A. Renteria, B. Holland, Yiwu Huang, J. Cooper, B. Donahue
Anne S. Renteria, MD, Bart K. Holland, MPH, PhD, Yiwu Huang, MD, PhD, Jay S. Cooper, MD, and Bernadine Donahue, MD Bone Marrow Transplant Program, The Tisch Cancer Institute, Mount Sinai Medical Center, New York; Preventive Medicine, Biostatistics, UMDNJ New Jersey Medical School, Newark; Hematology Oncology Department and Radiation Oncology Department, Maimonides Cancer Center, Brooklyn, New York
Anne S. Renteria，医学博士，Bart K. Holland，公共卫生硕士，博士，Yiwu Huang，医学博士，医学博士，Jay S. Cooper，医学博士，和Bernadine Donahue，医学博士骨髓移植项目，Tisch癌症研究所，西奈山医学中心，纽约;预防医学，生物统计学，纽瓦克UMDNJ新泽西医学院;纽约布鲁克林迈蒙尼德癌症中心血液肿瘤科和放射肿瘤科
{"title":"Locally advanced pancreatic cancer in a socio-economically challenged population","authors":"A. Renteria, B. Holland, Yiwu Huang, J. Cooper, B. Donahue","doi":"10.12788/J.CMONC.0030","DOIUrl":"https://doi.org/10.12788/J.CMONC.0030","url":null,"abstract":"Anne S. Renteria, MD, Bart K. Holland, MPH, PhD, Yiwu Huang, MD, PhD, Jay S. Cooper, MD, and Bernadine Donahue, MD Bone Marrow Transplant Program, The Tisch Cancer Institute, Mount Sinai Medical Center, New York; Preventive Medicine, Biostatistics, UMDNJ New Jersey Medical School, Newark; Hematology Oncology Department and Radiation Oncology Department, Maimonides Cancer Center, Brooklyn, New York","PeriodicalId":72649,"journal":{"name":"Community oncology","volume":"10 1","pages":"220-226"},"PeriodicalIF":0.0,"publicationDate":"2013-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"66797929","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
J. Watkins, Patricia L. Watkins, M. Laszewski, T. Dufan, M. Rodacker, N. Koleilat
Methods Eligible patients were diagnosed with Gleason score 8-10 at diagnostic biopsy and prostate-specific antigen (PSA) 30 ng/mL, treated with primary radical prostatectomy, without clinical evidence of distant metastatic disease, seminal vesicle invasion, or lymph node involvement. Demographic, treatment, and outcome data were retrospectively collected and analyzed from a clinical database. Survival analysis methods were employed to assess disease control and survival rates, as well as association of patient-, tumor-, and treatment-specific factors for endpoints.
{"title":"High-grade prostate adenocarcinoma: survival and disease control after radical prostatectomy","authors":"J. Watkins, Patricia L. Watkins, M. Laszewski, T. Dufan, M. Rodacker, N. Koleilat","doi":"10.12788/J.CMONC.0044","DOIUrl":"https://doi.org/10.12788/J.CMONC.0044","url":null,"abstract":"Methods Eligible patients were diagnosed with Gleason score 8-10 at diagnostic biopsy and prostate-specific antigen (PSA) 30 ng/mL, treated with primary radical prostatectomy, without clinical evidence of distant metastatic disease, seminal vesicle invasion, or lymph node involvement. Demographic, treatment, and outcome data were retrospectively collected and analyzed from a clinical database. Survival analysis methods were employed to assess disease control and survival rates, as well as association of patient-, tumor-, and treatment-specific factors for endpoints.","PeriodicalId":72649,"journal":{"name":"Community oncology","volume":"10 1","pages":"197-201"},"PeriodicalIF":0.0,"publicationDate":"2013-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"66798607","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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. 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. 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. 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. The data speak to omacetaxine’s safety in patients with advanced CML. Myelosuppression is by far the most common and serious toxicity of treatment. The myelosuppression may be delayed and profound. Otherwise, the subcutaneous injections are well tolerated. Omacetaxine’s efficacy is modest with 18%-20% major cytogenetic response in CML patients in chronic phase but none in those in accelerated phase. Hematologic responses were more frequent and one obvious role for omacetaxine in clinical practice is as a therapeutic bridge to allogeneic transplant when patients are progressing on secondor third-line TKI therapy. Are there any other roles? The availability of an orally administered third-generation TKI, ponatinib, that is also active after resistance to two or more other TKIs, even when the T315I mutation is present, suggests that omacetaxine will be relegated to last-line therapy when all or most TKIs have already been tried. Even then, in the absence of a plan for transplant, treatment goals are largely palliative since the cytogenetic responses induced by omacetaxine are of relatively short duration (median, 12 months). Hydroxyurea may provide more convenient and less expensive palliation. All other roles for omacetaxine are currently investigational.
