nongenetics providers or the inclusion of a genetics professional in the community setting as part of multidisciplinary patient care. These approaches can leverage the expertise of genetics professionals while allowing patients to remain in their community and enjoy better access to resources for long-term follow-up care.

*Click on the link to the left for a PDF of the full article.

Many professional entities endorse the need to deliver cancer genetics risk assessment (CGRA) services through a multidisciplinary team that includes trained genetics professionals. However, market forces, a lack of regulation of genetic testing, patent laws, cost barriers, and a limited workforce in genetics have resulted in an increasing number of community practitioners who order and interpret genetic testing. In addition, varying state-level laws and licensure requirements for genetic counselors may contribute to the nonuniform delivery of CGRA services across the United States. Those who perform genetic testing without having adequate training or expertise may incur liability risks. Moreover, the patient might not enjoy the maximum benefit of testing at the hands of an inadequately trained individual. In the setting of a limited number of professional who are trained in CGRA and a dearth of education and training resources, it is a challenge to integrate genetic testing services into clinical care. With advances in genomics and the implementation of personalized medicine, the problem will only be magnified, and it is critical that there are more opportunities for high quality education and training in clinical cancer genetics free of commercial bias. Successful strategies for delivering comprehensive CGRA services include academic-community partnerships that focus on collaboration with nongenetics providers or the inclusion of a genetics professional in the community setting as part of multidisciplinary patient care. These approaches can leverage the expertise of genetics professionals while allowing patients to remain in their community and enjoy better access to resources for long-term follow-up care.

*Click on the link to the left for a PDF of the full article.

The advent of BCR-ABL1 tyrosine kinase inhibitors (TKIs) for the treatment of chronic myeloid leukemia (CML) has dramatically changed the management of patients with CML. With continuous long-term TKI therapy, CML can be managed like a chronic condition, and most patients can expect to have a normal life expectancy. Given the prospect of lifelong therapy, however, issues related to adherence become particularly important and warrant greater attention since attainment of favorable long-term survival depends in large part on consistent, appropriate treatment administration over years, if not decades. As the multidisciplinary care team approach to cancer care has gained traction at academic centers and community practices, midlevel providers, including nurse practitioners and physician assistants, have taken on greater patient-related responsibilities. Midlevel providers have the potential to foster and maintain meaningful provider-patient relationships that may span years, and are well positioned to recognize and manage problems that patients may have with adherence. Here we discuss the importance of achieving and maintaining responses to TKI therapy, describe the clinical consequences of poor adherence to TKI therapy in CML, and outline factors behind poor adherence. We also share strategies that we use at our center to improve adherence to long-term TKI therapy for CML.

*Click on the link to the left for a PDF of the full article.  

The advent of BCR-ABL1 tyrosine kinase inhibitors (TKIs) for the treatment of chronic myeloid leukemia (CML) has dramatically changed the management of patients with CML. With continuous long-term TKI therapy, CML can be managed like a chronic condition, and most patients can expect to have a normal life expectancy. Given the prospect of lifelong therapy, however, issues related to adherence become particularly important and warrant greater attention since attainment of favorable long-term survival depends in large part on consistent, appropriate treatment administration over years, if not decades. As the multidisciplinary care team approach to cancer care has gained traction at academic centers and community practices, midlevel providers, including nurse practitioners and physician assistants, have taken on greater patient-related responsibilities. Midlevel providers have the potential to foster and maintain meaningful provider-patient relationships that may span years, and are well positioned to recognize and manage problems that patients may have with adherence. Here we discuss the importance of achieving and maintaining responses to TKI therapy, describe the clinical consequences of poor adherence to TKI therapy in CML, and outline factors behind poor adherence. We also share strategies that we use at our center to improve adherence to long-term TKI therapy for CML.

*Click on the link to the left for a PDF of the full article.  

The advent of BCR-ABL1 tyrosine kinase inhibitors (TKIs) for the treatment of chronic myeloid leukemia (CML) has dramatically changed the management of patients with CML. With continuous long-term TKI therapy, CML can be managed like a chronic condition, and most patients can expect to have a normal life expectancy. Given the prospect of lifelong therapy, however, issues related to adherence become particularly important and warrant greater attention since attainment of favorable long-term survival depends in large part on consistent, appropriate treatment administration over years, if not decades. As the multidisciplinary care team approach to cancer care has gained traction at academic centers and community practices, midlevel providers, including nurse practitioners and physician assistants, have taken on greater patient-related responsibilities. Midlevel providers have the potential to foster and maintain meaningful provider-patient relationships that may span years, and are well positioned to recognize and manage problems that patients may have with adherence. Here we discuss the importance of achieving and maintaining responses to TKI therapy, describe the clinical consequences of poor adherence to TKI therapy in CML, and outline factors behind poor adherence. We also share strategies that we use at our center to improve adherence to long-term TKI therapy for CML.

*Click on the link to the left for a PDF of the full article.  

