C Blake Gilks

Vancouver General Hospital, Vancouver, British Columbia, Canada

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Publications (220)1085.98 Total impact

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    ABSTRACT: Therapies that target overexpression of human epidermal growth factor receptor 2 (HER2) rely on accurate and timely assessment of all patients with new diagnoses. This study examines HER2 testing of primary breast cancer tissue when performed with immunohistochemistry (IHC) and additional in situ hybridization (ISH) for negative cases (IHC 0/1+). The analysis focuses on the rate of false-negative HER2 tests, defined as IHC 0/1+ with an ISH ratio ≥ 2.0, in eight pathology centers across Canada.
    Journal of clinical oncology : official journal of the American Society of Clinical Oncology. 11/2014;
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    ABSTRACT: Formalin-fixed, paraffin-embedded unstained archived diagnostic tissue sections are frequently exchanged between clinical laboratories for immunohistochemical staining. The manner in which such sections are prepared represents a type of preanalytical variable that must be taken into account given the growing importance of immunohistochemical assays, especially predictive and prognostic tests, in personalized medicine.
    American Journal of Clinical Pathology 11/2014; 142(5):629-33. · 2.88 Impact Factor
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    ABSTRACT: Context .- Immunohistochemical (IHC) testing for HER2/neu is becoming the standard of care for guiding adjuvant treatment of gastric carcinoma with trastuzumab. Objective .- To assess interlaboratory variation in IHC staining and interpretation across multiple laboratories. Design .- A tissue microarray consisting of 45 cores from 28 gastric cancers was distributed to 37 laboratories for HER2/neu assessment. The IHC results were compared against expert scores at an academic institution and correlated with in situ hybridization results from the originating specimen. Interlaboratory agreement was calculated using Cohen κ statistic. Results .- The survey demonstrated several variations in IHC methods, including the primary antibodies in use. There was excellent agreement among laboratories in HER2/neu(+) (IHC 3(+)) cases (κ = 0.80 ± 0.01) and very good agreement among laboratories in HER2/neu(-) (IHC 0 or 1(+)) cases (κ = 0.58 ± 0.01). Less agreement was observed among laboratories when scoring equivocal (IHC 2(+)) cases (κ = 0.22 ± 0.01). Sensitivity and specificity of HER2/neu IHC were 99% and 100%, respectively, when measured against expert review and consensus score as a reference standard. Conclusions .- There is substantial interlaboratory agreement in the interpretation of HER2/neu IHC despite variability in protocols. Although HER2/neu IHC is a highly sensitive and specific test, primary antibody selection may significantly affect IHC results. Furthermore, gastric tumors require a unique scoring system and expertise in interpretation. Intratumoral heterogeneity has a significant effect on HER2/neu scoring by IHC. Ongoing quality assurance exercises among laboratories will help ensure optimized HER2/neu testing.
    Archives of pathology & laboratory medicine 11/2014; 138(11):1495-502. · 2.78 Impact Factor
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    ABSTRACT: AimsEndometrial clear cell carcinomas (CCC) constitute less than 5% of all carcinomas of the endometrium. There is currently little known regarding the genetic basis of endometrial CCC.Methods and ResultsWe performed genomic and immunohistochemical analyses on 14 rigorously reviewed pure endometrial CCC. The genomic analysis consisted of sequencing the coding regions of 26 genes previously implicated in endometrial carcinoma. Twelve of fourteen tumors displayed a prototypic CCC immunophenotype (napsin A+, HNF1β+ and estrogen receptor-) and all showed intact mismatch repair protein expression. We detected mutations in 11 of 14 tumors and there was a predominance of mutations involving genes that are more frequently mutated in endometrial serous carcinomas than in endometrioid carcinomas. Two tumors displayed prototypical serous carcinoma mutation profile (concurrent TP53 and PPP2R1A mutations, without PTEN, CTNNB1 or ARID1A mutation). There were no mutations in PTEN, CTNNB1 or POLE identified.Conclusions The overall mutation profile of this cohort of endometrial CCC appears to be more serous-like than endometrioid-like, with a minor subset in the TP53-mutated CCC showing serous carcinoma profile. These findings provide new insights into the molecular features of morphologically prototypical endometrial CCC, and underscore the needs for further investigations into the oncogenesis of endometrial CCC.This article is protected by copyright. All rights reserved.
