Saturday, September 15, 2012
Green tea and green tea catechin extracts: An overview of the clinical evidence
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Green tea and green tea catechin extracts: An overview of the clinical evidence
Publication year: 2012Source:Maturitas
Rachel Johnson, Susan Bryant, Alyson L. Huntley
Background Tea leaves contain varying amounts of polyphenols of which the majority are catechins. There has been a sizable amount of research on the potential effect of green tea catechins for cancer risk, cardiovascular disease risk and weight loss; all conditions that are relevant to mid-life health. The aim was to produce an overview of the evidence for green tea for these three important health conditions. Methods The databases Medline (& Medline in process) and Embase, were searched for systematic reviews and meta-analyses using customised search strategies performed up until April 2012. Assessment of Multiple Systematic Reviews criteria were used to assess the quality of the included reviews. Relevant data were extracted into predefined tables. The results are described and discussed narratively. Results We included eight systematic reviews and meta-analyses covering the topics of cancer risk (n =2), cardiovascular risk (n =4) and weight loss (n =2). Conclusions The evidence for green tea and cancer risk is inadequate and inconclusive. However there is some positive evidence for risk reduction of breast, prostate, ovarian and endometrial cancers with green tea. RCTs of green tea and cardiovascular risk factors suggest that green tea may reduce low-density lipoproteins and total cholesterol, although studies are of short duration. There is no robust evidence to support a reduction in coronary artery disease risk in green tea drinkers. There are a considerable number of RCTs to suggest that green tea does reduce body weight in the short term, but this not likely to be of clinical relevance.
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Outcomes of cancer patients after unplanned admission to general intensive care units, Acta Oncologica, Informa Healthcare
Outcomes of cancer patients after unplanned admission to general intensive care units, Acta Oncologica, Informa Healthcare
Abstract
Background.
Acute admission to an intensive care unit (ICU) of cancer patients is
considered with increasing frequency due to a better life expectancy and
more aggressive therapies. The aim of this study was to determine the
characteristics and outcomes of cancer patients with unplanned
admissions to general ICUs, and to compare these with outcomes of
critically ill patients without cancer.
Material and methods. All
unplanned ICU admissions in the Netherlands collected in the National
Intensive Care Evaluation registry between January 2007 and January 2011
were analyzed.
Results and conclusion. Of the 140,154 patients
with unplanned ICU admission 10.9% had a malignancy. Medical cancer
patients were more severely ill on ICU admission in comparison with
medical non-cancer patients, as reflected by higher needs for mechanical
ventilation (50.8% vs. 46.4%, p < 0.001) and vasopressors within 24
hours after admission (41.5% vs. 33.0%, p < 0.001), higher Acute
Physiology and Chronic Health Evaluation (APACHE) IV scores (88.1 vs.
67.5, p < 0.001) and a longer ICU stay (5.1 vs. 4.6 days, p
< 0.001). In contrast, surgical cancer patients only displayed a
modestly higher APACHE IV score on admission when compared with
non-cancer surgical patients, whereas the other afore mentioned
parameters were lower in the surgical cancer patients group. In-hospital
mortality was almost twice as high in medical cancer patients (40.6%)
as in medical patients without cancer (23.7%). In-hospital mortality of
surgical cancer patients (17.4%) was slightly higher than in patients
without cancer (14.6%). These data indicate that unplanned ICU admission
is associated with a high mortality in patients with cancer when
admitted for medical reasons.
Hereditary Gynecological Malignancies: Advances in Screening
Hereditary Gynecological Malignancies: Advances in Screening and Treatment
DOI: 10.1111/his.12028
© 2012 Blackwell Publishing Ltd
Additional Information(Show All)
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Cell-cell and cell-matrix dynamics in intraperitoneal cancer metastasis.
Cell-cell and cell-matrix dynamics in intraperitoneal cancer metastasis.
