Thursday, September 20, 2012
When Cancer Treatment Causes Menopause: Tips for Preparing and Coping
http://www.onclive.com/publications/contemporary-oncology/2012/Spring-2012/When-Cancer-Treatment-Causes-Menopause-Tips-for-Preparing-and-Coping
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Wednesday, September 19, 2012
Molecular abnormalities in ovarian carcinoma: clinical, morphological and therapeutic correlates
Molecular abnormalities in ovarian carcinoma: clinical, morphological and therapeutic correlates
Abstract
The histopathological classification of ovarian surface epithelial carcinomas (referred to hereafter as "ovarian carcinoma") has shifted over the past 10 years to better reflect our understanding of molecular events during carcinogenesis. Ovarian carcinoma is no longer viewed as a singular entity but as multiple disease processes, with each having different molecular pathways altered during oncogenesis, resulting in differences in clinical and pathological features, such as biomarker expression, pattern of spread, and response to chemotherapy. There are five subtypes of ovarian carcinoma that are sufficiently distinct and well characterized that they should be considered to be different diseases i.e. high-grade serous, clear cell, endometrioid, mucinous and low-grade serous, from most to least common, respectively. This review summarizes the molecular abnormalities of these five ovarian carcinoma subtypes, relating them to clinical and pathological features.
© 2012 Blackwell Publishing Ltd
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Serial measurements of serum PDGF-AA, PDGF-BB, FGF2, and VEGF in multiresistant ovarian cancer patients treated with bevacizumab
Serial measurements of serum PDGF-AA, PDGF-BB, FGF2, and VEGF in multiresistant ovarian cancer patients treated with bevacizumab
IntroductionAnti-VEGF treatment has proven effective in recurrent ovarian cancer. However, the identification of the patients most likely to respond is still pending. It is well known that the angiogenesis is regulated by several other pro-angiogenic proteins, e.g. the platelet - derived growth factor (PDGF) system and the fibroblast growth factor (FGF) system. These other signaling pathways may remain active or become upregulated during anti-VEGF treatment.The aim of the present study was to investigate if potential changes of PDGF-BB, PDGF-AA, and FGF2 before and during bevacizumab treatment had predictive value for early progression or survival. Furthermore, we wanted to investigate the importance of serum VEGF in the same cohort.Methods:
This study included 106 patients with chemotherapy-resistant epithelial ovarian cancer who were treated with single agent bevacizumab as part of a biomarker protocol. Patients were evaluated for response by the Response Evaluation Criteria In Solid Tumors (RECIST) and/ or Gynecologic Cancer Intergroup (GCIG) CA125 criteria. Serum samples were collected at baseline and prior to each treatment. FGF2, PDGF-BB, PDGF-AA were quantified simultaneously using the Luminex system, and VEGF-A was measured by ELISA. Eighty-eight baseline samples were avaliable for FGF2, PDGF-BB, PDGF-AA analysis, and 93 baseline samples for VEGF
Results:
High baseline serum VEGF was related to poor overall survival. Furthermore, high serum PDGF-BB and FGF2 was of prognostic significance. None of the markers showed predictive value, neither at baseline level nor during the treatment.
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HE4 and ROMA Index in Czech Postmenopausal Women
HE4 and ROMA Index in Czech Postmenopausal Women
Aim: The first aim of the project was to evaluate the benefits of the determination of human epididymis protein 4 (HE4) and the risk of ovarian malignancy algorithm (ROMA) index for primary detection of ovarian cancer in a population of Czech women. The second aim was to study the advantages HE4, cancer antigen 125 (CA125) and ROMA index for distinguishing between benign and malignant tumors. Aware of the age distribution of ovarian cancer, we focused on postmenopausal patients. Patients and Methods: Our group of patients consisted of 256 females, 21 with ovarian cancer and 235 with benign ovarian tumors. All diagnoses were histologically verified. We determined the serum levels of HE4 and CA125 and calculated the ROMA2 index for postmenopausal women. Serum levels of the analytes were measured using an Architect 1000i instrument. Serum samples were collected prior to surgery or any other form of treatment and the results of the two groups of patients were compared (malignant vs. benign). Results: There was a significant difference in the serum levels for all parameters studied between the groups of patients with malignant and those with benign diagnoses (Wilcoxon test, p<0.0001). When all parameters were evaluated at 95% specificity, the HE4 cut-off was 112 pmol/l at a sensitivity of 71.42%, a positive predictive value (PPV) of 55.56%, a negative predictive value (NPV) of 97.14% and an area under the curve (AUC) of 0.9152. The CA125 cut-off was 81 IU/l at a sensitivity of 80.95%, a PPV of 58.62%, a NPV of 98.23% and an AUC of 0.9731. ROMA2 index had a cut-off 37.70% at a sensitivity of 85.71%, a PPV of 62.06%, a NPV of 98.65% and an AUC of 0.9803. The highest diagnostic efficiency was achieved by the ROMA2 index. Conclusion: Determination of HE4 along with CA125 and ROMA2 index calculation is a suitable method for the improvement of the primary detection of ovarian cancer. This approach also improves the differential diagnostic possibilities for distinguishing between malignant and benign tumors.