    Histopathology 10/2014; · 2.86 Impact Factor
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    ABSTRACT: The contemporary oncologic pathology report conveys diagnostic, prognostic, predictive, and hereditary predisposition information. Each component may be premised on a morphologic feature or a biomarker. Clinical validity and reproducibility are paramount as is standardization of reporting and clinical response to ensure individualization of patient care. Regarding hereditary predisposition, morphology-based genetic referral systems in some instances have eclipsed genealogy-based systems, for example, cell type in ovarian cancer and BRCA screening. In other instances such as Lynch syndrome, morphology-based schemas supplement clinical schemas and there is an emerging standard of care for reflex biomarker testing. Hereditary leiomyomatosis and renal cell carcinoma (HLRCC) syndrome predisposes patients to uterine and cutaneous leiomyomas (LMs) and renal cell carcinomas (RCCs). Several authors have emphasized the role pathologists may play in identifying this syndrome by recognizing the morphologic characteristics of syndromic uterine LMs and RCCs. Recently immunohistochemical overexpression of S-(2-succinyl) cysteine (2SC) has been demonstrated as a robust biomarker of mutation status in tumors from HLRCC patients. In this blinded control-cohort study we demonstrate that the proposed morphologic criteria used to identify uterine LMs in HLRCC syndrome are largely irreproducible among pathologists and lack sufficient robustness to serve as a trigger to triage cases for 2SC immunohistochemistry or patients for further family/personal history inquiry. Although refinement of morphologic criteria can be considered, in view of the availability of a clinically robust biomarker, consideration should be given to reflex testing of uterine LMs with an appropriate age cut off or in the setting of a suspicious family history.
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    ABSTRACT: Uterine sarcomas and carcinosarcomas are an aggressive group of uterine malignancies. The frequency of mismatch repair (MMR) protein loss by immunohistochemical evaluation has not been comprehensively characterized in this group of tumors; hence, the appropriateness of applying an immunohistochemical panel to screen for Lynch syndrome in these tumors remains unclear. We examined for the immunohistochemical loss of 4 MMR proteins (MLH1, MSH2, MSH6, and PMS2) in a series of 67 uterine carcinosarcomas and 51 uterine sarcomas (20 leiomyosarcomas, 11 adenosarcomas, 9 low-grade endometrial stromal sarcomas, 8 high-grade endometrial stromal sarcomas/undifferentiated endometrial sarcomas, and 3 rhabdomyosarcomas) at our institution. Four of the 67 (6.0%) carcinosarcomas demonstrated abnormal MMR protein expression. Two tumors showed concurrent loss of MLH1 and PMS2 in both the carcinomatous and sarcomatous components. One tumor showed the loss of only PMS2 in both components. The remaining tumor showed an isolated loss of MLH1 and PMS2 in only the small cell carcinoma component, whereas the non-small-cell carcinoma and sarcoma components demonstrated normal staining patterns for MMR proteins. Two of 20 leiomyosarcomas (10%) showed the loss of MMR proteins: one with loss of PMS2 and the other with loss of MSH2 and MSH6. All other uterine sarcoma types examined showed intact MMR protein expression. These observations provide a basis for MMR protein screening in uterine carcinosarcomas and leiomyosarcomas but not in other types of uterine mesenchymal or mixed epithelial/mesenchymal malignancies.
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    ABSTRACT: The evolution of cancer genomes within a single tumor creates mixed cell populations with divergent somatic mutational landscapes. Inference of tumor subpopulations has been disproportionately focused on the assessment of somatic point mutations, whereas computational methods targeting evolutionary dynamics of copy number alterations (CNA) and loss of heterozygosity (LOH) in whole genome sequencing data remain under-developed. We present a novel probabilistic model, TITAN, to infer CNA and LOH events while accounting for mixtures of cell populations, thereby estimating the proportion of cells harboring each event. We evaluate TITAN on idealized mixtures, simulating clonal populations from whole genome sequences taken from genomically heterogeneous ovarian tumor sites collected from the same patient. In addition, we show in 23 whole genomes of breast tumors that inference of CNA and LOH using TITAN critically inform population structure and the nature of the evolving cancer genome. Finally, we experimentally validated subclonal predictions using fluorescence in situ hybridization (FISH) and single-cell sequencing from an ovarian cancer patient sample, thereby recapitulating the key modeling assumptions of TITAN.
