OVARIAN CANCER and US

Blog Archives: Nov 2004 - present

#ovariancancers



Special items: Ovarian Cancer and Us blog best viewed in Firefox

Search This Blog

Monday, May 02, 2016

Surgical management of recurrent ovarian cancer



abstract

Most patients with advanced-stage epithelial ovarian cancer will experience a relapse of disease despite a complete response after surgical cytoreduction and platinum-based chemotherapy. Treatment of recurrent ovarian cancer mainly comprises various combinations of systemic chemotherapy with or without targeted agents. The role of cytoreductive surgery for recurrent ovarian cancer is not well established. Although the literature on survival benefit of cytoreductive surgery for recurrent disease has expanded steadily over the past decade, most studies were retrospective, single-institution series with small numbers of patients. Given the balance between survival benefit and surgery-related morbidity during maximum cytoreductive surgical effort, it is essential to establish the optimal selection criteria for identifying appropriate candidates who will benefit from surgery without worsening quality of life. Three phase III randomized trials for this issue are currently underway. Herein, we present contemporary evidence supporting the positive role of cytoreductive surgery and offer selection criteria for optimal candidates for surgery in the treatment of recurrent ovarian cancer.

The Limited Utility of Currently Available Venous Thromboembolism Risk Assessment Tools in Gynecologic Oncology Patients. - PubMed - NCBI



abstract

BACKGROUND:

Use of risk assessment tools, such as the Caprini score or Rogers score, is recommended by national societies to stratify surgical patients by venous thromboembolism (VTE) risk and guide prophylaxis. However, these tools were not developed in a gynecologic oncology patient population and their utility in this population is unknown.

OBJECTIVE:

To examine the ability of both the Caprini and Rogers score to stratify gynecologic oncology patients by risk of VTE.
 

CONCLUSIONS:

Gynecologic oncology patients score very high on current VTE risk assessment models. The Caprini score is limited in its ability to discriminate relative VTE risk among gynecologic oncology patients as 97% are in the highest-risk category. Sub-stratification of the highest risk groups allows for relative VTE risk stratification among gynecologic oncology patients suggesting that further evaluation of risk stratification is needed in gynecologic oncology surgery.

ReCAP: Oncologists' Selection of Genetic and Molecular Testing in the Evolving Landscape of Stage II Colorectal Cancer



abstract

CONTEXT AND QUESTION ASKED:

Genetic testing can be used in the diagnosis of Lynch syndrome, formerly known as hereditary nonpolyposis colorectal cancer (CRC), the most common inherited disorder that increases the risk for CRC; however, test results related to Lynch syndrome screening may also be used for predictive and prognostic purposes in patients with stage II CRC. Although national guidelines recommend the use of several genetic and molecular tests for patients with CRC, little is known about how guidelines, particularly the complex testing recommendations for Lynch syndrome, are translated into clinical practice. In this study, we asked: how does the family history of patients with stage II CRC influence medical oncologists' selection of genetic and molecular testing, both related and unrelated to Lynch syndrome?

SUMMARY ANSWER:

We found that oncologists' self-reported ordering of Lynch syndrome-related tests was strongly associated with the strength of CRC family history, but even so, not all oncologists would order germline testing for mismatch repair (MMR) genes, much less screen for Lynch syndrome by ordering microsatellite instability and/or immunohistochemistry for MMR proteins, in a patient scenario with the strongest family history of CRC (Table 2)....

METHODS:

In 2012 and 2013, we surveyed medical oncologists in the Cancer Care Outcomes Research and Surveillance Consortium (CanCORS) and evaluated their selection of microsatellite instability and/or immunohistorchemistry for MMR proteins, germline testing for MMR genes, BRAF and KRAS mutation analysis, and Oncotype DX in stage II CRC......

BIAS, CONFOUNDING FACTORS, DRAWBACKS:

Although we surveyed a large cohort of oncologists from diverse geographic and practice settings, there were several limitations to this study.....

REAL-LIFE IMPLICATIONS:

The high lifetime risk of CRC and other cancers among affected individuals and family members and low detection rates led the Centers for Disease Control and Prevention to recommend universal Lynch syndrome screening of all patients newly diagnosed with CRC. Previous efforts to increase the identification of patients and family members with Lynch syndrome have unfortunately achieved limited success. It remains to be seen whether the recapitulation by the National Comprehensive Cancer Network of the Centers for Disease Control and Prevention recommendation to screen all incident CRC specimens for Lynch syndrome can increase diagnoses. Undertesting related to Lynch syndrome screening and overtesting involving molecular tests among surveyed oncologists highlight the need for improved implementation, targeted education, and evaluation of organizational and financial arrangements to promote the appropriate use of genetic and molecular tests.


quick search: clinical trials: ovarian cancer- ClinicalTrials.gov



Search of: ovarian cancer | Open Studies | Exclude Unknown | received from 01/01/2016 to 02/04/2016 - List Results - ClinicalTrials.gov

 28 studies found for:    ovarian cancer | Open Studies | Exclude Unknown | received from 01/01/2016 to 02/04/2016

How U.S. Reporters Are Using Facebook, Twitter › Communication Breakdown



Communication
  http://www.scilogs.com/communication_breakdown/wp-content/blogs.dir/111/files/SocMed-Journo-2016-HEADER.jpg 
Image credit: Sean MacEntee. Retrieved via Flickr and shared under a Creative Commons license.