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Health-related Quality of Life During Sequential Chemotherapy with Carboplatin Followed by Weekly Paclitaxel in Advanced Ovarian Cancer: A Multicenter Phase II Study of the North Eastern German Society of Gynecological Oncology
Health-related Quality of Life During Sequential Chemotherapy with Carboplatin Followed by Weekly Paclitaxel in Advanced Ovarian Cancer: A Multicenter Phase II Study of the North Eastern German Society of Gynecological Oncology
Aim: We describe the impact of a sequential dose-dense schedule of carboplatin and paclitaxel on the quality of life (QoL) of patients with ovarian cancer. Patients and Methods: In this multicenter phase II trial, four cycles of carboplatin followed by 12 cycles of weekly paclitaxel were applied after cytoreductive surgery. QoL was assessed using the QoL questionnaires EORTC QLQ-C30 and QLQ-OV28 before chemotherapy (baseline), after four cycles of carboplatin, at the end of treatment (EOT), and after 6, 12, and 24 months. Results: Out of 104 eligible patients 87 (84%) participated in at least one QoL assessment. At baseline, all QLQ-C30 scales and symptoms were significantly worse than age-adjusted values for the general population. Subsequently QoL improved in general. During chemotherapy with paclitaxel, most functioning scales and symptoms worsened slightly (not significantly). However, peripheral neuropathy and chemotherapy-related side-effects increased to clinically important levels. At the end of treatment, most QoL scores were similar to those of the general population, but physical functioning and fatigue were worse. Sexual functioning and peripheral neuropathy remained problematic. Conclusion: QoL was affected mainly by the weekly paclitaxel schedule, but effects were in most cases only temporary. A dose-dense regimen using a sequential protocol may be favourable in terms of QoL.
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Salvage Chemotherapy Using Gemcitabine for Taxane/Platinum-resistant Recurrent Ovarian Cancer: A Single Institutional Experience
Salvage Chemotherapy Using Gemcitabine for Taxane/Platinum-resistant Recurrent Ovarian Cancer: A Single Institutional Experience
Background: The purpose of this study was to report on the safety and efficacy of gemcitabine used as salvage chemotherapy for ovarian cancer. Patients and Methods: From January 2002 to October 2011, 27 patients were treated with gemcitabine for platinum-resistant recurrent ovarian cancer. Gemcitabine (800 mg/m2) was given on days 1, 8, and 15 of every 28 days. The patients' medical records were retrospectively reviewed. Results: All 27 patients had previously received paclitaxel/carboplatin doublet and their disease had become platinum-resistant. The median number of previous chemotherapy regimens was 2 (range 1-7). A total of 114 cycles of single-agent gemcitabine were administered, with a median of 3 (range 1-10). No complete responses were observed. Partial response (PR) was observed in five patients (18.5%). Eight patients demonstrated stable disease (SD). The median duration of response for 5 responders was 4 months (range 2-6 months). The median survival time was 15 months. Patients with PR or SD (n=13) had significantly better survival compared with the group with progressive disease (n=14) (p=0.03, by univariate analysis). In addition, multivariate Cox proportional hazards analysis revealed that responses to gemcitabine were a significant factor for survival (hazard ratio=0.08, 95% confidence interval=0.0138 to 0.5614, p=0.01). Cases with hematological toxicity included 10 patients (37.0%) with grade 3/4 neutropenia, 3 patients (11.1%) with grade 3 thrombocytopenia, and 3 patients (11.1%) with grade 3 anemia. Non-hematological toxicity was well-tolerated. Conclusion: Gemcitabine (800 mg/m2) used for recurrent ovarian cancer possesses a modest activity and a well-tolerated toxicity.