Abstract
The peritoneal metastatic route of cancer dissemination is shared by cancers of the ovary and gastrointestinal tract. Once initiated, peritoneal metastasis typically proceeds rapidly in a feed-forward manner. Several factors contribute to this efficient progression. In peritoneal metastasis, cancer cells exfoliate into the peritoneal fluid and spread locally, transported by peritoneal fluid. Inflammatory cytokines released by tumor and immune cells compromise the protective, anti-adhesive mesothelial cell layer that lines the peritoneal cavity, exposing the underlying extracellular matrix to which cancer cells readily attach. The peritoneum is further rendered receptive to metastatic implantation and growth by myofibroblastic cell behaviors also stimulated by inflammatory cytokines. Individual cancer cells suspended in peritoneal fluid can aggregate to form multicellular spheroids. This cellular arrangement imparts resistance to anoikis, apoptosis, and chemotherapeutics. Emerging evidence indicates that compact spheroid formation is preferentially accomplished by cancer cells with high invasive capacity and contractile behaviors. This review focuses on the pathological alterations to the peritoneum and the properties of cancer cells that in combination drive peritoneal metastasis.
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Influence of a family history of breast and/or ovarian cancer on breast cancer outcomes.
Influence of a family history of breast and/or ovarian cancer on breast cancer outcomes.
Influence of a family history of breast and/or ovarian cancer on breast cancer outcomes.
Exp Ther Med. 2011 9;2(5):917-923
Authors: Cao AY, He M, DI GH, Wu J, Lu JS, Liu GY, Shen ZZ, Shao ZM
Abstract
Various published studies have been inconclusive in attempting to relate a family history of breast and/or ovarian cancer (BOC) to the survival of breast cancer patients. The aim of the study was to investigate the association of a family history of BOC with tumor characteristics, treatment response and the difference between the prognosis of familial breast cancer (FBC) patients and sporadic breast cancer (SBC) patients. Data on 348 operable FBC patients and 345 SBC patients were retrospectively analyzed. The overall survival (OS) and recurrence/metastasis-free survival (RFS) were compared for both groups. FBC cases were diagnosed at a relatively younger age (51.1±10.4 vs. 53.7±11.0 years, P=0.054) and presented a lower T stage (P=0.000) than the SBC cases. Patients with a family history of BOC had a significantly greater risk of recurrence/metastasis (P= 0.04) and a non-significantly increased risk of death (P=0.06) compared to the SBC patients. In a multivariate analysis, family history of BOC was an independent predictive factor for both recurrence/metastasis rate (P=0.01, HR=0.012, 95% CI 0.02-0.57) and mortality (P=0.044, HR=0.43, 95% CI 0.19-0.98) in the hormone receptor-positive population. Our results found that women diagnosed with FBC had an early onset of disease in the population studied, and the poor outcome of patients with a family history of BOC associated with survival was restricted to the hormone receptor-positive population.
PMID: 22977598 [PubMed - as supplied by publisher]
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Friday, September 14, 2012
Gregory Pawelski on Expert Opinion: A US Perspective On Beating Cancer (ovarian....)
Gregory Pawelski on Expert Opinion: A US Perspective On Beating Cancer:
I first came across in 2003, the disparities in cancer care between the US and the UK in a clinical trial by Dr. Ian Cree, studying how well chemosensitivity assays predict response to chemotherapy in patients with persistent, refractory, or recurrent ovarian epithelial, peritoneal, or fallopian tube cancer. The results were highly suggestive of an effect due to the assay, and the most successful drug regimens used were nearly all developed using the assay. However, UK results in cancer are always lower than in the US for a variety of reasons. Part of this is probably lead time bias, but data on surgical debulking may be part of the explanation. Patients in the US get a whole lot more surgery along the way than in Europe. Even in the underpowered Cree, et al study, the use of his ATP assay changed treatment decisions in something like 90% of the cases, but the study was too small to show that the changed treatment decisions were to the benefit of the patient, in terms of long survival. The study allowed the physician's choice arm to include Dr. Cree's own drug combination as the trial accrued (BMC Cancer. 2003: 3:19). This experience taught me to look at those disparities closer, particularly when it comes to the British National Institute for Clinical Excellence (NICE). Based on clinical trials, results showing no difference between single-agent platinums versus platinum/taxol (GOG Trial #132, ICON3, ICON4), NICE determined that platinum/taxol should no longer be considered as standard therapy, and that a range of therapies are equally acceptable (Lancet 2002;360:500-501, 505-515). In the US, where the administration of platinum/taxol had been much more profitable to the treating oncologist than single-agent platinum, there had been the dogged insistance that platinum/taxol remained standard, despite clear lack of support for this position, based on the entirety of the clinical trials literature. Platinum-taxol is not superior to single-agent carboplatin and single-agent cisplatin. I wrote a paper "Who Needs Taxol?" One of the researchers listed in the foot notes of the paper (Carcinomatous Meningitis: Taxane-Induced) which found what is called "dissemination after taxane-based chemotherapy," had told me that the study he finally published in the journal Oncology, was rejected by all other American & European cancer journals (Journal of Clinical Oncology, Cancer, Annals of Oncology, European Journal of Cancer, International Journal of Cancer) where it had been submitted. The journal were reluctant to publish such a scientific report, simply because taxanes (both taxol and taxotere) were at the time very intensively advertised in these journals. Why would the UK look to the US with a tinge of envy about what we do when it comes to providing cancer care? Yes, the problem is we can't afford to keep doing this, while NICE is trying to do something about it.