 8 April 2016

 Social media are used to connect with people and share information, so it is not surprising that reporters are using social media platforms in their work – connecting with sources and collecting information are fundamental aspects of journalism. A recent paper offers insights into how, and to what extent, newspaper journalists are using Facebook and Twitter in their reporting.....
 Only 22.7 percent of study participants said that Facebook was either an “important” or “very important” tool for their reporting. On the other hand, 51.7 percent of participants said Twitter was an important or very important tool.

Assessing Critical Situations in Cancer Care (eg. sepsis; hypotension...)



Cancer Network

Dogs' hearts beat in sync with their owners says study



media

open access: The topography of mutational processes in breast cancer genomes



Nature Communications

...Finally, the signature-based genomic variation seen here drives home a fundamental point regarding genomic analyses forthwith: statistical models involving mutability cannot assume uniform genomic mutation rates and must consider signature-dependent variation as a factor in all future analyses.

Five new breast cancer genes and range of mutations pave way for personalised treatment



medical news

The largest-ever study to sequence the whole genomes of breast cancers has uncovered five new genes associated with the disease and 13 new mutational signatures that influence tumour development. The results of two papers published in Nature and Nature Communications also reveal what genetic variations exist in breast cancers and where they occur in the genome.
Dr Serena Nik-Zainal of the Wellcome Trust Sanger Institute led analysis of 560 breast cancer genomes; 556 from women and four from men. This international collaboration included breast cancer patients from around the world, including the USA, Europe and Asia.
The results reveal more about the causes of breast tumours and provide evidence that breast cancer genomes are highly individual......

 Dr Nik-Zainal's team hunted for mutations that encourage cancers to grow and looked for mutational signatures in each patient's tumour. They found that women who carry the BRCA1 or BRCA2 gene, and so have increased risk of developing breast and ovarian cancer, had whole cancer genome profiles that were highly distinctive from each other and were also very different to other breast cancers. This discovery could be used to classify patients more accurately for treatment.

OncoPilot: Navigating the Cancer Journey Cancer Resources



OncoPilot

The Cancer Community's Next Steps for the Moonshot Initiative



National Cancer Institute

Bobby Umar - background plus message from twitter - share your stories



 Blogger's Note: see background and request - use at your own risk

Bobby Umar - Google Search

twitter request:
 
 
  Dee Sparacio @womenofteal
     
#gyncsm Ovarian Cancer survivors - opportunity to share your story reach out to Bobby. twitter.com/raehanbobby/st… - Apr 26
    More Tweets
  Dee Sparacio @womenofteal
     
@ovariancancers Do you still need stories @raehanbobby ? - May 01
Bobby Umar @raehanbobby
 
   
 

Assessing biases of information contained in pedigrees for the classification of BRCA-genetic variants (ENIGMA)



Assessing biases of information contained in pedigrees for the classification of BRCA-genetic variants: a study arising from the ENIGMA analytical working group | Hereditary Cancer in Clinical Practice | Full Text 
 

Conclusion

Clinical scores change significantly over time for BRCAm families. This may be due to differences in follow-up, but also to differences in cancer risks from carrying a pathogenic variant in a highly penetrant gene. To reduce bias, models for VUS classification should incorporate FH collected at intake.

Table of Contents Apr 2016: 10th Intl Symposium on Advanced Ovarian Cancer



Blogger's Note: this journal is subscriber based for full access ($$$)

Table of Contents

  • 10th International Symposium on Advanced Ovarian Cancer: Optimal Therapy. Update, 6 March 2015, Valencia, Spain
Volume 27 suppl 1 April 2016

symposium articles

Sunday, May 01, 2016

Estrogen and colorectal cancer incidence and mortality



abstract

BACKGROUND

The preponderance of observational studies describe an association between the use of estrogen alone and a lower incidence of colorectal cancer. In contrast, no difference in the incidence of colorectal cancer was seen in the Women's Health Initiative (WHI) randomized, placebo-controlled trial with estrogen alone after a mean intervention of 7.1 years and cumulative follow-up of 13.2 years. This study extends these findings by providing detailed analyses of the effects of estrogen alone on the histology, grade, and stage of colorectal cancer, relevant subgroups, and deaths from and after colorectal cancer.

Population-based analysis of colorectal cancer risk after oophorectomy



 Blogger's Notes: WHI/post-WHI studies indicated that HRT had a protective effect on colorectal cancer (info needs to be updated) eg. estrogen

abstract

Background

The development of colorectal cancer is influenced by hormonal factors. Oophorectomy alters endogenous levels of sex hormones, but the effect on colorectal cancer risk is unclear. The aim of this cohort study was to examine colorectal cancer risk after oophorectomy for benign indications.

Methods

Women who had undergone oophorectomy between 1965 and 2011 were identified from the Swedish Patient Registry. Standard incidence ratios (SIRs) and 95 per cent confidence intervals for colorectal cancer risk were calculated compared with those in the general population. Stratification was carried out for unilateral and bilateral oophorectomy, and hysterectomy without specification of whether the ovaries were removed or not. Associations between the three oophorectomy options and colorectal cancer risk in different locations were assessed by means of hazard ratios (HRs) and 95 per cent confidence intervals calculated by Cox proportional hazards regression modelling.