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Treatment Decision-making Processes in the Systemic Treatment of Ovarian Cancer: Review of the Scientific Evidence
Treatment Decision-making Processes in the Systemic Treatment of Ovarian Cancer: Review of the Scientific Evidence
Background: The systemic treatment of epithelial ovarian cancer (OC) is one of the cornerstones in the multimodal management of advanced OC in both primary and recurrent stages of this disease. In most situations various treatment options are available but only few data exists about the treatment decision-making process. Therefore, we conducted a review of the current literature regarding the decision-making process concerning the systemic therapy in patients with advanced ovarian cancer. Materials and Methods: The electronic database MEDLINE (PubMed) was systematically reviewed for studies that evaluate the treatment decision-making processes in patients with advanced OC. Results: The PubMed database was searched in detail for all titles and abstracts of potentially relevant studies published between 1995 and 2011. An initial search identified 15 potentially relevant studies, but only seven met all inclusion criteria. Factors that influence treatment decisions in patients with OC include not only rational arguments and medical reasons, but also individual attitudes, fears, existential questions, various projections resulting from the physician patient relationship and the social environment. The physician's personal experience with OC treatment seems to be an important factor, followed by previous personal experience with medical issues, and the fear of side-effects and future metastases. Family and self-support organisations also seem to play a significant role in the treatment decision-making process. Conclusion: This review underlines the need for more research activities to explore the treatment decision-making process to enable the best individual support for patients in treatment decision-making. It is a challenge for clinicians to determine the individual information needs of women with OC and to involve them during the decision-making process to the extent they wish.
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Gemcitabine-induced Pulmonary Toxicity
Gemcitabine-induced Pulmonary Toxicity
Background: Gemcitabine is the only approved cytotoxic agent for the treatment of pancreatic cancer by the Food and Drug Administration. In addition, gemcitabine is also commonly used for the management of breast, ovarian, and non-small cell lung cancer. Myelosuppression is the most common toxicity of gemcitabine therapy. Pulmonary toxicities due to gemcitabine have, however, been reported. Dyspnea occurs in approximately 25% of patients treated with gemcitabine, whereas serious pulmonary toxicities are much less common, approximately 0.3%. Here, we present a case of gemcitabine-induced pneumonitis, encountered during treatment of pancreatic cancer, and review the literature of this rare, but dangerous complication. Case Report: A 56-year old male being treated for stage IV pancreatic cancer developed progressive dyspnea on exertion, chest tightness, and palpitations. Oxygen saturation was 82-84%. Computerized-tomography (CT) angiography of the chest demonstrated new diffuse groundglass opacities in the bilateral lower lobes when compared to the CT of the chest without intravenous contrast, 5 weeks prior. Mild to moderate emphysema was also seen, but no pulmonary emboli were detected. Myocardial infraction was ruled-out by normal electrocardiogram and normal cardiac biomarkers. Conclusion: We report another case of gemcitabine-induced pneumonitis. Physicians seeing such patients should be aware of this rare but real pulmonary toxicity. A delay in diagnosis and treatment can lead to potentially fatal outcomes.
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Loss of function germline mutations in RAD51D in women with ovarian carcinoma.
Loss of function germline mutations in RAD51D in women with ovarian carcinoma.
Loss of function germline mutations in RAD51D in women with ovarian carcinoma.
Gynecol Oncol. 2012 Sep 14;
Authors: Wickramanyake A, Bernier G, Pennil C, Casadei S, Agnew KJ, Stray SM, Mandell J, Garcia RL, Walsh T, King MC, Swisher EM
Abstract
OBJECTIVE: RAD51D, a gene in the Fanconi Anemia-BRCA homologous recombination pathway, has recently been shown to harbor germline mutations responsible for ovarian carcinoma in multiply affected families. We aimed to extend these results to ovarian carcinoma in the general population. METHODS: We sequenced RAD51D in germline DNA from 360 individuals with primary ovarian, peritoneal or fallopian tube carcinoma who were not selected for age of cancer onset or family history. We also sequenced RAD51D in 459 probands from 226 high risk breast cancer families who were wild type for 21 breast and ovarian cancer genes. RESULTS: Of 360 cases, three (0.8%) carried loss-of-function mutations in RAD51D. All three subjects had ovarian carcinoma; one was also diagnosed with a synchronous endometrial carcinoma. Only one of the three subjects had a family history of breast or ovarian cancer. Combined with previous data for this series, 23.9% of women with unselected ovarian, fallopian tube, or peritoneal carcinoma carried a germline loss-of-function mutation in any of 13 tumor suppressor genes. Among the 449 women and 10 men with familial breast cancer, none carried a loss of function mutation in RAD51D. CONCLUSIONS: These data support the previous observation that loss-of-function mutations in RAD51D predispose to ovarian carcinoma but not to breast carcinoma. We conclude that inherited ovarian cancer is highly heterogeneous genetically, and that approximately one in four ovarian carcinoma patients carry a germline mutation in a known tumor suppressor gene that confers high risk.
