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Showing posts with label ovarian. Show all posts
Showing posts with label ovarian. Show all posts

Wednesday, April 04, 2012

abstract: Incidence, prevalence and risk factors for peritoneal carcinomatosis from colorectal cancer - Segelman - 2012 - British Journal of Surgery - Wiley Online Library




Peritoneal Carcinomatosis (Creighton University) includes a variety of tumors that present with extensive metastasis throughout the peritoneal cavity (inside surface of the abdomen) and can be found with gall bladder, liver, colon, appendix, ovarian, pancreas, mesothelioma, pseudomyxoma peritonei, rectal, small bowel and stomach cancers. It is a broad description in which multiple tumors develop in and line the peritoneal abdominal cavity and linings.

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 Incidence, prevalence and risk factors for peritoneal carcinomatosis from colorectal cancer - Segelman - 2012 - British Journal of Surgery

Abstract

Background:

This was a population-based cohort study to determine the incidence, prevalence and risk factors for peritoneal carcinomatosis (PC) from colorectal cancer.

Methods:

Prospectively collected data were obtained from the Regional Quality Registry. The Cox proportional hazards regression model was used for multivariable analysis of clinicopathological factors to determine independent predictors of PC.

Results:

All 11 124 patients with colorectal cancer in Stockholm County during 1995–2007 were included and followed until 2010. In total, 924 patients (8·3 per cent) had synchronous or metachronous PC. PC was the first and only localization of metastases in 535 patients (4·8 per cent). The prevalence of synchronous PC was 4·3 per cent (477 of 11 124). The cumulative incidence of metachronous PC was 4·2 per cent (447 of 10 646). Independent predictors for metachronous PC were colonic cancer (hazard ratio (HR) 1·77, 95 per cent confidence interval 1·31 to 2·39; P = 0·002 for right-sided colonic cancer), advanced tumour (T) status (HR 9·98, 3·10 to 32·11; P < 0·001 for T4), advanced node (N) status (HR 7·41, 4·78 to 11·51; P < 0·001 for N2 with fewer than 12 lymph nodes examined), emergency surgery (HR 2·11, 1·66 to 2·69; P < 0·001) and non-radical resection of the primary tumour (HR 2·75, 2·10 to 3·61; P < 0·001 for R2 resection). Patients aged > 70 years had a decreased risk of metachronous PC (HR 0·69, 0·55 to 0·87; P = 0·003).

Conclusion:

PC is common in patients with colorectal cancer and is associated with identifiable risk factors.

Sunday, March 25, 2012

open access - Revie: Unravelling modifiers of breast and ovarian cancer risk for BRCA1 and BRCA2 mutation carriers: update on genetic modifiers - Journal of Internal Medicine (references to Lynch Syndrome/Familial Melanoma)



Unravelling modifiers of breast and ovarian cancer risk for BRCA1 and BRCA2 mutation carriers: update on genetic modifiers - Journal of Internal Medicine

pdf file

Genetic variants associated with breast cancer risk for BRCA1 mutations carriers

Genetic variants associated with breast cancer risk for BRCA2 mutations carriers

Patterns of association and tumour characteristics

Genetic modifiers of ovarian cancer risk

Environmental, hormonal and reproductive modifiers of risk

Common alleles and cancer risks for mutation carriers

Future challenges     "Over the past 5 years, there has been substantial progress in our understanding of genetic factors that modify breast and ovarian cancer risk for BRCA1 and BRCA2 mutation carriers. This was made possible to a great extent because of the availability of large numbers of mutation carriers from the CIMBA consortium and GWAS data. However, the five loci described in this review that are associated with breast cancer risk for BRCA1 mutation carriers are estimated to explain only approximately 3% of the genetic variability in breast cancer risk for BRCA1 mutation carriers. Similarly, the 11 SNPs associated with breast cancer risk for BRCA2 mutation carriers are estimated to account for approximately 6% of the genetic variability in breast cancer risk for BRCA2 mutation carriers. Therefore, the majority of the genetic variability in breast cancer risk for mutation carriers still remains unexplained. Several more breast and ovarian cancer susceptibility alleles have been identified through GWAS in the general population, but have not yet been investigated in mutation carriers [61, 63, 72, 75]. Given the observed association patterns in mutation carriers with previously identified loci, it is expected that at least a subset of these will also be associated with breast or ovarian cancer risk for mutation carriers. Additional genetic modifiers of risk may also be identified through not only the ongoing GWAS in BRCA1 and BRCA2 mutation carriers but also other GWAS from the general population or by GWAS focusing on specific cancer subtypes such as oestrogen-receptor-negative or triple-negative breast cancers, or serous ovarian cancer. However, it is likely that several of the alleles identified through population-based GWAS may be associated with modest relative risks in the range of 1.05–1.10. Despite sample sizes of approximately 15 000 BRCA1 and 10 000 BRCA2 mutation carriers, CIMBA would still be underpowered to detect modifying polymorphisms conferring such modest relative risks. Given the rarity of BRCA1 and BRCA2 mutations, increasing sample sizes is currently only possible through increased collaboration between studies and through continued recruitment of mutation carriers........