Results

Of 195 973 women who had undergone oophorectomy, 3150 (1·6 per cent) were diagnosed with colorectal cancer at a later date (median follow-up 18 years). Colorectal cancer risk was increased after oophorectomy compared with that in the general population (SIR 1·30, 95 per cent c.i. 1·26 to 1·35). The risk was lower for younger age at oophorectomy (15–39 years: SIR 1·10, 0·97 to 1·23; 40–49 years: SIR 1·26, 1·19 to 1·33; P for trend < 0·001). The risk was highest 1–4 years after oophorectomy (SIR 1·66, 1·51 to 1·81; P < 0·001). In the multivariable analysis, women who underwent bilateral oophorectomy had a higher risk of rectal cancer than those who had only unilateral oophorectomy (HR 2·28, 95 per cent c.i. 1·33 to 3·91).

Conclusion

Colorectal cancer risk is increased after oophorectomy for benign indications.

Saturday, April 30, 2016

Effect of Noninfectious Wound Complications after Mastectomy on Subsequent Surgical Procedures and Early Implant Loss



abstract
 

Background

Noninfectious wound complications (NIWCs) after mastectomy are not routinely tracked and data are generally limited to single-center studies. Our objective was to determine the rates of NIWCs among women undergoing mastectomy and assess the impact of immediate reconstruction (IR).

Study Design

We established a retrospective cohort using commercial claims data of women aged 18 to 64 years with procedure codes for mastectomy from January 2004 through December 2011. Noninfectious wound complications within 180 days after operation were identified by ICD-9-CM diagnosis codes and rates were compared among mastectomy with and without autologous flap and/or implant IR.

Results

There were 18,696 procedures (10,836 [58%] with IR) among 18,085 women identified. The overall NIWC rate was 9.2% (1,714 of 18,696); 56% required surgical treatment. The NIWC rates were 5.8% (455 of 7,860) after mastectomy only, 10.3% (843 of 8,217) after mastectomy plus implant, 17.4% (337 of 1,942) after mastectomy plus flap, and 11.7% (79 of 677) after mastectomy plus flap and implant (p < 0.001). Rates of individual NIWCs varied by specific complication and procedure type, ranging from 0.5% for fat necrosis after mastectomy only, to 7.2% for dehiscence after mastectomy plus flap. The percentage of NIWCs resulting in surgical wound care varied from 50% (210 of 416) for mastectomy plus flap, to 60% (507 of 843) for mastectomy plus implant. Early implant removal within 60 days occurred after 6.2% of mastectomy plus implant; 66% of the early implant removals were due to NIWCs and/or surgical site infection.

Conclusions

The rate of NIWC was approximately 2-fold higher after mastectomy with IR than after mastectomy only. Noninfectious wound complications were associated with additional surgical treatment, particularly in women with implant reconstruction, and with early implant loss.

TAPUR: Testing the Use of FDA Approved Drugs That Target a Specific Abnormality in a Tumor Gene in People With Advanced Stage Cancer (Michigan/NC)



Full Text View - ClinicalTrials.gov


This study is currently recruiting participants. (see Contacts and Locations)
Verified April 2016 by American Society of Clinical Oncology
Sponsor:
Collaborators:
AstraZeneca
Bayer
Bristol-Myers Squibb
Eli Lilly and Company
Genentech, Inc.
Pfizer
Information provided by (Responsible Party):
American Society of Clinical Oncology
ClinicalTrials.gov Identifier:
NCT02693535
First received: February 11, 2016
Last updated: April 13, 2016
Last verified: April 2016
  Purpose
The purpose of the study is to learn from the real world practice of prescribing targeted therapies to patients with advanced cancer whose tumor harbors a genomic variant known to be a drug target or to predict sensitivity to a drug.

Condition Intervention Phase
Lymphoma, Non-Hodgkin
Multiple Myeloma
Advanced Solid Tumors
Drug: Erlotinib
Drug: Axitinib
Drug: Bosutinib
Drug: Crizotinib
Drug: Palbociclib
Drug: Sunitinib
Drug: Temsirolimus
Drug: Trastuzumab and Pertuzumab
Drug: Vemurafenib and Cobimetinib
Drug: Vismodegib
Drug: Cetuximab
Drug: Dasatinib
Drug: Regorafenib
Drug: Olaparib
Phase 2

Study Type: Interventional
Study Design: Allocation: Non-Randomized
Endpoint Classification: Safety/Efficacy Study
Intervention Model: Single Group Assignment
Masking: Open Label
Primary Purpose: Treatment
Official Title: Targeted Agent and Profiling Utilization Registry (TAPUR) Study

Resource links provided by NLM:


Further study details as provided by American Society of Clinical Oncology:

Primary Outcome Measures:
  • Objective Response Rate defined as % of participants in a cohort with complete or partial response or with stable disease according to standard response criteria [ Time Frame: Assessed at 16 weeks of treatment ] [ Designated as safety issue: No ]
    Each cohort includes participants with the same tumor type, genomic variant and study drug. For solid tumors, the Response Evaluation Criteria for Solid Tumors (RECIST) criteria will be used, for non-Hodgkin Lymphoma, the Lugano Criteria will be used, and for multiple myeloma, the International Uniform Response Criteria for Multiple Myeloma will be used.