PMID: 22986143 [PubMed - as supplied by publisher]
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Tuesday, September 18, 2012
Table of Contents — Abstract Book of the 37th ESMO Congress Vienna, Austria, 28 September – 2 October 2012
Table of Contents — September 2012, 23 (suppl 9)
- Abstract Book of the 37th ESMO Congress Vienna, Austria, 28 September – 2 October 2012
RCT: L-carnitine supplementation shows no benefit for fatigue in cancer patients - NeLM
RCT: L-carnitine supplementation shows no benefit for fatigue in cancer patients - NeLM
RCT: L-carnitine supplementation shows no benefit for fatigue in cancer patients
Reference:
J Clin Oncol published early online on 17 September 2012
Source:
J Clin Oncol
Date published:
18/09/2012 17:15
Summary
by:
Hina Radia
According to research published early online in the
Journal of Clinical Oncology, four weeks of L-carnitine supplementation
did not improve fatigue in patients with invasive malignancies and good
performance status.
A double-blind, placebo-controlled study was conducted to evaluate L-carnitine, a popular complementary medicine often used by cancer patients for the treatment of fatigue.
The study involved 376 patients randomised to receive treatment with either 2g per day of L-carnitine supplementation or placebo. The primary end point was the change in average daily fatigue from baseline to week 4 using the Brief Fatigue Inventory (BFI). The following results were reported:
• The primary outcome, fatigue, measured using the BFI, improved in both arms compared with baseline (L-carnitine: −0.96, 95% CI, −1.32 to −0.60; placebo: −1.11, 95% CI −1.44 to −0.78, p=0.57 – not statistically significant).
• Secondary outcomes, including fatigue measured by the Functional Assessment of Chronic Illness Therapy–Fatigue instrument, depression, and pain, did not show significant difference between arms.
• There were no statistically significant differences in incidence of adverse events reported across the two groups.
The researchers concluded that despite some of the limitations of the study, it appears that 2-g of L-carnitine supplementation per day does not improve symptoms of fatigue in cancer patients.
A double-blind, placebo-controlled study was conducted to evaluate L-carnitine, a popular complementary medicine often used by cancer patients for the treatment of fatigue.
The study involved 376 patients randomised to receive treatment with either 2g per day of L-carnitine supplementation or placebo. The primary end point was the change in average daily fatigue from baseline to week 4 using the Brief Fatigue Inventory (BFI). The following results were reported:
• The primary outcome, fatigue, measured using the BFI, improved in both arms compared with baseline (L-carnitine: −0.96, 95% CI, −1.32 to −0.60; placebo: −1.11, 95% CI −1.44 to −0.78, p=0.57 – not statistically significant).
• Secondary outcomes, including fatigue measured by the Functional Assessment of Chronic Illness Therapy–Fatigue instrument, depression, and pain, did not show significant difference between arms.
• There were no statistically significant differences in incidence of adverse events reported across the two groups.
The researchers concluded that despite some of the limitations of the study, it appears that 2-g of L-carnitine supplementation per day does not improve symptoms of fatigue in cancer patients.