Cochrane request: Take part in an innovative pilot study using your iPhone, iPad, or iPod Touch
Take part in an innovative pilot study using your iPhone, iPad, or iPod Touch:
Dear Cochrane colleagues
We are pleased to invite you to take part in an innovative research study using your iPhone, iPad, or iPod Touch. I realise many of you, myself included, don't have one of these devices...but we'd be really grateful if you could help us out by passing this invitation on to friends, relations and colleagues who do. We are particularly interested in recruiting people unfamiliar with Cochrane and EBM, including older school students.
External link for more information:
Contributor's name:
Caroline Struthers
Email address:
caroline.struthers@ndm.ox.ac.uk
DOD Announces Research Funding Opportunities
DOD Announces Research Funding Opportunities:
The following pre-announcement on a postdoctoral fellowship award may be of interest to those working on colon cancer/breast cancer or pancreatic cancer/breast cancer (BRCA2 mutations) research.
The fiscal year 2012 (FY12) Defense Appropriations Act provides $120 million to the Department of Defense Breast Cancer Research Program (BCRP) to support innovative, high-impact breast cancer research. The BCRP is administered by the U.S. Army Medical Research and Materiel Command through the Office of Congressionally Directed Medical Research Programs (CDMRP).
The FY12 BCRP program announcement and general application instructions for the following award are anticipated to be posted on grants.gov in October.
Eligibility
- Principal Investigator: doctoral graduates (PhD or MD). Clinical investigators are eligible to apply. Must have no more than two years experience in the proposed research setting and no more than four years of postdoctoral research experience as of the application deadline.
- Mentor or formal co-mentor must have breast cancer research experience, including current funding and publications.
- Supports the training of exceptionally talented recent doctoral or medical graduates who have demonstrated that they are the "best and brightest" of their peers.
- Individualized training program and mentorship should prepare the principal investigator for an independent career at the forefront of breast cancer research.
- Proposed research should address a critical problem in breast cancer.
- Maximum funding of $300,000 for direct costs ($100,000 per year, plus indirect costs).
- Period of performance not to exceed three years.
Position Opening: Executive Director | Society for Participatory Medicine
Position Opening: Executive Director | Society for Participatory Medicine
The Society for Participatory Medicine (SPM) seeks a part-time executive director. SPM is a nonprofit organization that promotes Participatory Medicine through its journal, online community, meetings, and other channels. Participatory Medicine is a cooperative model of healthcare that encourages and expects active involvement by all connected parties (patients, caregivers, healthcare professionals, etc.) as integral to the full continuum of care. The Executive Director will report to the Board of Directors and participate in bi-weekly executive committee meetings and other organizational meetings.
Major areas of responsibility include:...............
Non-steroidal anti-inflammatory drug use and ovarian cancer risk: findings from the NIH-AARP Diet and Health Study and systematic review.