Conclusions

As more cost-effective mutation screening techniques become available, the number of identified BRCA1 and BRCA2 mutation carriers in the population is likely to increase. Therefore, it will be important that all mutation carriers are provided with accurate information on their risk of developing breast and ovarian cancer, so that informed decisions on clinical management are made. Our understanding of factors influencing cancer risk variability in mutation carriers has increased over the last few years and is likely to improve further in the near future. Therefore, we are getting closer to the goal of being able to provide more individualized clinical management. Understanding how cancer risks are modified in BRCA1 and BRCA2 mutation carriers will also provide further insights for studying the biological mechanisms of cancer development in mutation carriers. These may lead to the development of novel therapies and more accurate prediction of breast and ovarian cancer progression in mutation carriers.
Studying genetic modifiers of breast and ovarian cancer risk for BRCA1 and BRCA2 mutation carriers has provided useful insights in study design, analytical methodology and applications, which could be used for studying modifiers of disease in carriers of other high-risk mutations such as the mismatch repair genes MSH2, MLH1, MSH6, PMS2 in colorectal cancer (Lynch Syndrome) and CDKN2A in melanoma but also other noncancer-related diseases.

 

 

 

 

 

 




Monday, January 09, 2012

open access: Jan 2012 - Assessing the malignant potential of ovarian inclusion cysts in postmenopausal women within the UK Collaborative Trial of Ovarian Cancer Screening (UKCTOCS): a prospective cohort study



Objective  To evaluate the malignant potential of ultrasound-detected ovarian inclusion cysts in the development of ovarian cancer (OC) in postmenopausal women.
Design  Prospective cohort study.
Setting  UK Collaborative Trial of Ovarian Cancer Screening (UKCTOCS).
Population  Postmenopausal women.

Conclusions  Postmenopausal women with ultrasound-detected inclusion cysts do not seem to be at increased risk of ovarian or breast/endometrial (hormone-dependent) cancers.

see also 

Table 1.   Details of ovarian cancers detected in the cohort of women with inclusion cysts in year 1 

Table 2.   Details of ovarian cancers detected in the cohort of women with normal scans in year 1 


Table 3.   Relative risks of developing gynaecological cancers in women with inclusion cysts 
 
 

Wednesday, March 30, 2011

Lynch Syndrome Hereditary Cancers Public Awareness Day | Fight Colorectal Cancer



Increased Risk of Cancer

If a parent carries a Lynch mutation there is a 50-50 chance that their child will inherit Lynch syndrome with
  • 60 to 80 percent increased lifetime risk of colorectal cancer.
  • 40 to 70 percent increased risk of endometrial cancer (cancer of the uterus lining).
  • 13 percent increased risk for stomach cancer
  • 12 percent increased risk of ovarian cancer.
  • smaller, but significant risk of small intestine, urinary tract, heptobiliary (liver, gall bladder and bile ducts), skin, and brain cancers.
  • Some families may also have increased risk for breast cancer.
Note: 
Lynch Syndrome is also noted for multiple primary cancers (different cancers in one person)





Saturday, March 19, 2011

Ovarian cancer patient ‘failed by consultant’ (The Bolton News) - case of misconduct



Blogger's note: odd that the story didn't mention how the patient is doing ??

"....The panel heard that at a later consultation, the progress of the condition was again not identified and acted on, with poor notes made.
A specialist was not consulted and clinical standards of care were not met...."