RCT: Patupilone vs. pegylated liposomal doxorubicin in patients with epithelial ovarian, primary fallopian tube, or primary peritoneal cancer - NeLM
RCT: Patupilone vs. pegylated liposomal doxorubicin in patients with epithelial ovarian, primary fallopian tube, or primary peritoneal cancer - NeLM
RCT: Patupilone vs. pegylated liposomal doxorubicin in
patients with epithelial ovarian, primary fallopian tube, or primary
peritoneal cancer
Reference:
J Clin Oncol published early online on 17 September 2012
Source:
J Clin Oncol
Date published:
18/09/2012 17:17
Summary
by:
Hina Radia
The Journal of Clinical Oncology has featured a phase
III study evaluating the safety and efficacy of patupilone vs.
pegylated liposomal doxorubicin (PLD) in patients with
platinum-refractory or -resistant epithelial ovarian, primary fallopian
tube, or primary peritoneal cancer.
The study involved a total of 829 patients who had received three or fewer prior regimens and who had received first-line taxane/platinum-based combination chemotherapy and were platinum refractory or resistant. Patients were randomised to receive either patupilone 10 mg/m2 intravenously every 3 weeks (n=412) or PLD 50 mg/m2 intravenously every 4 weeks (n=417). The primary endpoint was overall survival, and secondary endpoints were progression-free survival (PFS) and overall response rate (ORR). The following results were reported:
• The median overall survival rates were 13.2 months for patupilone and 12.7 months for PLD (Hazard ratio 0.93; 95% CI 0.79 to 1.09; p=0.195)
• The overall response rate (all partial responses) was higher in the patupilone arm than in the PLD arm (15.5% v s. 7.9%; odds ratio, 2.11; 95% CI, 1.36 to 3.29)
• Frequently observed adverse events of any grade included diarrhea (85.3%) and peripheral neuropathy (39.3%) in the patupilone arm and mucositis/stomatitis (43%) and hand-foot syndrome (41.8%) in the PLD arm.
The researchers concluded that patupilone did not demonstrate a statistically significant improvement compared to PLD in patients with platinum-refractory or -resistant epithelial ovarian, primary fallopian tube, or primary peritoneal cancer.
The study involved a total of 829 patients who had received three or fewer prior regimens and who had received first-line taxane/platinum-based combination chemotherapy and were platinum refractory or resistant. Patients were randomised to receive either patupilone 10 mg/m2 intravenously every 3 weeks (n=412) or PLD 50 mg/m2 intravenously every 4 weeks (n=417). The primary endpoint was overall survival, and secondary endpoints were progression-free survival (PFS) and overall response rate (ORR). The following results were reported:
• The median overall survival rates were 13.2 months for patupilone and 12.7 months for PLD (Hazard ratio 0.93; 95% CI 0.79 to 1.09; p=0.195)
• The overall response rate (all partial responses) was higher in the patupilone arm than in the PLD arm (15.5% v s. 7.9%; odds ratio, 2.11; 95% CI, 1.36 to 3.29)
• Frequently observed adverse events of any grade included diarrhea (85.3%) and peripheral neuropathy (39.3%) in the patupilone arm and mucositis/stomatitis (43%) and hand-foot syndrome (41.8%) in the PLD arm.
The researchers concluded that patupilone did not demonstrate a statistically significant improvement compared to PLD in patients with platinum-refractory or -resistant epithelial ovarian, primary fallopian tube, or primary peritoneal cancer.
Background on the Oncotype DX Colon Cancer Assay: QUASAR and C-07 video
http://www.oncologytube.com/index.php?page=videos§ion=view&vid_id=103062&utm_medium=email&utm_campaign=Video%3A+EMILIA+Trial+Results&utm_source=YMLP&utm_term=Background+on+the+Oncotype+DX+...
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Personalised medicine: a note of caution
Personalised medicine: a note of caution
Tailoring a patient's treatment to the particular biology of their cancer holds out the enticing prospect of avoiding over-treatment and reducing unnecessary toxicity – patients and cash-strapped health systems both stand to benefit. But delivering the right option for the right patient at the right time takes more than having the right biomarkers. And success in developing predictive biomarkers and targeted drugs has so far been modest when compared to the time, money and effort invested.All of which gives cause for concern that so many people are jumping on the 'personalised medicines' bandwagon and are pushing national and European policy makers to make this a priority.
The problem lies not with personalised medicine per se. Medicine has always been about tailoring treatment and care to a patient's particular disease, age, comorbidities and preferences. The problem is that when the term 'personalised medicine' is used today, the focus is on one aspect of tailored cancer treatment – the use of targeted drugs and predictive biomarkers.