{"title":"Other therapy options may relegate omacetaxine to last-line choice for chronic or accelerated phase CML","authors":"M. Kalaycio","doi":"10.12788/J.CMONC.0046","DOIUrl":"https://doi.org/10.12788/J.CMONC.0046","url":null,"abstract":"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. 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. 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. 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. The data speak to omacetaxine’s safety in patients with advanced CML. Myelosuppression is by far the most common and serious toxicity of treatment. The myelosuppression may be delayed and profound. Otherwise, the subcutaneous injections are well tolerated. Omacetaxine’s efficacy is modest with 18%-20% major cytogenetic response in CML patients in chronic phase but none in those in accelerated phase. Hematologic responses were more frequent and one obvious role for omacetaxine in clinical practice is as a therapeutic bridge to allogeneic transplant when patients are progressing on secondor third-line TKI therapy. Are there any other roles? The availability of an orally administered third-generation TKI, ponatinib, that is also active after resistance to two or more other TKIs, even when the T315I mutation is present, suggests that omacetaxine will be relegated to last-line therapy when all or most TKIs have already been tried. Even then, in the absence of a plan for transplant, treatment goals are largely palliative since the cytogenetic responses induced by omacetaxine are of relatively short duration (median, 12 months). Hydroxyurea may provide more convenient and less expensive palliation. All other roles for omacetaxine are currently investigational.","PeriodicalId":72649,"journal":{"name":"Community oncology","volume":"10 1","pages":"193-193"},"PeriodicalIF":0.0,"publicationDate":"2013-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"66798673","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Since President Richard Nixon declared war on cancer more than 40 years ago, there have been significant increases in the number of people who survive cancer. Alongside advances in screening, detection, and diagnosis, the development of targeted anticancer agents has been a major contributory factor to this success. We highlight some of the key developments that have shaped oncological practice in recent decades and those that will likely have a significant impact in the near future (Figure 1).
{"title":"Recent advances that are redefining oncology","authors":"J. D. Lartigue","doi":"10.12788/J.CMONC.0036","DOIUrl":"https://doi.org/10.12788/J.CMONC.0036","url":null,"abstract":"Since President Richard Nixon declared war on cancer more than 40 years ago, there have been significant increases in the number of people who survive cancer. Alongside advances in screening, detection, and diagnosis, the development of targeted anticancer agents has been a major contributory factor to this success. We highlight some of the key developments that have shaped oncological practice in recent decades and those that will likely have a significant impact in the near future (Figure 1).","PeriodicalId":72649,"journal":{"name":"Community oncology","volume":"10 1","pages":"178-185"},"PeriodicalIF":0.0,"publicationDate":"2013-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"66798233","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
When your beloved authors were studying research and statistics, around the time that Methuselah was celebrating his first birthday, we thought we knew the difference between hypothesis testing and hypothesis generating. With the former, you begin with a question, design a study to answer it, carry it out, and then do some statistical mumbo-jumbo on the data to determine if you have reasonable evidence to answer the question. With the latter, usually done after you’ve answered the main questions, you don’t have any preconceived idea of what’s going on, so you analyze anything that moves. We know that’s not really kosher, because the probability of finding something just by chance (a Type I error) increases astronomically as you do more tests. So, in the hypothesis generating phase, you don’t come to any conclusions; you just say, “That’s an interesting finding. Now we’ll have to do a real study to see if our observation holds up.” Well, we thought we knew the difference, but something must have changed over the past few centuries when we weren’t paying too much attention. The reason for our puzzlement is an article by Hurvitz et al about the relative effectiveness of trastuzumab emtansine (T-DM1) compared with trastuzumab plus docetaxel (HT) in patients with metastatic breast cancer. First, a bit about the study itself. This was a phase 2, multicenter open label randomized controlled trial. “Phase 2” means it’s not yet ready for prime time, and “open label” means that nobody was blinded regarding who got what. (“Multicenter” means a great opportunity for the investigators to rack up frequent flier points.) There were 137 women with HER2-positive metastatic breast cancer or recurrent locally advanced breast cancer, randomly divided between the 2 groups. The primary endpoints were progressionfree survival (PFS) and safety, both assessed by the investigators. Key secondary endpoints were overall survival (OS), objective response rate (ORR), quality of life (QOL), and a handful of