The FDA recently widened the approved use of nanoparticle albumin bound (nab) paclitaxel (nab-paclitaxel) to include first-line treatment for non–small-cell lung cancer (NSCLC), in combination with carboplatin. This approval was based on results of a global, phase 3 randomized trial conducted by Socinski et al that compared the use of nab-paclitaxel and solventbased paclitaxel injection in combination with carboplatin as first-line treatment of advanced NSCLC.1 Taxanes are the most widely used chemotherapeutic agents in solid tumor oncology. Paclitaxel and docetaxel are effective in the treatment of NSCLC and are frequently used for adjuvant therapy after resection, in combination with radiation for locally advanced disease and for treatment of patients with advanced disease. They are usually used in combination with platinum agents or as single-agent therapy in the relapsed refractory setting. Paclitaxel and docetaxel require synthetic solvents for intravenous administration, which can cause life-threatening allergic reactions and significant toxicity. Nab-paclitaxel is a novel, solvent-free formulation of paclitaxel, which can be administered without the need for steroid and antihistamine premedication. Furthermore, nab-paclitaxel delivers high concentrations of the drug’s active ingredient into the cancer cell with a reduced incidence of side effects compared with the solvent-based formulation. As summarized in the Community Translations article on page 166, the administration of nab-paclitaxel as firstline therapy in combination with carboplatin was efficacious and resulted in a significantly improved overall response rate (ORR), compared with paclitaxel (33% vs 25%, respectively; response rate ratio [RRR], 1.313; 95% CI, 1.082-1.593; P .005), and it achieved the study’s primary end point. Of note, ORR was significantly greater with nab-paclitaxel in patients with squamous cell histology (41% vs 24%; RRR, 1.680; P .001), with no difference between treatments being observed in patients with nonsquamous histology (ORR, 26% vs 25%) or adenocarcinoma (ORR, 26% vs 27%). There was no difference in PFS or survival between the 2 arms.

The FDA recently widened the approved use of nanoparticle albumin bound (nab) paclitaxel (nab-paclitaxel) to include first-line treatment for non–small-cell lung cancer (NSCLC), in combination with carboplatin. This approval was based on results of a global, phase 3 randomized trial conducted by Socinski et al that compared the use of nab-paclitaxel and solventbased paclitaxel injection in combination with carboplatin as first-line treatment of advanced NSCLC.1 Taxanes are the most widely used chemotherapeutic agents in solid tumor oncology. Paclitaxel and docetaxel are effective in the treatment of NSCLC and are frequently used for adjuvant therapy after resection, in combination with radiation for locally advanced disease and for treatment of patients with advanced disease. They are usually used in combination with platinum agents or as single-agent therapy in the relapsed refractory setting. Paclitaxel and docetaxel require synthetic solvents for intravenous administration, which can cause life-threatening allergic reactions and significant toxicity. Nab-paclitaxel is a novel, solvent-free formulation of paclitaxel, which can be administered without the need for steroid and antihistamine premedication. Furthermore, nab-paclitaxel delivers high concentrations of the drug’s active ingredient into the cancer cell with a reduced incidence of side effects compared with the solvent-based formulation. As summarized in the Community Translations article on page 166, the administration of nab-paclitaxel as firstline therapy in combination with carboplatin was efficacious and resulted in a significantly improved overall response rate (ORR), compared with paclitaxel (33% vs 25%, respectively; response rate ratio [RRR], 1.313; 95% CI, 1.082-1.593; P .005), and it achieved the study’s primary end point. Of note, ORR was significantly greater with nab-paclitaxel in patients with squamous cell histology (41% vs 24%; RRR, 1.680; P .001), with no difference between treatments being observed in patients with nonsquamous histology (ORR, 26% vs 25%) or adenocarcinoma (ORR, 26% vs 27%). There was no difference in PFS or survival between the 2 arms.

The FDA recently widened the approved use of nanoparticle albumin bound (nab) paclitaxel (nab-paclitaxel) to include first-line treatment for non–small-cell lung cancer (NSCLC), in combination with carboplatin. This approval was based on results of a global, phase 3 randomized trial conducted by Socinski et al that compared the use of nab-paclitaxel and solventbased paclitaxel injection in combination with carboplatin as first-line treatment of advanced NSCLC.1 Taxanes are the most widely used chemotherapeutic agents in solid tumor oncology. Paclitaxel and docetaxel are effective in the treatment of NSCLC and are frequently used for adjuvant therapy after resection, in combination with radiation for locally advanced disease and for treatment of patients with advanced disease. They are usually used in combination with platinum agents or as single-agent therapy in the relapsed refractory setting. Paclitaxel and docetaxel require synthetic solvents for intravenous administration, which can cause life-threatening allergic reactions and significant toxicity. Nab-paclitaxel is a novel, solvent-free formulation of paclitaxel, which can be administered without the need for steroid and antihistamine premedication. Furthermore, nab-paclitaxel delivers high concentrations of the drug’s active ingredient into the cancer cell with a reduced incidence of side effects compared with the solvent-based formulation. As summarized in the Community Translations article on page 166, the administration of nab-paclitaxel as firstline therapy in combination with carboplatin was efficacious and resulted in a significantly improved overall response rate (ORR), compared with paclitaxel (33% vs 25%, respectively; response rate ratio [RRR], 1.313; 95% CI, 1.082-1.593; P .005), and it achieved the study’s primary end point. Of note, ORR was significantly greater with nab-paclitaxel in patients with squamous cell histology (41% vs 24%; RRR, 1.680; P .001), with no difference between treatments being observed in patients with nonsquamous histology (ORR, 26% vs 25%) or adenocarcinoma (ORR, 26% vs 27%). There was no difference in PFS or survival between the 2 arms.