We know that translating scientific know how into clinical reality is a highly uncertain business. History is littered with scientific failures that once appeared highly promising but ended up on the scrap heap. So far only a minority of cancer patients have derived significant benefit from targeted drugs, and that is not likely to change much in the immediate future. Arguing in favour of putting all our eggs in the 'personalised medicine' basket is therefore a flawed strategy that risks creating unrealistic public expectations.
It also takes the focus away from addressing obstacles to delivering personalised care that we do know how to overcome. Much more public funding is needed to conduct the optimisation studies that can show how best to use the the therapies we already have. Then there is the question of delivering personalised cancer care in everyday practice. Urgent action is required to improve cancer services, so every patient receives the attention of the right mix of specialists, to plan and deliver care tailored to their needs.
And finally, while we certainly need to vigorously pursue the potential for developing therapies designed using our knowledge of cancer genetics, the current heavy focus on drugs is too narrow. What about the potential for more precise tailoring of surgical and radiotherapy strategies, which currently account for only a tiny fraction of research into personalised therapies?
We need to be careful about the messages we send out. The biggest potential for improving cancer outcomes over the coming years lies in redesigning health systems to give all patients, regardless of cancer type, access to high-quality treatment and care from a multidisciplinary team of specialists. If we call for policymakers to focus instead on a scientific potential that might never reach the mainstream, we risk giving them a green light to shirk their duty to do what they must do to improve th...
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HE4 protein and SMRP: Potential novel biomarkers in ovarian cancer detection.
HE4 protein and SMRP: Potential novel biomarkers in ovarian cancer detection.
HE4 protein and SMRP: Potential novel biomarkers in ovarian cancer detection.
Oncol Lett. 2012 Sep;4(3):385-389
Abstract
Epithelial ovarian cancer has the highest mortality of all gynecological cancers, and its progression is often without symptoms. Clinical outcome and survival may be improved if the disease is identified in the early stages. The objective of the study was to evaluate the utility of the serum biomarkers human epididymis protein 4 (HE4), soluble mesothelin-related protein (SMRP) and CA125 in the detection of ovarian cancer. In this retrospective study, the serum concentrations of CA125, HE4 protein and SMRP were measured in a cohort of 70 patients with epithelial ovarian cancer (EOC) compared with 78 healthy controls. Median serum levels of CA125 for ovarian cancer cases were 503.55±560.7 U/ml vs. 9.28±14.47 U/ml in the control group (p<0.001); for SMRP 5.13±7.64 nM vs. 1.02±0.89 nM (p<0.01); and for HE4 597.95±934.59 pM vs. 56.75±43.79 pM (p<0.001), respectively. Positive correlations between the clinical stage of EOC and CA125, HE4 and SMRP serum concentrations were found [(R=0.83; p<0.001); (R=0.64; p<0.001); (R=0.45; p<0.001), respectively]. Data analysis for the whole study group also revealed a significant correlation between plasma concentrations of CA125 and HE4 (R=0.45; p<0.001), between CA125 and SMRP (R=0.38; p<0.001) as well as HE4 and SMRP (R=0.51; p<0.001). Similar significant correlations between serum biomarker concentrations were also found in the ovarian cancer group [CA125 and HE4 (R=0.31; p<0.01); CA125 and SMRP (R=0.25; p<0.05); HE4 and SMRP (R=0.44, p<0.001), respectively]. A significant correlation was observed between the serous histological type of EOC and serum concentration of HE4 in the study group compared with other non-serous types of ovarian cancer (p<0.01). In conclusion, measuring CA125 in combination with new biomarkers such as SMRP and HE4 may improve the accuracy of ovarian cancer diagnosis, particularly in early detection of the disease.
PMID: 22984370 [PubMed - as supplied by publisher]
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Monday, September 17, 2012
Sept 24th Webinar for Outpatient Oncology Providers + information on preventing infections in cancer patients
Webinar for Outpatient Oncology Providers
Webinar for Outpatient Oncology Providers
Centers for Disease Control and Prevention (CDC) sent this bulletin at 09/17/2012 01:05 PM EDT Doctors and nurses who care for cancer patients can take steps to help prevent infections. Join us for a free webinar featuring experts from CDC and other organizations. This webinar is a must-attend for every doctor, nurse, and health care provider who works with cancer patients. The webinar will—- Help doctors make sure their clinic is following recommended infection control standards to reduce their patients' risk of getting infections.
- Feature new information and tools that providers can use to help prevent infections.