    Genome research. 07/2014;
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    ABSTRACT: Previously reported findings in Austrian BRCA1/2 mutation carriers suggested a possible dependency of embryos with BRCA1/2 mutations on so-called low alleles of the fragile X mental retardation 1 (FMR1) gene, characterized by less than 26 CGG repeats (CGGn<26). The hypothesis arose from a study reporting highly statistically significant enrichment of low FMR1 alleles, significantly exceeding low allele prevalence in a general population, suggesting embryo lethality of BRCA1/2 mutations, "rescued" by presence of low FMR1 alleles. Such a dependency would also offer an explanation for the so-called "BRCA-paradox," characterized by BRCA1/2 deficient embryonic tissues being anti-proliferative (thereby potentially causing embryo-lethality) but proliferative in malignant tumors, including breast and ovarian cancers. Follow up investigations by other investigators, however, at most demonstrated trends towards enrichment but, mostly, no enrichment at all, raising questions about the original observation and hypothesis. We in this study, therefore, investigated CGGn of the FMR1 gene of 86 anonymized DNA samples from women with various forms of ovarian cancer, and were unable to demonstrate differences in prevalence of low FMR1 alleles either between positive and negative ovarian cancer patients for BRCA1/2 or between ovarian cancer patients and reported rates in non-cancer populations. This raises further questions about a suggested dependency between BRCA1/2 and FMR1, but also raises the possibility that investigated Austrian BRCA1/2 carrier populations differ from those in other countries. Either only selected BRCA1/2 mutations, therefore, interact with low FMR1 alleles or the Austrian data reflect only coincidental observations.
    PLoS ONE 07/2014; 9(7):e102370. · 3.53 Impact Factor
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    ABSTRACT: The pathogenesis of vulvar squamous cell carcinoma follows 1 of 2 distinct pathways. A precursor lesion in the human papilloma virus-independent pathway, differentiated vulvar intraepithelial neoplasia (dVIN), was only recently characterized in detail and is infrequently diagnosed without an associated component of invasive carcinoma. Aberrant p53 immunostaining is frequently seen in dVIN, and in approximately 25% to 30% of cases it manifests as a complete loss or a p53-null pattern. The abrupt transition between p53 loss and basal p53 expression in lesional versus nonlesional epithelium allows clear demarcation between neoplastic and non-neoplastic epithelium. For this study, 14 specimens from 10 patients were identified from the pathology archives of 2 teaching hospitals on the basis of: (1) a diagnosis of dVIN, with or without invasive carcinoma; and (2) p53-null immunostaining pattern in lesional cells. Ten specimens had associated invasive carcinoma. All sections from each specimen that showed the specimen resection margin were stained for p53 and reviewed together with all hematoxylin and eosin sections. Detailed morphologic assessment of the p53-null epithelium was made and compared with the adjacent benign squamous epithelium. The status of the resection margins based on the original pathologic assessment was compared with that assessed with p53 immunohistochemistry. One specimen showed p53 loss in the invasive carcinoma but patchy basal positivity in the region originally diagnosed as dVIN, supporting interpretation as a benign hyperplastic focus, rather than dVIN. In the remaining 13 specimens the areas originally diagnosed as dVIN, as well as the associated invasive carcinoma (if present), were p53-null. In 8 of these specimens, on the basis of the presence of p53-null immunostaining and subtle morphologic abnormalities, dVIN was more extensive than originally recognized. The spectrum of morphologic changes in p53-null regions that were in continuity with areas originally recognized as dVIN were subtle and typically consisted of an abrupt change in maturation of the squamous epithelium (loss of keratohyaline granules and parakeratosis), tinctorial alterations in the keratinocytes, with cells containing more abundant eosinophilic cytoplasm, and minimal basal nuclear atypia. Margin status changed from negative to positive in 4 of 13 specimens and from focally to more extensively positive in an additional 3 specimens. In summary, the clonal in situ component of non-human papilloma virus vulvar squamous cell carcinoma can be characterized by very subtle morphologic abnormalities that may be misinterpreted as benign change. This results in underestimation of the extent of dVIN, and, as a result, resection margin involvement may be significantly underestimated. dVIN can also be overdiagnosed in areas of reactive change. Better tools for diagnosis of dVIN are needed; until such tools are developed the limitations in the current diagnosis of dVIN should be recognized.