Non-steroidal anti-inflammatory drug use and ovarian cancer risk: findings from the NIH-AARP Diet and Health Study and systematic review.:
| Related Articles |
Cancer Causes Control. 2012 Sep 13;
Abstract
BACKGROUND: Chronic inflammation has been proposed as a risk factor for ovarian cancer. Some data suggest that anti-inflammatory medications may be protective against ovarian cancer; however, results have been inconsistent. METHODS: We evaluated the risk of epithelial ovarian cancer with regular use of NSAIDs prospectively in the NIH-AARP Diet and Health Study, using Cox proportional hazard models. We also examined the risk of common subtypes of epithelial ovarian cancer (serous, mucinous, endometrioid, clear cell, and other epithelial) with regular use of NSAIDs. In addition, we performed meta-analyses summarizing the risk of ovarian cancer with "regular use" of NSAIDs in previously published studies. RESULTS: We did not observe a significant association between regular use of NSAIDs with ovarian cancer risk in the AARP cohort (aspirin: RR 1.06, 95 % CI 0.87-1.29; non-aspirin NSAIDs: RR 0.93, 95 % CI 0.74-1.15); however, summary estimates from prospective cohort studies demonstrated that use of non-aspirin NSAIDs may reduce the risk of ovarian cancer (RR 0.88, 95 % CI 0.77-1.01). Although not significant, we found that mucinous tumors were inversely associated with non-aspirin NSAID use (RR 0.69, 95 % CI 0.23-2.10) in the AARP cohort, which was supported by the meta-analysis (RR 0.69, CI 0.50-0.94.) CONCLUSION: Although results from the NIH-AARP cohort study were not statistically significant, our meta-analysis suggests that non-aspirin NSAIDs may be protective against ovarian cancer. Additional analyses, focusing on dose, duration, and frequency of NSAID use and accounting for ovarian cancer heterogeneity are necessary to further elucidate the association between NSAID use and ovarian cancer risk.
PMID: 22972000 [PubMed - as supplied by publisher]
Frequency of mismatch repair deficiency in ovarian cancer: a systematic review This article is a US Government work and, as such, is in the public domain of the United States of America.
Frequency of mismatch repair deficiency in ovarian cancer: a systematic review This article is a US Government work and, as such, is in the public domain of the United States of America
Int J Cancer. 2011 Oct 15;129(8):1914-22
Abstract
Loss of mismatch repair (MMR) capacity may represent an important tumor initiating mechanism in ovarian cancer. We conducted a systematic review to analyze the frequency of microsatellite instability (MSI), immunohistochemical (IHC) staining for MMR proteins, and hypermethylation of the MLH1 promoter region in ovarian cancers. Studies examining MSI, loss of MMR gene expression by IHC staining and MLH1 promoter hypermethylation in ovarian cancer were identified by a systematic literature search of the PubMed electronic database through August 31, 2009. Pertinent data was extracted from eligible studies and estimates for pooled proportions were computed using random effects models. The pooled proportion of MSI detection was 0.10 (95% CI, 0.06-0.14) among 1,234 cases in 22 studies. Dinonucleotide markers had a higher frequency of instability than mononucleotide markers. The pooled proportion of MLH1 or MSH2 staining loss was 0.06 (95% CI, 0.01-0.17) among 474 cases in three studies, with a higher frequency of loss in MLH1. The pooled proportion of MLH1 methylation was 0.10 (95% CI, 0.06-0.15) among 672 cases in seven studies. Data reporting MSI and loss of MMR staining in the same cases was limited. Although MMR deficiency was found in all histologic subtypes, endometrioid cancers had the highest proportion.
Approximately 10% of unselected ovarian cancers are related to MMR deficiency. While MMR deficiency is associated with improved survival in other MMR-deficiency related cancer sites, epidemiological and clinical factors related to the MMR-deficient phenotype have not been adequately studied in ovarian cancer to date.
PMID: 21140452 [PubMed - indexed for MEDLINE]
Paclitaxel inhibits ovarian tumor growth by inducing epithelial cancer cells to benign fibroblast-like cells - Corrected Proof
Paclitaxel inhibits ovarian tumor growth by inducing epithelial cancer cells to benign fibroblast-like cells - Corrected Proof:
Highlights:
► Paclitaxel can induce the EMT of epithelial cancer.