Tuesday, January 18, 2011

full free access: Absence of microsatellite instability in mucinous carcinomas of the breast (Lynch Syndrome)



Note: some key excerpt; see also Supplemental Tables 1-4

"Microsatellite instability (MSI) is a form of genetic instability that results from defects in DNA mismatch repair. MSI is reported to be rare in unselected breast cancers, however it is a common feature in subsets of colorectal, ovarian and endometrial cancers. In these anatomical sites, MSI-high carcinomas often display a mucinous histology. The aim of this study was to determine whether mucinous carcinomas of the breast would more frequently display MSI-high than invasive ductal carcinomas of no special type (IDC-NSTs). The expression of four MSI markers (i.e. MSH2, MSH6, MLH1 and PMS2) was immunohistochemically assessed in 35 mucinous breast carcinomas and 35 histological grade- and oestrogen receptor (ER) status-matched IDC-NSTs, and in a series of 245 invasive breast cancers...........
........
Subsets of colorectal [24], gastric [31], pancreatic [31], ovarian [32] and endometrial tumours [22,31,33], and particularly those occurring in the hereditary nonpolyposis colorectal cancer (HNPCC) or Lynch syndrome [31], are characterised by microsatellite instability. Interestingly, however, MSI-H appears to be vanishingly rare in breast cancer [21,34]. Likewise, breast cancers displaying an MSI-L status are remarkably rare, whereas in tumours from other anatomical sites, such as colorectal, endometrial or ovarian cancers [27], this phenomenon is not as uncommon. Of note, in some anatomical sites (e.g. colorectal and ovarian), tumours displaying microsatellite instability often display a mucinous histology [32,35,36]. However, the prevalence of MSI in mucinous carcinomas of the breast has not yet been systematically addressed........
...........All 35 pure mucinous carcinomas of the breast analysed were positive for MLH1 and MSH6 as determined by IHC, and 33 out of 35 (94.2%) and 32 out of 34 cases (94.1%) showed expression of MSH2 and PMS2, respectively (Table 2 and Figure 1)............cont'd

Sunday, November 14, 2010

Does the time interval between first and last birth influence the risk of endometrial and ovarian cancer?



CONCLUSION: Our findings suggest that the risk of endometrial cancer is significantly decreased for women having at least a difference of 10 years between their first and last birth. Ovarian cancer does not seem to be influenced by the time interval between first and last birth.

Sunday, October 10, 2010

8th Symposium on Advanced Ovarian Cancer 2011 (Spain) - GEICO - ESMO - European Society for Medical Oncology



It is a great honor and privilege for us to present you this 8th International Symposium on Advanced Ovarian Cancer: Optimal Therapy. Update, organized since 2009 in partnership between the Spanish Ovarian Cancer Research Group (GEICO) and the European Society for Medical Oncology.

This comprehensive multidisciplinary symposium covers all of the hot and innovative topics surrounding the diagnosis, biology, and therapy of ovarian cancer. In fact our meeting has grown to be recognized internationally as a classical educational event, offering a platform for many of you to gather, to teach, to learn, and also to discuss both the value and the methodology of how standard, as well as new approaches are being incorporated into the management of ovarian cancer.

More than 350 participants from all over the world attended the last edition of the meeting in 2009. It will be a pleasure to welcome all of you on 4th March 2011 in Valencia. Please reserve the date today!

On behalf of the Organizing Committee,

Andrés Poveda & Jan B Vermorken
Symposium Directors

For further information, please visit: www.doctaforum.com/aocsymp

Sunday, August 08, 2010

A prospective study of dietary acrylamide intake and the risk of breast, endometrial, and ovarian cancers — Cancer Epidemiology, Biomarkers & Prevention



WHO website: What is acrylamide?


Abstract

Background
Acrylamide is a probable human carcinogen formed during cooking of many common foods. Epidemiological studies of acrylamide and breast cancer risk have been null; however, positive associations with ovarian and endometrial cancers have been reported. We studied acrylamide intake and risk of breast, endometrial, and ovarian cancers in a prospective cohort study.

Methods
We assessed acrylamide intake among 88,672 women in the Nurses' Health Study using food frequency questionnaires administered every four years. Between 1980 and 2006 we identified 6301 cases of invasive breast cancer, 484 cases of invasive endometrial adenocarcinoma, and 416 cases of epithelial ovarian cancer. We used Cox proportional hazards models to study the association between acrylamide and cancer risk.

Results
We found no association between acrylamide intake and breast cancer overall or according to estrogen and progesterone receptor status. We found an increased risk of endometrial cancer among high acrylamide consumers (adjusted relative risk [RR] for highest versus lowest quintile=1.41, 95% CI: 1.01-1.97, p-value for trend=0.03). We observed a non-significant suggestion of increased risk for ovarian cancer overall (RR 1.25, CI: 0.88-1.77, p-trend=0.12), with a significantly increased risk for serous tumors (RR 1.58, CI: 0.99-2.52, p-trend=0.04). Associations did not differ by smoking status.