    American Journal of Surgical Pathology 07/2014; · 4.87 Impact Factor
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    ABSTRACT: Women with Lynch syndrome (LS) are at increased risk for the development of epithelial ovarian cancer (OC). Analogous to previous studies on BRCA1/2 mutation carriers, there is evidence to suggest a histotype-specific association in LS-associated OCs (LS-OC). Whereas the diagnosis of high-grade serous carcinoma is an indication for BRCA1/2 germline testing, in contrast, there are no screening guidelines in place for triaging OC patients for LS testing based on histotype. We performed a centralized pathology review of tumor subtype on 20 germline mutation-confirmed LS-OCs, on the basis of morphologic assessment of hematoxylin and eosin-stained slides, with confirmation by immunohistochemistry when necessary. Results from mismatch-repair immunohistochemistry (MMR-IHC) and microsatellite instability (MSI) phenotype status were documented, and detailed pedigrees were analyzed to determine whether previously proposed clinical criteria would have selected these patients for genetic testing. Review of pathology revealed all LS-OCs to be either pure endometrioid carcinoma (14 cases), mixed carcinoma with an endometrioid component (4 cases), or clear cell carcinoma (2 cases). No high-grade or low-grade serous carcinomas or mucinous carcinomas of intestinal type were identified. Tumor-infiltrating lymphocytes were prominent (≥40 per 10 high-powered fields) in 2 cases only. With the exception of 1 case, all tumors tested for MMR-IHC or MSI had an MMR-deficient phenotype. Within this cohort, 50%, 55%, 65%, and 85% of patients would have been selected for genetic workup by Amsterdam II, revised Bethesda Guidelines, SGO 10% to 25%, and SGO 5% to 10% criteria, respectively, with <60% of index or sentinel cases detected by any of these schemas. To further support a subtype-driven screening strategy, MMR-IHC reflex testing was performed on all consecutive non-serous OCs diagnosed at 1 academic hospital over a 2-year period; MMR deficiency was identified in 10/48 (21%) cases, all with endometrioid or clear cell histology. We conclude that there is a strong association between endometrioid and clear cell ovarian carcinomas and hereditary predisposition due to MMR gene mutation. These findings have implications for the role of tumor subtype in screening patients with OC for further genetic testing and support reflex MMR-IHC and/or MSI testing for newly diagnosed cases of endometrioid or clear cell ovarian carcinoma.