Secondary Outcome Measures:
  • Overall survival (OS) [ Time Frame: Duration of survival from registration on study until death from any cause, assessed throughout end of study, up to 3 years ] [ Designated as safety issue: No ]
    OS will be estimated using the Kaplan-Meier method


Estimated Enrollment: 730
Study Start Date: March 2016
Estimated Primary Completion Date: March 2019 (Final data collection date for primary outcome measure)
Arms Assigned Interventions
Group 1 (VEGFR)
Participants receive axitinib - dosage, frequency and duration per label VEGFR mutation, amplification or overexpression)
Drug: Axitinib
drug
Other Name: Inlyta
Group 2 (Bcr-abl, SRC, LYN, LCK)
Participants receive bosutinib- dosage, frequency and duration per label Bcr-abl, SRC, LYN, LCK mutations
Drug: Bosutinib
drug
Other Name: Bosulif
Group 3 (ALK, ROS1, MET)
Participants receive crizotinib - dosage, frequency and duration per label ALK, ROS1, MET mutations
Drug: Crizotinib
drug
Other Name: Xalkori
Group 4 (CDKN2A/p16, CDK4, CDK6)
Participants receive palbociclib - dosage, frequency and duration per label CDKN2A/p16 loss, CDK4, CDK6 amplifications
Drug: Palbociclib
drug
Other Name: Ibrance
Group 5 (CSF1R, PDGFR, VEGFR)
Participants receive sunitinib - dosage, frequency and duration per label CSF1R, PDGFR, VEGFR mutations
Drug: Sunitinib
drug
Other Name: Sutent
Group 6 (mTOR, TSC)
Participants receive temsirolimus - dosage, frequency and duration per label mTOR, TSC mutations
Drug: Temsirolimus
drug
Other Name: Torisel
Group 7 (EGFR)
Participants receive erlotinib - dosage, frequency and duration per label EGFR mutations
Drug: Erlotinib
drug
Other Name: Tarceva
Group 8 (ERBB2)
Participants receive trastuzumab and pertuzumab - dosage, frequency and duration per label (ERBB2 amplifications)
Drug: Trastuzumab and Pertuzumab
drug
Other Name: Herceptin and Perjeta
Group 9 (BRAFV600E)
Participants receive vemurafenib and cobimetinib - dosage, frequency and duration per label BRAFV600E mutations
Drug: Vemurafenib and Cobimetinib
drug
Other Name: Zelboraf and Cotellic
Group 10 (PTCH1)
Participants receive vismodegib - dosage, frequency and duration per label PTCH1 deletion or inactivating mutations
Drug: Vismodegib
drug
Other Name: Erivedge
Group 11 (KRAS, NRAS and BRAF)
Participants receive cetuximab - dosage, frequency and duration per label KRAS, NRAS and BRAF wildtype
Drug: Cetuximab
drug
Other Name: Erbitux
Group 12 (Bcr-abl, SRC, KIT, PDGFRB, EPHA2, FYN, LCK, YES1)
Participants receive dasatinib- dosage, frequency and duration per label Bcr-abl, SRC, KIT, PDGFRB, EPHA2, FYN, LCK, YES1 mutations
Drug: Dasatinib
drug
Other Name: Sprycel
Group 13 (RET,VEGFR1/2/3,KIT,PDGFRβ,RAF-1,BRAF
Participants receive regorafenib- dosage, frequency and duration per label RET, VEGFR1, VEGFR2, VEGFR3, KIT, PDGFRβ, RAF-1, BRAF mutations/amplifications
Drug: Regorafenib
drug
Other Name: Stivarga
Group 14 (BRCA1/BRCA2; ATM)
Participants receive olaparib- dosage, frequency and duration per label Germline or somatic BRCA1/BRCA2 inactivating mutations; ATM mutations or deletions
Drug: Olaparib
drug
Other Name: Lynparza

Detailed Description:
The Targeted Agent and Profiling Utilization Registry (TAPUR) Study is a non-randomized clinical trial that aims to describe the safety and efficacy of commercially available, targeted anticancer drugs prescribed for treatment of patients with advanced cancer that has a potentially actionable genomic variant. TAPUR will study Food and Drug Administration (FDA)-approved targeted therapies that are contributed by collaborating pharmaceutical companies, catalogue the choice of molecular profiling test by clinical oncologists and develop hypotheses for additional clinical trials.
  Eligibility