Conclusions
We observed no association between acrylamide and breast cancer. Risk of endometrial cancer and possibly ovarian cancer was greater among high acrylamide consumers.

Impact
This is the second prospective study to report positive associations with endometrial and ovarian cancers. These associations should be further evaluated to inform public health policy.

Saturday, July 31, 2010

Press Release: Canada's Leading Ovarian Cancer "Patient" Advocate Speaks at Sask Conference






 

OCATS

Ovarian Cancer Awareness & Treatment in Saskatchewan
A SUPPORT & ACTION GROUP FOR ANYONE AFFECTED BY GYNECOLOGIC CANCERS

M E D I A   R E L E A S E


CANADA’S LEADING OVARIAN CANCER “PATIENT” ADVOCATE SPEAKS AT SASK CONFERENCE

For Immediate Release
REGINA, July 26, 2010  - Conference Co-Chairs Scott Livingstone, CEO Sask Cancer Agency and Darlene Gray, President, OCATS, in partnership with CNT Management Group, invite survivors, support people and the medical community to the first ever Gynecologic Cancer Conference, Strategies for Survival on September 24, 2010 at the Regina Inn.  Early Bird registration fees available until the end of July for this important event featuring some of the province’s most knowledgeable specialists in female reproductive cancers.  Experts will address clinical study trials for new drug therapies, managing cancer recurrence, the emotional aspects of cancer diagnoses, identifying families with hereditary risks, alternative and complimentary therapies available and the roles of our nurses, general practitioners, and pharmacists in cancer care delivery.

A conference highlight will be a presentation by Canada’s leading ovarian cancer “patient” advocate, Sandi Pniauskas.  Other experts presenting at the conference include the following.

Dr. Christopher Giede, Gynecologic Oncologist at the Royal University Hospital, Saskatoon and the team leader of Saskatchewan gynecologic oncology team of female reproductive cancer specialists.
Dr. Muhammad Salim, Medical Oncologist at the Allan Blair Cancer Centre, Regina and the specialist of all our Clinical Study Trials. 
Dr. Vicki Holmes, Medical Director of the Women’s Mid-Life Health Centre in Saskatoon. Dr. Holmes developed the concept of this centre and is the resident physician at the centre.
Rosalee Longmoore, RN, a Registered Nurse for 34 years with a wide range of experience on all Saskatchewan medical nursing issues.
Andrew Gilbertson, Pharmacist and owner of Hill Avenue Drugs, Regina, Regina’s first and currently only pharmacy that specializes in compounding custom prescription medications.
Dr. Heather Fox, Naturopath, a health specialist with over 30 years experienced and a registered doctor of Natural Medicine through the Examining Board of Natural Medicine Practitioners, Canada.
Monica Milas, Personal Growth and Healing Services Counsellor and Therapist.
Wendy Stoeber, Genetic Counsellor at the Division of Medical Genetics, Royal University Hospital, Saskatoon.
And a member of the Gynecologic Oncology Program Working Group, Scott Livingstone, the new CEO of the Sask Cancer Agency, will speak about Saskatchewan’s new Gynecologic Oncology Program.

The conference will include an exhibit hall marketplace and be followed by the OCATS Annual Benefit Gala and Silent Auction featuring Jack Semple and presentation of the OCATS 2010 Catleya Award of Collaboration & Vision.  Conference on-line registration at  http://guest.cvent.com/EVENTS/Info/Summary.aspx?e=ce9c4a0f-157e-4a42-ab49-0f19dae902e3. A group guestroom rate is available at the Regina Inn by asking for the OCATS event.  Discounted conference fees available for OCATS members and all students.  For more information please contact Darlene at 306-775-1848 or CNT Management Group Claire Bélanger-Parker [claire.belanger-parker@cntgrp.ca].

For more info contact Darlene Gray at OCATS at 306-775-1848, cell 529-3199 or darlenegray@sasktel.netdarlenegray@sasktel.net
# # #

Sunday, July 11, 2010

PET in women with high risk for breast or ovarian cancer : The Lancet Oncology



Summary

Data on the use of PET in women with genetic or familial high-risk for breast or ovarian cancer are scarce.