others. What they found was that the median PFS was 9.2 months with HT, compared with 14.2 months for T-DM1; and an ORR of 58.0% in the HT group and 64.4% in the T-DM1 group; both were statistically significant. However, “preliminary OS results were similar between treatment arms.” So, let’s begin looking at the study. It may help if you jotted down all of the abbreviations that were used; we listed 15 before we ran out of lead for our pencils, and we never even got to the ones from statistics we were familiar with. We can’t fault the authors for this; it appears to be an editorial policy to abbreviate everything and not provide a table of them to help readers. Ink must be a very precious commodity. But back to the study. The paper states that “This study had a hypothesis-generating statistical design.” If you go back over all of the papers we have written for this journal, looking for a definition of “hypothesisgenerating statistical design,” you will look in vain. If you
{"title":"When is an answer not an answer","authors":"D. Streiner, G. Norman","doi":"10.12788/J.CMONC.0037","DOIUrl":"https://doi.org/10.12788/J.CMONC.0037","url":null,"abstract":"When your beloved authors were studying research and statistics, around the time that Methuselah was celebrating his first birthday, we thought we knew the difference between hypothesis testing and hypothesis generating. With the former, you begin with a question, design a study to answer it, carry it out, and then do some statistical mumbo-jumbo on the data to determine if you have reasonable evidence to answer the question. With the latter, usually done after you’ve answered the main questions, you don’t have any preconceived idea of what’s going on, so you analyze anything that moves. We know that’s not really kosher, because the probability of finding something just by chance (a Type I error) increases astronomically as you do more tests. So, in the hypothesis generating phase, you don’t come to any conclusions; you just say, “That’s an interesting finding. Now we’ll have to do a real study to see if our observation holds up.” Well, we thought we knew the difference, but something must have changed over the past few centuries when we weren’t paying too much attention. The reason for our puzzlement is an article by Hurvitz et al about the relative effectiveness of trastuzumab emtansine (T-DM1) compared with trastuzumab plus docetaxel (HT) in patients with metastatic breast cancer. First, a bit about the study itself. This was a phase 2, multicenter open label randomized controlled trial. “Phase 2” means it’s not yet ready for prime time, and “open label” means that nobody was blinded regarding who got what. (“Multicenter” means a great opportunity for the investigators to rack up frequent flier points.) There were 137 women with HER2-positive metastatic breast cancer or recurrent locally advanced breast cancer, randomly divided between the 2 groups. The primary endpoints were progressionfree survival (PFS) and safety, both assessed by the investigators. Key secondary endpoints were overall survival (OS), objective response rate (ORR), quality of life (QOL), and a handful of others. What they found was that the median PFS was 9.2 months with HT, compared with 14.2 months for T-DM1; and an ORR of 58.0% in the HT group and 64.4% in the T-DM1 group; both were statistically significant. However, “preliminary OS results were similar between treatment arms.” So, let’s begin looking at the study. It may help if you jotted down all of the abbreviations that were used; we listed 15 before we ran out of lead for our pencils, and we never even got to the ones from statistics we were familiar with. We can’t fault the authors for this; it appears to be an editorial policy to abbreviate everything and not provide a table of them to help readers. Ink must be a very precious commodity. But back to the study. The paper states that “This study had a hypothesis-generating statistical design.” If you go back over all of the papers we have written for this journal, looking for a definition of “hypothesisgenerating statistical design,” you will look in vain. If you ","PeriodicalId":72649,"journal":{"name":"Community oncology","volume":"10 1","pages":"189-190"},"PeriodicalIF":0.0,"publicationDate":"2013-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"66798281","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Nanoparticle albumin-bound (nab-) paclitaxel is a solvent-free paclitaxel formulation that has been designed to reduce adverse reactions associated with conventional solvent-based paclitaxel formulations and to improve paclitaxel tumor penetration by exploiting the physiologic transport properties of albumin. In a recently reported phase 3 trial that compared nab-paclitaxel and solvent-based paclitaxel injection in combination with carboplatin as first-line treatment of advanced non– small-cell lung cancer (NSCLC), nab-paclitaxel was associated with a significantly greater overall response rate (ORR), the primary end point, and a reduced risk of neuropathy. The findings in this international trial, combined with the demonstration of paclitaxel efficacy in this setting, supported the recent approval of nab-paclitaxel combined with carboplatin as first-line treatment of advanced NSCLC. Subset analyses in the trial suggested some potential response and survival advantages with nab-paclitaxel treatment. Of 