Ages Eligible for Study:   18 Years and older
Genders Eligible for Study:   Both
Accepts Healthy Volunteers:   No
Criteria
Inclusion Criteria:
  • 18 years of age or older
  • Histologically-proven locally advanced or metastatic solid tumor, multiple myeloma or B cell non-Hodgkin lymphoma who is no longer benefitting from standard anti-cancer treatment or for whom, in the opinion of the treating physician, no such treatment is available or indicated
  • Performance status 0-2 (Per Eastern Cooperative Oncology Group (ECOG )criteria)
  • Patients must have acceptable organ function as defined below. However, as noted above, drug-specific inclusion/exclusion criteria specified in the protocol appendix for each agent will take precedence for this and all inclusion criteria:
    1. Absolute neutrophil count ≥ 1.5 x 106/µl
    2. Hemoglobin > 9.0 g/dl
    3. Platelets > 75,000/µl
    4. Total bilirubin < 2.0 mg/ dl
    5. Aspartate aminotransferase (AST) serum glutamic-oxaloacetic transaminase (SGOT) and alanine aminotransferase (ALT) serum glutamic-pyruvic transaminase (SGPT) < 2.5 x institutional upper limit of normal (ULN) (or < 5 x ULN in patients with known hepatic metastases)
    6. Serum creatinine ≤ 1.5 × ULN or calculated or measured creatinine clearance ≥ 50 mL/min/1.73 m2
  • Patients must have measurable or evaluable disease (per RECIST v1.1 for solid tumor, Lugano criteria for non Hodgkin lymphoma or International Myeloma Working Group criteria for multiple myeloma), defined, per RECIST 1.1, as at least one lesion that can be accurately measured in at least one dimension (longest diameter to be recorded for non-nodal lesions and short axis for nodal lesions) as ≥20 mm with conventional techniques or as ≥10 mm with spiral computed tomography (CT) scan, Magnetic Resonance Imaging (MRI), or a subcutaneous or superficial lesion that can be measured with calipers by clinical exam. For lymph nodes, the short axis must be ≥15 mm. Patients who have assessable disease by physical or radiographic examination but do not meet these definitions of measurable disease are eligible and will be considered to have evaluable disease. Patient's whose disease cannot be objectively measured by physical or radiographic examination (e.g., elevated serum tumor marker only) are NOT eligible
  • Results must be available from a genomic test or immunohistochemistry (IHC) test for protein expression performed in a Clinical Laboratory Improvement Amendments (CLIA)-certified, College of American Pathologists (CAP) -accredited, New York State accredited (for labs offering services to residents of NY) laboratory that has registered the test with the National Institutes of Health (NIH) Genetic Test Registry or has established an integration with the TAPUR platform. The genomic or IHC test used to qualify a patient for participation in TAPUR may have been performed on any specimen of the patient's tumor obtained at any point during the patient's care at the discretion of the patient's treating physician. Genomic assays performed on cell-free DNA in plasma ("liquid biopsies") will also be acceptable if the genomic analysis is performed in a laboratory that meets the criteria described above.

interview: (Government) Showdown With The (Ontario) Doctors



TVO.org The Agenda with Steve Paik


Air Date: 
Apr 29, 2016
Length: 
14:56

About this Video
Ontario spends $50 billion a year on health care. According to the Ministry of Health, one in five of those dollars goes to doctor compensation. It's the latest in the war of words between the minister and his physician colleagues. Dr. Eric Hoskins, minister of health and long-term care, joins The Agenda to discuss the province's point of view.

(interview) Ontario Doctors vs. the Government



TVO.org The Agenda with Steve Paikin
 
Air Date: 
Apr 29, 2016
Length: 
14:17

About this Video
The negotiations between Ontario doctors and the provincial government have stalled for a year. This week, the province asked the doctors to come back to the negotiating table, using statistics on how much doctors are paid, including that two per cent of doctors take 10 per cent of total billings. The Ontario Medical Association's past president Ved Tandan joins The Agenda to respond.

A personalized paradigm in the treatment of platinum-resistant ovarian cancer - A cost utility analysis of genomic-based vs cytotoxic therapy



Abstract

OBJECTIVE:

To assess the cost-effectiveness of a strategy employing genomic-based tumor testing to guide therapy for platinum-resistant ovarian cancer.

METHODS:

A decision model was created to compare standard of care (SOC) cytotoxic chemotherapy to a genomic-based treatment strategy. The genomic arm included tumor testing with treatment directed at targets identified. Overall survival was assumed to be similar between strategies; quality of life (QOL) was assumed superior during targeted therapy compared to chemotherapy. Pertinent uncertainties (cost of targeted therapy and genomic testing, response to targeted therapy, probability of a tumor having a targetable alteration, and impact on QOL) were evaluated in a series of one-and two-way sensitivity analyses.

RESULTS:

The genomic testing strategy was more expensive ($90,271 vs. $74,926) per patient than SOC. The incremental cost-effectiveness ratio (ICER) of the genomic strategy was $479,303 per quality-adjusted life year saved (QALY). Model results were insensitive to the cost of genomic testing, differences in QOL, and the probability of identifying a targetable alteration. However, the model was sensitive to the cost of targeted therapy. For example, when the cost of targeted therapy was reduced to 56% of its current cost (or $6400/cycle), the genomic strategy became more cost-effective with an ICER of $96,612/QALY.

CONCLUSIONS:

Genomic-based tumor testing and targeted therapy in patients with platinum-resistant ovarian cancer is not cost-effective compared with SOC. However, reducing the cost of targeted therapy (independently, or in combination with reducing the cost of the genomic test) provides opportunities for improved value in cancer care.

Poor adherence to staging guidelines for children with malignant ovarian tumors



abstract

Purpose

Historically, surgical staging practices for pediatric malignant ovarian tumors mirrored adult guidelines. In 2004, the Children's Oncology Group (COG) developed guidelines specific to pediatric patients with ovarian germ cell tumors. We sought to characterize the operative management of pediatric ovarian lesions and adherence to COG surgical staging guidelines.

Methods

We conducted a single institution, retrospective study of pediatric patients who underwent surgical intervention for ovarian lesions between 1995 and 2012. The primary outcome was adherence to COG staging guidelines.