Open issues include the complementary use of dedicated breast-PET scanners in patients at high-risk for breast cancer, the relation between pathological characteristics of cancer diagnosed in BRCA carriers and 18F-fluorodeoxyglucose (18F-FDG)-avidity, and the predictive value of PET in patients at high-risk for ovarian cancer presenting with a pelvic mass or potential chemical markers. Therefore, the use of PET in high-risk patients with unproven malignant disease needs to be investigated in well designed clinical trials.

Once breast or ovarian cancer is diagnosed, indications for 18F-FDG-PET or PET—CT imaging are similar for high-risk patients and patients with sporadic cancer. However, PET can provide data that are beyond tumour detection per se. Future directions of PET in high-risk patients might include monitoring the response of BRCA carriers to new treatments such as poly-ADP ribose polymerase (PARP) inhibitors, personalisation of treatment, and the use of new PET tracers to investigate the tissue changes related to increased risk for breast and ovarian cancer.

Tuesday, June 29, 2010

summary: Targeted therapies for rare gynaecological cancers : The Lancet Oncology



"Some gynaecological cancers are uncommon, such as sex cord-stromal tumours, malignant germ-cell tumours, vulvar carcinoma, melanoma of the female genital tract, clear-cell carcinoma of the ovary and endometrium, neuroendocrine tumours of the cervix, and gestational trophoblastic neoplasia. All these cancers have different clinicopathological characteristics, suggesting different molecular biological pathogeneses. Despite aggressive treatment, some cancers recur or respond poorly to therapy. Comprehensive knowledge of the molecular biology of each cancer might help with development of novel treatments that maximise efficacy and minimise toxic effects. Targeted therapy is a new treatment strategy that has been investigated in various tumours in clinical and laboratory settings. Since these cancers are rare and large clinical trials are difficult to do, molecular biological techniques might allow rapid proof-of-principle experiments in few patients. Novel targeted agents either alone or in combination with other treatments offer promising therapeutic options."

Monday, June 28, 2010

Marjie - The support of 'family'



"...Margie is in the midst of a battle with colon, ovarian, and uterus cancer, and Saturday was her first time attending...."

Friday, June 25, 2010

(another amazing) job posting - Ovarian Cancer Canada



Note: see prior blog posting "BSB4uD" (Be Smart Before You Donate) - +$1million dollars in salaries and rising

Job Categories: Program / Project Evaluation & Development
Position Type: Part Time
Job Region: QC - Quebec City
Location(s): 4950 chemin Queen Mary
Career Level: Experienced (Non-manager)
Ad Online Since: 06/22/2010
Application Deadline: 07/06/2010

Tuesday, May 25, 2010

A genomic and transcriptomic approach for a differential diagnosis between primary and secondary ovarian carcinomas in patients with a previous history of breast cancer.



ABSTRACT:
BACKGROUND: The distinction between primary and secondary ovarian tumors may be challenging for pathologists. The purpose of the present work was to develop genomic and transcriptomic tools to further refine the pathological diagnosis of ovarian tumor after a previous history of breast cancer.

METHODS: Sixteen paired breast-ovary tumors from patients with a former diagnosis of breast cancer were collected.. ... A hierarchical clustering of these samples was performed, combined with a dataset of well-identified primary and secondary ovarian tumors.

RESULTS: In 12 of the 16 paired tumors analyzed, the comparison of genomic profiles confirmed the pathological diagnosis of primary ovarian tumor (n = 5) or metastasis of breast cancer (n = 7). Among four cases with uncertain pathological diagnosis, genomic profiles were clearly distinct between the ovarian and breast tumors in two pairs, thus indicating primary ovarian carcinomas, and showed common patterns in the two others, indicating metastases from breast cancer.
CONCLUSIONS: In patients with ovarian carcinoma and a previous history of breast cancer, SNP array analysis can be used to distinguish primary and secondary ovarian tumors. Transcriptomic analysis may be used when primary breast tissue specimen is not available.

Wednesday, April 21, 2010

Gene link to cancer risk in families - protein RAD51C (news item) breast and ovarian



Note: this report is worthwhile reading especially for those who test negative for BRCA 1/2

"No significant mutations were found in RAD51C in the 620 families with breast cancer only.  However, when they looked at the breast and ovarian cancer families, things got really interesting.  In all, they were able to identify a total of 6 mutations in the 480 families that had sufficient evidence to implicate them in the breast and ovarian cancer susceptibility.  Thus, in this German study of women with unexplained familial breast and ovarian cancer, the cancer susceptibility in 1.3% of the families could be explained by heterozygous mutations in the RAD51C gene."