► Fibroblast-like cells induced by paclitaxel are benign in nature.
► Epithelial cancer cells and benign fibroblasts may be interchangeable.
Abstract: Paclitaxel is commonly used to treat multiple human malignancies, but its mechanism of action is still poorly defined. Human ovarian cancer SKOV3 cells (parental SKOV3) were treated with paclitaxel (1μM) for 2days, and the morphologic changes in the cells were monitored for more than 4months. Parental SKOV3 underwent a markedly morphologic transition from the epithelial to fibroblast-like phenotype following treatment with paclitaxel; the resulting cells were designated as SKOV3-P. The SKOV3-P cells’ proliferative ability was assessed via a 3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide (MTT) assay. The molecular characteristics of these cells were assessed via immunocytochemical staining and Western blot analysis. Their invasiveness and tumor formation ability was evaluated via wound-scratch and colony formation assays. The tumorigenicity of SKOV3-P cells was assessed in vivo after subcutaneous injection of tumor cells between injections of parental and paclitaxel-treated cells in nude mice. SKOV3-P cells have decreased the proliferation and invasion ability, decreased colony-forming ability when cultured in Matrigel and lost their tumor formation as compared with parental SKOV3 cells when injected in nude mice. SKOV3-P cells have decreased expression of E-cadherin, cytokeratin, Snail, PI3K, and P-Akt-Ser473, and increased expression of fibronectin, vimentin, Slug, P27, and PTEN. These results demonstrated that paclitaxel can inhibit tumor growth by inducing ovarian cancer epithelial cells toward a benign fibroblast-like phenotype through dysregulation of previously known pathways involved in the regulation of epithelial to mesenchymal transition (EMT), which may represent a novel mechanism for paclitaxel-induced tumor suppression.
A Phase 2 Study of the IDO Inhibitor INCB024360 Versus Tamoxifen for Subjects With Biochemical-recurrent-only EOC, PPC or FTC Following Complete Remission With First-line Chemotherapy
A Phase 2 Study of the IDO Inhibitor INCB024360 Versus Tamoxifen for Subjects With Biochemical-recurrent-only EOC, PPC or FTC Following Complete Remission With First-line Chemotherapy:
Conditions: Biochemical-recurrent Only Epithelial Ovarian Cancer; Primary Peritoneal Carcinoma; Fallopian Tube Cancer
Interventions: Drug: INCB024360; Drug: tamoxifen
Sponsors: Incyte Corporation; Incyte Corporation
Recruiting - verified September 2012
A Phase 2 Study of the IDO Inhibitor INCB024360 Versus Tamoxifen for Subjects With Biochemical-recurrent-only EOC, PPC or FTC Following Complete Remission With First-line Chemotherapy
A Phase 2 Study of the IDO Inhibitor INCB024360 Versus Tamoxifen for Subjects With Biochemical-recurrent-only EOC, PPC or FTC Following Complete Remission With First-line Chemotherapy:
Conditions: Biochemical-recurrent Only Epithelial Ovarian Cancer; Primary Peritoneal Carcinoma; Fallopian Tube Cancer
Interventions: Drug: INCB024360; Drug: tamoxifen
Sponsors: Incyte Corporation;
Recruiting - verified September 2012
Cancer: Heat Bio vaccine to target bladder, ovarian cancers | MedCity News
"...Heat is in phase 2 clinical trials studying its vaccine candidate HS-110 to treat nonsmall cell lung cancer. The company plans to start additional clinical studies in bladder and ovarian cancer this year. Heat's proprietary Immune Pan-Antigen Cytotoxic Therapy, or ImPACT, reprograms live tumor cells to continually produce antigens that prompt the body's immune system to fight disease. ImPACT is used to make off-the-shelf vaccines that can be used by a general population of patients, unlike some of the personalized medicine therapies that are patient specific....
http://medcitynews.com/2012/01/vaccine-developer-heat-biologics-lands-250k-clinical-trials-for-bladder-ovarian-cancers-planned/
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Thursday, September 13, 2012
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