Results

Among 502 patients, 44 (8.8%) had malignant ovarian tumors. Two patients (2/44, 4.5%) underwent correct surgical staging. Therefore, 95.5% (42/44) underwent incorrect surgical staging by omitting recommended maneuvers (surgical understaging) or performing clinically unnecessary surgical staging steps (surgical overstaging). Of the 42 patients with incorrect surgical staging, 85.7% (36/42) were surgically overstaged and 76.2% (32/42) were surgically understaged. In the entire cohort, 12 (27.3%) patients had complete staging procedures, including 10 surgically overstaged patients (10/12, 83.3%). Staging practices were not significantly different before and after the release of the 2004 COG guidelines.

Conclusion

Incorrect surgical staging of pediatric ovarian malignancies is commonplace. These data stress the need for greater education among all surgeons caring for children with malignant ovarian tumors.

A pure primary transitional cell carcinoma of the ovary: A rare case report with literature review



Abstract

 Primary transitional cell carcinoma (TCC) of the ovary is a rare and recently recognized subtype of ovarian surface epithelial-stromal cancer. Pure forms of the TCC ovary account for only 1% of surface epithelial carcinomas. The clinical presentation is indistinguishable from other types of ovarian cancers. They have a favorable response to chemotherapy than other surface epithelial cancers. We report a case of 55-year-old woman who presented with a hard mass in the abdomen. Computed tomography-diagnosed it as a carcinoma of the ovary. Tumor was immunoreactive with Wilms' tumor protein-1 and nonreactive with cytokeratin 7 (CK7) and CK20. Histopathology diagnosis of primary TCC of the ovary was made. These tumors are needed to be differentiated from metastatic TCC from other sites and undifferentiated carcinomas of ovaries. Clinical features and immunohistochemistry are helpful. Surgical resection is the primary therapeutic approach followed by standardized chemotherapy.

Loss of PAX8 in high-grade serous ovarian cancer reduces cell survival despite unique modes of action in the fallopian tube and ovarian surface epithelium



open access (technical)

 In summary, this study reveals a distinctive role for PAX8 in the ovary compared to the fallopian tube that increases migration, proliferation, and EMT. These findings highlight the importance of deciphering a tumor’s cell of origin because of the unique pathways that are deregulated depending on a tumor’s progenitor cell. Yet despite the unique role of PAX8 in the ovary compared to the fallopian tube, these findings suggest HGSC cells are reliant on PAX8.

An international survey of surveillance schemes for unaffected BRCA1/BRCA2 mutation carriers



Abstract

 Female BRCA1/BRCA2 mutation carriers are at substantially increased risk for developing breast and/or ovarian cancer, and are offered enhanced surveillance including screening from a young age and risk-reducing surgery (RRS)-mastectomy (RRM) and/or salpingo-oophorectomy (RRSO). While there are established guidelines for early detection of breast cancer in high-risk women who have not undergone RRM, there are less developed guidelines after RRM. We evaluated the schemes offered before and after RRS in internationally diverse high-risk clinics. An e-mailed survey was distributed to high-risk clinics affiliated with CIMBA. Overall, 22 centers from 16 countries responded. Pre RRS surveillance schemes overwhelmingly included breast imaging (primarily MRI) from 18 to 30 years and clinical breast exam (CBE) at 6-12 month intervals. For ovarian cancer, all but 6 centers offered semiannual/annual gynecological exam, transvaginal ultrasound, and CA 125 measurements. Post RRM, most centers offered only annual CBE while 4 centers offered annual MRI, primarily for substantial residual breast tissue. After RRSO only 4 centers offered specific gynecological surveillance. Existing guidelines for breast/ovarian cancer detection in BRCA carriers are being applied pre RRS but are not globally harmonized, and most centers offer no specific surveillance post RRS. From this comprehensive multinational study it is clear that evidence-based, long-term prospective data on the most effective scheme for BRCA carriers post RRS is needed.

open access version: SSRI use and clinical outcomes in epithelial ovarian cancer | Christensen | Oncotarget



open access
 
Histology (n) Serous 582 Other 189





Ovarian cancer patients from a 6-site study between 1994 and 2010 were included.
 To date, no studies have examined effects of SSRIs among patients already diagnosed with ovarian cancer and the influence SSRIs may have on survival and disease progression in these patients. Moreover, no studies have explored the effect of 5-HT or SSRIs on ovarian neoplastic cell growth. To address these knowledge gaps, we characterized 5-HT receptor expression in ovarian cancer cells and investigated the functional and biological roles of 5-HT using in vitro and in vivo models. In addition, this multicenter study examined effects of SSRIs on survival and disease progression in patients diagnosed with epithelial ovarian cancer.....


Patient characteristics
Demographic and clinical characteristics of the sample are listed in Table 1
 
 

Proteomic Mapping of p53 Immunogenicity in Pancreatic, Ovarian, and Breast Cancers



abstract


 ep·i·tope

(ĕp′ĭ-tōp′)n. A localized region on the surface of an antigen capable of eliciting an immune response and of combining with a specific antibody to counter that response.

Purpose

Mutations in TP53 induce autoantibody immune responses in a subset of cancer patients, which have been proposed as biomarkers for early detection. Here, we investigate the association of p53 specific autoantibodies with multiple tumor subtypes and determine the association with p53 mutation status and epitope specificity.

Experimental Design

IgG p53 autoantibodies (p53-AAb), were quantified in 412 serum samples using a programmable ELISA assay from patients with serous ovarian, pancreatic adenocarcinoma, and breast cancer. To determine if patients generated mutation specific autoantibodies we designed a panel of the most relevant 51 p53 point mutant proteins....