1,052 patients with nonresectable stage 3B or stage 4 NSCLC, 521 received a weekly nab-paclitaxel 100 mg/m infusion and 531 received conventional solventbased paclitaxel 200 mg/m every 3 weeks. All of the patients received carboplatin at area under the concentrationtime curve (AUC) 6 once every 3 weeks. Steroid/antihistamine premedication was required in the solvent-based paclitaxel group and was used at investigator discretion in the nab-paclitaxel group. Patients were to receive at least 6 cycles of treatment. The primary endpoint was ORR. The median age of the patients was 60 years in the nab-paclitaxel and solvent-based paclitaxel groups, with 14% and 15% of patients, respectively, being 70 years or older; 75% of patients in both groups were men, and 80% and 82% were white. Global geographic distribution was balanced, with most patients being from Russia (46% and 44%) and Ukraine (23% and 25%), followed by Japan (14% and 14%) and the United States (12% and 11%). ECOG performance status was 1 in 74% of the nabpaclitaxel group, and 78% of the solvent-based paclitaxel group. Histology consisted of adenocarcinoma in 49% and 50% of patients, and squamous cell carcinoma in 44% and 42%; and 79% of each group had stage IV disease. In
{"title":"Nab-paclitaxel in first-line treatment of advanced non-small-cell lung cancer","authors":"J. Abraham, C. Aggarwal","doi":"10.12788/J.CMONC.0039","DOIUrl":"https://doi.org/10.12788/J.CMONC.0039","url":null,"abstract":"Nanoparticle albumin-bound (nab-) paclitaxel is a solvent-free paclitaxel formulation that has been designed to reduce adverse reactions associated with conventional solvent-based paclitaxel formulations and to improve paclitaxel tumor penetration by exploiting the physiologic transport properties of albumin. In a recently reported phase 3 trial that compared nab-paclitaxel and solvent-based paclitaxel injection in combination with carboplatin as first-line treatment of advanced non– small-cell lung cancer (NSCLC), nab-paclitaxel was associated with a significantly greater overall response rate (ORR), the primary end point, and a reduced risk of neuropathy. The findings in this international trial, combined with the demonstration of paclitaxel efficacy in this setting, supported the recent approval of nab-paclitaxel combined with carboplatin as first-line treatment of advanced NSCLC. Subset analyses in the trial suggested some potential response and survival advantages with nab-paclitaxel treatment. Of 1,052 patients with nonresectable stage 3B or stage 4 NSCLC, 521 received a weekly nab-paclitaxel 100 mg/m infusion and 531 received conventional solventbased paclitaxel 200 mg/m every 3 weeks. All of the patients received carboplatin at area under the concentrationtime curve (AUC) 6 once every 3 weeks. Steroid/antihistamine premedication was required in the solvent-based paclitaxel group and was used at investigator discretion in the nab-paclitaxel group. Patients were to receive at least 6 cycles of treatment. The primary endpoint was ORR. The median age of the patients was 60 years in the nab-paclitaxel and solvent-based paclitaxel groups, with 14% and 15% of patients, respectively, being 70 years or older; 75% of patients in both groups were men, and 80% and 82% were white. Global geographic distribution was balanced, with most patients being from Russia (46% and 44%) and Ukraine (23% and 25%), followed by Japan (14% and 14%) and the United States (12% and 11%). ECOG performance status was 1 in 74% of the nabpaclitaxel group, and 78% of the solvent-based paclitaxel group. Histology consisted of adenocarcinoma in 49% and 50% of patients, and squamous cell carcinoma in 44% and 42%; and 79% of each group had stage IV disease. In","PeriodicalId":72649,"journal":{"name":"Community oncology","volume":"10 1","pages":"166-168"},"PeriodicalIF":0.0,"publicationDate":"2013-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"66798321","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Patients with gastrointestinal stromal tumors (GIST) used to have a poor prognosis due to the very low response rate of these tumors to conventional chemotherapy and radiation therapy. However, following the introduction of imatinib as a targeted therapeutic agent with efficacy in GIST, survival outcomes have improved remarkably for patients in the advanced/metastatic and adjuvant settings. Imatinib is now approved for both indications and has become the standard of care for patients with GIST. Despite the mounting evidence demonstrating the clinical benefits of extending imatinib treatment beyond 1 year, the optimal duration of imatinib therapy has not yet been determined. Similarly, whether chronic or extended adjuvant imatinib therapy can further improve clinical outcomes in patients with GIST remains to be determined. In this review, we present recent findings from various clinical trials which indicate that prolonged, uninterrupted imatinib treatment can have durable clinical benefits in patients who underwent resection of primary, operable GIST, as well as patients with advanced, unresectable, or metastatic GIST. We also summarize data showing that treatment interruption can result in disease progression in both the adjuvant and advanced/metastatic settings. Finally, we present evidence from different trials that long-term imatinib therapy is feasible and safe (ie, without cumulative toxicities) in patients with GIST.