Webinar: Infection Control and Prevention in Outpatient Oncology Clinics
Monday, September 24, 2012, 1:00–2:00 p.m. EDT
More Information about Preventing Infections in Cancer PatientsMonday, September 24, 2012, 1:00–2:00 p.m. EDT
If I Paint a Rosy Picture, Will You Promise Not to Cry? The Art of Oncology series
If I Paint a Rosy Picture, Will You Promise Not to Cry?
“Am I going to be OK, doc?”“Yes. Yes, you are.”“How do you know?”“Because I'm a doctor.”
These are powerful words, and it is impressive how very much we want to say them. The patient is in distress. The physician's
voice is calm, reassuring.
“You're going to be OK. I'm a doctor. I know.”....
A Phase I Trial of Trastuzumab and Alvespimycin
A Phase I Trial of Trastuzumab and Alvespimycin:
Purpose: We conducted a phase I dose-escalation study to define the maximum tolerated dose (MTD), pharmacokinetics (PK), and pharmacodynamics of alvespimycin (17-DMAG), a heat shock protein 90 (Hsp90) inhibitor, given in combination with trastuzumab.
Experimental Design: Patients were treated with trastuzumab followed by intravenous alvespimycin on a weekly schedule. Hsp90 client proteins were measured at baseline and serially in peripheral blood lymphocytes (PBL) during cycle 1. Patients with advanced solid tumors progressing on standard therapy were eligible.
Results: Twenty-eight patients (25, breast; 3, ovarian) were enrolled onto three dose cohorts: 60 (n = 9), 80 (n = 13), and 100 mg/m2 (n = 6). Dose-limiting toxicities (DLT) were: grade III left ventricular systolic dysfunction presenting as congestive heart failure in 1 patient (100 mg/m2), and reversible grade III keratitis in two patients (80 mg/m2). Drug-related grade III toxicity included one episode each of fatigue, diarrhea, myalgia, and back pain. Common mild to moderate toxicities included diarrhea, fatigue, myalgia, arthralgia, nausea, blurry vision, headache, back pain, and dry eyes. There was one partial response and seven cases of stable disease (range, 4–10 months), all in HER2+ MBC. In addition, an ovarian cancer patient had complete resolution of ascites and pleural effusion that lasted 24.8 months. There was no change in PK upon weekly dosing. Hsp70 effect continued to increase across four weeks and was most pronounced at 80 and 100 mg/m2.
Conclusion: The combination of alvespimycin and trastuzumab is safe and tolerable at MTD. Antitumor activity was seen in patients with refractory HER2+ MBC and ovarian cancer. The recommended dose of alvespimycin for further study in this combination is 80 mg/m2 weekly. Clin Cancer Res; 18(18); 5090–8. ©2012 AACR.
message from Genetic Alliance: Genetic Alliance wants to hear from you about your experience with biobanks and registries
16/09/2012
Genetic Alliance is
conducting a short, anonymous survey about biobanks. (We are defining
biobank as a collection of human biological samples, such as blood or
tissue samples and the information associated with
these samples, such as health information, that are stored for future
use and managed according to professional standards.) We are asking
current biobank participants and those who may be interested in
participating in biobanking in the future. This survey
has been approved by the Genetic Alliance Institutional Review Board
#IORG0003358.
Help us
recruit additional participants for our survey! The more people that
respond, the more accurately we can take the pulse of the community on
biobanking. Please consider sending this to your
clients/members (below)/network. We want to be sure ordinary people are well represented!
Dear Member/client/friend…,
An
umbrella group (or network – your choice) called Genetic Alliance to
which we belong, is asking people who have banked biological samples
anywhere (in a hospital surgery, in a biobank, in a
research project or clinical trial) or donated health information, to
reply to a short survey. They are working to understand what people who bank these samples and health information
are concerned about.to
make sure policies to protect participants are in place, and also to
understand what people who bank these samples are concerned about. The
survey has been
approved by the Genetic Alliance Institutional Review Board. Please
respond ASAP: Take
the survey
Best,
You
As always, we will share the results with you!
Thanks very much!
Sharon
Best,
Sharon
===========================
Sharon F. Terry | President
and CEO
Genetic
Alliance | 4301 Connecticut Avenue, NW | Suite 404 | Washington, DC
20008 | Phone: 202.966.5557 x 201 | Fax: 202.966.8553
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