Results

We detected p53-AAb with sensitivities of 58.8% (ovarian), 22% (pancreatic), 32% (triple negative breast cancer), and 10.2% (HER2+ breast cancer) at 94% specificity. Sera with p53-AAb contained broadly-reactive autoantibodies to 51 displayed p53 mutant proteins, demonstrating a polyclonal response to common epitopes. All p53-AAb displayed broad polyclonal immune response to both continuous and discontinuous epitopes at the N- and C-terminus as well as the DNA binding domain.

Conclusion and clinical relevance

In this comprehensive analysis, mutations in tumor p53 induce strong, polyclonal autoantibodies with broadly reactive epitope specificity.

Friday, April 29, 2016

Follow-up of Women With Negative Pap Test Results and Abnormal Clinical Signs or Symptoms | American Journal of Clinical Pathology



abstract American Journal of Clinical Pathology

Objectives: Abnormal signs or symptoms recorded on Papanicolaou (Pap) test requisitions may reflect disease not detected with Pap testing. Since 2009, these cases have been reviewed in our laboratory by a second cytotechnologist and a cytopathologist. The objective of this study was to document follow-up findings on these patients.
Methods: A search for Pap test results of “Negative for intraepithelial lesion or malignancy, abnormal clinical signs or symptoms” was performed for cases from January 1, 2009, to October 10, 2013. Clinical information and follow-up findings were documented.
Results: 1,104 cases were identified. Signs and symptoms were abnormal bleeding 897 (81%), polyps 83 (8%), pelvic mass 54 (5%), visible cervical lesions 48 (4%), vaginal lesions 17 (2%) and endometrial masses 6 (0.5%). Six hundred sixty-seven (60%) had follow-up results, including 517 with histopathologic diagnoses. Two-hundred thirty-three (45%) had nonspecific benign diagnoses, 216 (42%) had benign tumor-like conditions, 28 (4%) had insufficient specimens, 16 (3%) had precancerous diagnoses and 23 (4%) had malignancies. Endometrial malignancy was identified in 14 (61%), ovarian in 6 (26%), and miscellaneous in 3 (13%). No cervical cancers were identified.
Conclusions: We report follow-up findings from patients with abnormal clinical signs or symptoms, negative Pap test results, and follow-up recommendations highlighting reported abnormal signs or symptoms. Abnormal clinical signs and symptoms should routinely be considered in assessment and management of patients with negative cervical screening test results.

HLA superfamily assignment is a predictor of immune response to cancer testis antigens and survival in ovarian cancer



abstract

OBJECTIVES:

To characterize the association between major histocompatibility complex (MHC) types and spontaneous antibody development to the cancer testis (CT) antigen NY-ESO-1.

METHODS:

Tumor expression of NY-ESO-1 and serum antibodies to NY-ESO-1 were characterized in addition to human leukocyte antigen (HLA) type for patients with epithelial ovarian cancer. HLA types were assigned to structure-based superfamilies and statistical associations were examined. HLA types were compared to existing reference libraries of HLA frequencies in a European-Caucasian American population.

RESULTS:

Out of 126 patients identified, 81% were expression positive and 48% had spontaneous antibody responses to NY-ESO-1. There was an association between HLA-B superfamily and seropositivity among patients with tumors expressing NY-ESO-1 (p<0.001). The differences in HLA-B superfamily assignment were driven by HLA-B44. Among all patients, the B27 superfamily was over-represented compared with the general population (p<0.001).

CONCLUSIONS:

HLA type appears to be associated with spontaneous anti-CT antigen antibodies, as well as with the overall risk of ovarian cancer.

AACR Annual Meeting 2016: Survivors Bring Broader Perspective



Cancer Today

The American Association for Cancer Research (AACR) Annual Meeting 2016 wrapped up in New Orleans April 20 with a crescendo as Vice President Joe Biden addressed thousands of cancer researchers, asking the scientists to collaborate and break down walls in research.

In the days leading up to the vice president’s address, less prominent supporters of cancer research—34 cancer survivors and advocates participating in the AACR Scientist↔Survivor Program (SSP)—took part in panel discussions, attended scientific sessions and presented posters describing their advocacy efforts during the Annual Meeting, held April 16-20.

Cancer survivors offered personal accounts of their struggles and perspectives—amid a backdrop of highly sophisticated scientific discussions of topics such as companion diagnostic assays, immunotherapy drugs and genetic testing.....
 
.... The AACR Annual Meeting also included policy symposia, including a packed-room discussion of the Affordable Care Act (ACA), often called “Obamacare,” and a panel discussion on how to get the latest cancer treatments to patients more quickly. During the session on the ACA, ovarian cancer survivor and patient advocate Mary Jackson Scroggins talked about perceptions and misconceptions of the ACA...... 

The science of cancer spread (general)



The science of cancer spread

Hutch News

The science of cancer spread

The how and why of metastasis — and what it might take to stop it


April 28, 2016
 

Editor’s note: This is the second in a two-part series on metastasis. Read part one, about patients living with metastatic breast cancer, here.