{"title":"Continuous imatinib therapy in patients with gastrointestinal stromal tumors","authors":"A. Hendifar, S. Chawla","doi":"10.12788/j.cmonc.0025","DOIUrl":"https://doi.org/10.12788/j.cmonc.0025","url":null,"abstract":"Patients with gastrointestinal stromal tumors (GIST) used to have a poor prognosis due to the very low response rate of these tumors to conventional chemotherapy and radiation therapy. However, following the introduction of imatinib as a targeted therapeutic agent with efficacy in GIST, survival outcomes have improved remarkably for patients in the advanced/metastatic and adjuvant settings. Imatinib is now approved for both indications and has become the standard of care for patients with GIST. Despite the mounting evidence demonstrating the clinical benefits of extending imatinib treatment beyond 1 year, the optimal duration of imatinib therapy has not yet been determined. Similarly, whether chronic or extended adjuvant imatinib therapy can further improve clinical outcomes in patients with GIST remains to be determined. In this review, we present recent findings from various clinical trials which indicate that prolonged, uninterrupted imatinib treatment can have durable clinical benefits in patients who underwent resection of primary, operable GIST, as well as patients with advanced, unresectable, or metastatic GIST. We also summarize data showing that treatment interruption can result in disease progression in both the adjuvant and advanced/metastatic settings. Finally, we present evidence from different trials that long-term imatinib therapy is feasible and safe (ie, without cumulative toxicities) in patients with GIST.","PeriodicalId":72649,"journal":{"name":"Community oncology","volume":"10 1","pages":"169-174"},"PeriodicalIF":0.0,"publicationDate":"2013-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"66798010","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Rhabdomyosarcomas are a rare group of soft tissue neoplasms of mesenchymal origin. RMS is common among childhood cancers, but it is among the rarest of adult tumors. They account for about 5% of all childhood cancers. Soft-tissue sarcomas account for less than 1% of adult malignancies, and RMS account for only 3% of those sarcomas. Here, we report a case of RMS in the neck, which led to dysphagia due to external compression of the esophagus.
{"title":"Rhabdomyosarcoma in an adult with HIV","authors":"S. Jhawar, G. Sharma, H. Ballard","doi":"10.12788/J.CMONC.0041","DOIUrl":"https://doi.org/10.12788/J.CMONC.0041","url":null,"abstract":"Rhabdomyosarcomas are a rare group of soft tissue neoplasms of mesenchymal origin. RMS is common among childhood cancers, but it is among the rarest of adult tumors. They account for about 5% of all childhood cancers. Soft-tissue sarcomas account for less than 1% of adult malignancies, and RMS account for only 3% of those sarcomas. Here, we report a case of RMS in the neck, which led to dysphagia due to external compression of the esophagus.","PeriodicalId":72649,"journal":{"name":"Community oncology","volume":"10 1","pages":"175-177"},"PeriodicalIF":0.0,"publicationDate":"2013-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"66798395","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The ATLAS trial For decades, 5 years of tamoxifen has been the standard of care for the adjuvant therapy of women with estrogen receptor positive breast cancer, although in recent years for postmenopausal women this treatment has been largely replaced with aromatase inhibitors (AIs). Would extending tamoxifen therapy to 10 years provide further benefit or merely increase toxicity? Do the results of the ATLAS trial, in which nearly 13,000 women were recruited and randomized to receive 5 more years of tamoxifen or to stop tamoxifen at 5 years, provide us with a new standard of care for premenopausal women?
{"title":"From ATLAS to HORIZONTAL: musings on five key trials","authors":"B. Mason","doi":"10.12788/j.cmonc.0038","DOIUrl":"https://doi.org/10.12788/j.cmonc.0038","url":null,"abstract":"The ATLAS trial For decades, 5 years of tamoxifen has been the standard of care for the adjuvant therapy of women with estrogen receptor positive breast cancer, although in recent years for postmenopausal women this treatment has been largely replaced with aromatase inhibitors (AIs). Would extending tamoxifen therapy to 10 years provide further benefit or merely increase toxicity? Do the results of the ATLAS trial, in which nearly 13,000 women were recruited and randomized to receive 5 more years of tamoxifen or to stop tamoxifen at 5 years, provide us with a new standard of care for premenopausal women?","PeriodicalId":72649,"journal":{"name":"Community oncology","volume":"10 1","pages":"186-188"},"PeriodicalIF":0.0,"publicationDate":"2013-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"66798298","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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