    The American journal of surgical pathology. 07/2014;
  • C. Blake Gilks
    Gynecologic Oncology 07/2014; 134(1):1–2. · 3.93 Impact Factor
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    ABSTRACT: Objective To assess the uptake and perioperative safety of bilateral salpingectomy (BS) as an ovarian cancer risk-reduction strategy in low-risk women following a regional initiative aimed at general gynecologists in the province of British Columbia (BC), Canada. Study Design This population-based retrospective cohort study evaluated 43,931 women in BC between 2008-2011 who underwent hysterectomy performed with and without bilateral salpingectomy (BS) or bilateral salpingo-oophorectomy, or underwent surgical sterilization by means of BS or tubal ligation. Parameters examined include patient age, operating time, surgical approach, indication, length of hospital stay, and perioperative complications. Results There was an increase in the uptake of hysterectomy with BS (5→35%, p< 0.001) and BS for sterilization (0.5→33%, p<0.001) over the study period, particularly in women <50 years of age. Minimal additional surgical time is required for hysterectomy with BS (16 minutes, p<0.001) and BS for sterilization (10 minutes, p<0.001) compared with hysterectomy alone or tubal ligation, respectively. No significant differences were observed in the risks of hospital readmission or blood transfusions in women who underwent hysterectomy with BS (aOR=0.91 95%CI (0.75,1.10) and aOR=0.86 95%CI (0.67,1.10)) or BS for sterilization (aOR=0.8 95%CI (0.56,1.21) and aOR=0.75 95%CI (0.32,1.73)), respectively. From 2008-2011 the proportion of hysterectomies with BS performed by open laparotomy decreased from 77→44% with uptake in laparoscopic, vaginal, and combined procedures (p<0.001). Conclusions Following our 2010 educational initiative there has been a shift in surgical paradigm in our province. This cancer prevention approach does not increase the risk of operative/perioperative complications and appears both feasible and safe.
    American journal of obstetrics and gynecology 05/2014; · 3.28 Impact Factor
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    ABSTRACT: The revised FIGO 2013 staging for carcinomas of the ovary, fallopian tube and peritoneum has introduced a single system for tumours originating at these sites. The system requires pathologists to assign a primary site (ovary, tube or peritoneum) but does not provide guidance to aid this assignment. This is particularly problematic in cases of advanced stage (stage II or greater) high-grade serous carcinoma (HGSC) where there is commonly involvement of two or more sites by tumour and practice amongst pathologists in determining where a tumour has arisen varies widely. This has significant implications for recording of tumour incidence and mortality, data collection by cancer registries and entry into clinical trials. We propose guidelines for assigning primary site of HGSC based on careful macroscopic and histological assessment. The use of these guidelines, in conjunction with the new FIGO staging system, is intended to act as an impetus to promote debate and a uniform and consistent approach in assigning primary tumour site which will facilitate comparison of data between centres. This article is protected by copyright. All rights reserved.
    Histopathology 03/2014; · 2.86 Impact Factor
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    ABSTRACT: The Ovarian Task Force of the Gynecologic Cancer Steering Committee convened a clinical trials planning meeting on October 28-29, 2011, with the goals to identify key tumor types, associated molecular pathways, and biomarkers for targeted drug intervention; review strategies to improve early-phase screening, therapeutic evaluation, and comparison of new agents; and optimize design of randomized trials in response to an evolving landscape of scientific, regulatory, and funding priorities. The meeting was attended by international clinical and translational investigators, pharmaceutical industry representatives, government regulators, and patient advocates. Panel discussions focused on disease types, early-phase trials, and randomized trials. A manuscript team summarized the discussions and assisted with formulating key recommendations. A more integrated and efficient approach for screening new agents using smaller selective randomized trials in specific disease-type settings was endorsed, together with collaborative funding models between industry and the evolving national clinical trials network, as well as efforts to enhance public awareness and study enrollment through advocacy.
    CancerSpectrum Knowledge Environment 03/2014; · 14.07 Impact Factor
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    ABSTRACT: Malignant melanoma of the vulva and vagina is relatively uncommon and accounts for <5% of all melanomas in women. The aim of our study was to establish the biological properties and evaluate potential therapeutic targets in these tumors. We collected a series of 65 cases from three centers and re-evaluated the tumor tissue for predominant growth pattern (superficial spreading, nodular, and mucosal lentiginous) and tumor thickness. KIT (CD117) expression was detected immunohistochemically. In addition, tumors were screened for BRAF, NRAS, and KIT mutations by PCR and DNA sequencing as well as for KIT amplifications by fluorescence in situ hybridization. None of the cases contained BRAF mutations. NRAS mutations and KIT amplifications were detected in similar frequency (∼12%) in tumors of the vulva and vagina. In contrast, KIT mutations were present in 18% of primary melanomas of the vulva, but in none of the tumors arising in the vagina. Moderate or strong KIT protein expression was detected in 30 cases, including all tumors with KIT mutations and 6 of the 7 with KIT amplifications. In conclusion, BRAF mutations are virtually absent in melanomas originating from the vulva or vagina, whereas NRAS mutations and KIT amplifications occur in both locations. KIT mutations appear to be specific for melanomas of the vulva, suggesting that in spite of the anatomic proximity, the development of vulvar and vaginal melanomas involves different molecular alterations which may be targeted by novel treatment approaches.Modern Pathology advance online publication, 7 March 2014; doi:10.1038/modpathol.2013.211.