In some ways, cancer is maddeningly uniform. Different cells in a tumor aren’t all identical, but in a general sense, they are driven by the same, unifying goal: grow and divide, grow and divide, grow and divide. But one day, after enough growing and dividing, a tiny minority of those cells bucks the trend and does something different.
They metastasize.
Metastasis, or cancer spread, is complex and still largely mysterious. Those maverick cells have to go through myriad changes as they traverse the path from their original home in the primary tumor to new tumors they seed and form throughout the body.
They change from stationary to mobile, actively pushing their way out of their tumor home. They breech the walls of blood vessels or lymph nodes. They survive the strange new environment and physical forces of the circulatory system. And at their final destination, they do all these steps again in reverse, setting up shop anew and triggering the growth of a metastatic tumor.
Metastasis is very inefficient. Some large tumors may shed upward of a million cells into the bloodstream every day, but only a few of these cells actually form new metastatic tumors. If it weren’t so deadly the feat of those few cells would be almost awe-inspiring — nearly all deaths from solid tumor cancers are due to metastatic disease, according to the American Cancer Society.
Even so, there’s still a ton researchers don’t understand about the process, let alone how to stop it, said Fred Hutchinson Cancer Research Center postdoctoral fellow Dr. Minna Roh-Johnson, who studies the biology of melanoma metastasis.
“The more I learn about metastasis from my work and other people’s work, the more outstanding questions I feel like get added to the list of outstanding questions,” she said. “Almost every step is an unknown.”
 

Step one: First steps

Step two: Breaking barriers and surviving torrents

Step three: Finding a new home

Step four: Waking up

It’s not clear why some metastatic cells stay dormant for so long while others wake up relatively soon after spreading. About one in five metastatic breast cancer patients won’t get metastases until 10 years after they’ve been treated, Ghajar said.
“You can imagine how crushing that is,” he said. “It’s crushing across the board, but you go 10 years after treatment, you think you’re cured, and all of a sudden you have a relapse.”....

Postscript: Can metastasis be stopped before it starts?

WHI Informs on Links Between Diabetes, Metformin, and Cancer



Medscape
 
A new analysis from the Women's Health Initiative (WHI) shows that, compared with women without diabetes, adult postmenopausal women with type 2 diabetes are at a significant 13% increased risk of invasive cancer and have a 46% higher risk for cancer death.
The latest WHI data, reported in the April 15 issue of the International Journal of Cancer, also suggest that long-term metformin therapy — the first go-to medicine for type 2 diabetes — may be linked with a reduced risk of cancer mortality.....

But Does Metformin Really Reduce Cancer Deaths?
 
Dr Fonseca explained to Medscape Medical News that it is difficult, in the WHI, to determine whether metformin may reduce the risk of cancer mortality in a realistic sense.
He feels that the message this kind of study sends is that other drugs used to treat diabetes are "bad," which is not true.
"Metformin is standard therapy and is typically used in relatively healthy individuals, while other medications are used in patients with progressive diabetes; in short, in sicker patients," he noted.
Dr Horton agreed. "Indeed, metformin is contraindicated in patients with significantly impaired kidney function," he said.
Sicker patients have additional comorbidities that may well contribute to the risk of cancer and cancer mortality, Dr Fonseca pointed out.
"Randomized studies have not shown that other drugs used to treat diabetes are associated with a higher risk for cancer mortality," he added......


And another endocrinologist warns about interpretation of this type of work. "Such studies [as the WHI] need to be viewed with caution," Vivian A Fonseca, MD, Tullis–Tulane Alumni Chair in Diabetes and chief of the section of endocrinology at Tulane University, New Orleans, told Medscape Medical News .
Dr Fonseca explained that studies linking diabetes and cancer and metformin use with decreased cancer mortality are confounded by selection bias and lack of randomization.

Expression-of-Interest for consumer participation - Cancer Australia



Expression-of-Interest for consumer participation in Grant Review Committees for the Priority-driven Collaborative Cancer Research Scheme | Cancer Australia

Cancer Australia has developed an innovative, annual cancer research projects funding scheme called the Priority-driven Collaborative Cancer Research Scheme (PdCCRS). The PdCCRS is conducted by Cancer Australia in partnership with other funders of cancer research.
Cancer Australia invites consumers interested in assessing cancer research applications submitted to the PdCCRS to submit an Expression-of-Interest to Cancer Australia. Expression-of-interest submissions will be assessed by a panel, which will include consumer representation.
For more information click here.

New Cancer Australia Framework to guide targeted efforts in gynaecological cancer control



Cancer Australia
 News Type: 
  • Announcement
As the Government’s lead national agency in cancer, Cancer Australia has today released the National Framework for Gynaecological Cancer Control to reduce the impact of gynaecological cancer in Australia.
This year around 5,500 Australian women will be diagnosed with a gynaecological cancer. While the number of women surviving gynaecological cancer in Australia is rising, outcomes remain poor for some cancer types and population groups. For many women, treatment for gynaecological cancer may have physical and psychological effects for years after their diagnosis.
The National Framework identifies priority areas for action and provides targeted strategies to guide efforts for improving outcomes for women with gynaecological cancer and ensure best practice and culturally-appropriate care is provided to all women across Australia.
Cancer Australia encourages health professionals and service providers, researchers, cancer organisations and the community to identify and apply relevant strategies in the Framework to their own stream of work, in a coordinated effort to reduce the impact of gynaecological cancer.

Pattern of Duplicate Presentations at National Hematology-Oncology Meetings: Influence of the Pharmaceutical Industry



ASCO Reading Room - open access (pdf)

Preventive Medicine - journal index



ScienceDirect