    Modern Pathology 03/2014; · 5.25 Impact Factor
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    Chris MJ Conklin, C Blake Gilks
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    ABSTRACT: The five main subtypes of ovarian surface epithelial carcinoma (high-grade serous, low-grade serous, endometrioid, clear cell and mucinous) are different diseases, with differences in genetic and environmental risk factors, precursor lesions, molecular events during oncogenesis, patterns of spread and response to treatment. With recent advances in surgical pathology, it is possible to reproducibly diagnose these subtypes in routine surgical pathology practice. This review examines these subtypes of ovarian carcinoma, focusing on differential diagnosis, molecular features and current treatment strategies. The increasing understanding of the molecular abnormalities associated with each subtype is leading to exploration and introduction of more subtype-specific treatment of ovarian carcinoma.
    Expert Review of Obstetrics &amp Gynecology 01/2014; 8(1).
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    Dataset: CD10article
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    ABSTRACT: To assess the variation in ovarian carcinoma type diagnosis among gynaecological pathologists from Nordic countries, and whether a rationally designed panel of immunohistochemical markers could improve diagnostic reproducibility. Eight pathologists from four countries (Sweden, Denmark, Norway and Finland) received an educational lecture on diagnosis of ovarian carcinoma type. All tumour-containing slides from 54 ovarian carcinoma cases were independently reviewed by the participants, who 1) determined type based purely on histology, 2) indicated whether they would apply immunohistochemistry in their routine practice, and 3) determined type after reviewing the staining results. The results for 6 markers (WT1, TP53, P16, HNF-1beta, ARID1A and PR) were determined for all 54 cases, by staining a tissue microarray. The median concordance with central review diagnosis was 86%, significantly improving to 90% with incorporation of immunostaining results (p=0.0002). The median interobserver agreement was 78%, significantly improving to 85% with incorporation of immunostaining results. (p=0.0002). Use of the immunostaining results significantly improved both diagnostic accuracy and interobserver agreement. These results indicate that ovarian carcinoma type can be reliably diagnosed by pathologists from different countries, and further demonstrates that immunohistochemistry has an important role in improving diagnostic accuracy and agreement between pathologists. This article is protected by copyright. All rights reserved.
    Histopathology 12/2013; · 2.86 Impact Factor
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    ABSTRACT: It is known that thyroid transcription factor-1 (TTF-1) is expressed in a small percentage of primary gynaecological adenocarcinomas. Following the observation of TTF-1 positivity in a number of endometrioid adenocarcinomas of the uterine corpus which behaved aggressively, we stained a large series of endometrial adenocarcinomas of various types to investigate whether its expression is of prognostic significance. TTF-1 immunohistochemistry was performed on tissue microarrays containing 102 low grade (grade 1 or 2) endometrioid adenocarcinomas, 101 grade 3 endometrioid adenocarcinomas, 89 serous adenocarcinomas and 29 clear cell carcinomas. All categories of endometrial adenocarcinoma exhibited TTF-1 staining in a small subset of cases (2% low grade endometrioid, 11% grade 3 endometrioid, 9% serous, 7% clear cell). TTF-1 was less expressed in low grade endometrioid adenocarcinomas compared to other subtypes. Endometrioid adenocarcinomas which expressed TTF-1 had a statistically significant worse prognosis with poorer disease specific survival and this was also statistically significant in the group of low grade endometrioid adenocarcinomas. Our study confirms that TTF-1 is positive in a small, but not insignificant, proportion of endometrial adenocarcinomas. TTF-1 positivity in low grade endometrioid adenocarcinomas is a poor prognostic factor. This article is protected by copyright. All rights reserved.
    Histopathology 11/2013; · 2.86 Impact Factor
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    ABSTRACT: Up to 15% of ovarian cancers are etiologically linked with hereditary susceptibility. Within this group, germline mutations in mismatch repair (MMR) genes, known otherwise as Lynch syndrome (LS), account for the majority of cases that are not associated with mutations in BRCA1 or BRCA2. Clinical schemas specific for gynecologic cancers have been developed to identify patients with LS; however, many of the recommendations are poorly defined. Few case series of germline-confirmed LS-associated ovarian cancers have been reported, limited by small sample size and often lacking central pathology review. Much insight has been gained from studies of unselected cohorts, using immunohistochemical assessment of MMR protein expression or microsatellite instability analysis. In spite of contradictory results, likely reflective of differences in study design, sample size and methodology, a recurring observation is the overrepresentation of "endometriosis-associated tumors," namely, endometrioid and clear cell subtypes, in the group of ovarian tumors with MMR deficiency. In this review, we summarize the clinical and histomorphologic features of LS-associated/MMR-deficient ovarian epithelial cancers and recommend that reflex testing be performed on the basis of tumor subtype.
    Advances in anatomic pathology 11/2013; 20(6):378-386. · 3.22 Impact Factor

Publication Stats

7k Citations
1,085.98 Total Impact Points


  • 1989–2014
    • Vancouver General Hospital
      • Department of Pathology and Laboratory Medicine (UBC)
      Vancouver, British Columbia, Canada
  • 1987–2014
    • University of British Columbia - Vancouver
      • • Department of Pathology and Laboratory Medicine
      • • Department of Obstetrics and Gynaecology
      • • Department of Pediatrics
      • • Genetic Pathology Evaluation Center (GPEC)
      • • Division of Neurology
      • • Faculty of Medicine
      Vancouver, British Columbia, Canada
  • 2013
    • University Health Network
      • Department of Laboratory Hematology
      Toronto, Ontario, Canada
    • Barts Health NHS Trust
      Londinium, England, United Kingdom
    • Kuwait University
      Al Kuwayt, Al Asimah Governorate, Kuwait
  • 2012–2013
    • Belfast Health and Social Care Trust
      Béal Feirste, N Ireland, United Kingdom
    • Washington Hospital Center
      Washington, Washington, D.C., United States
  • 2011–2013
    • Memorial Sloan-Kettering Cancer Center
      • Department of Pathology
      New York City, NY, United States
    • Memorial University of Newfoundland
      St. John's, Newfoundland and Labrador, Canada
    • Mount Sinai Hospital, Toronto
      Toronto, Ontario, Canada
  • 2010–2013
    • University of Toronto
      • Department of Laboratory Medicine and Pathobiology
      Toronto, Ontario, Canada
    • Cincinnati Children's Hospital Medical Center
      • Division of Immunobiology
      Cincinnati, OH, United States
    • Tabriz University of Medical Sciences
      • Department of Pathology
      Tabrīz, East Azarbaijan, Iran
  • 2004–2011
    • The University of Calgary
      • Department of Pathology and Laboratory Medicine
      Calgary, Alberta, Canada
    • University of Louisville
      Louisville, Kentucky, United States
  • 2002–2011
    • Stanford University
      • • Department of Pathology
      • • Department of Biochemistry
      Stanford, CA, United States
  • 2007–2010
    • King Fahad Hospital Medina La Munawarah Kingdom Of Saudi Arabia
      Al Madīnah al Munawwarah, Al Madīnah, Saudi Arabia
  • 2008
    • Vancouver Coastal Health
      Vancouver, British Columbia, Canada
    • Child & Family Research Institute
      Vancouver, British Columbia, Canada
    • BC Cancer Agency
      Vancouver, British Columbia, Canada
  • 2003–2004
    • Howard Hughes Medical Institute
      Ashburn, Virginia, United States
  • 1991–1993
    • Fox Chase Cancer Center
      • • Department of Medical Oncology
      • • Department of Pathology
      Philadelphia, PA, United States
    • Harvard Medical School
      • Department of Pathology
      Boston, MA, United States