C Blake Gilks

Vancouver General Hospital, Vancouver, British Columbia, Canada

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Publications (222)1175.58 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Uterine carcinosarcoma is a clinically aggressive malignancy composed of a mix of carcinomatous and sarcomatous elements. We performed targeted next-generation sequencing of 27 uterine cancer and sarcoma genes together with immunohistochemical analyses of selected proteins in 30 uterine carcinosarcomas. This included 13 cases in which the distinct carcinoma and sarcoma components were sequenced separately and 10 cases where the metastatic tumors were analyzed in addition to the primary tumors. We identified non-synonymous somatic mutations in 90% of the cases, with 27 of 30 cases (90%) harboring TP53 alterations. The PI3K pathway was the most commonly mutated signaling pathway with mutations identified in PIK3CA, PTEN, PIK3R1, and/or PIK3R2 in two-thirds of the cases. Mutations in FBXW7, PPP2R1A, ARID1A and KRAS were demonstrated in a minority of cases. In cases where the carcinomatous and sarcomatous components were separately analyzed, most of the mutations identified were present in both components, indicating a common origin for the two components. Furthermore, the same TP53 alterations and/or PI3K pathway mutations seen in the primary tumors were also identified in the metastatic sites. Overall, carcinosarcomas exhibited heterogeneous molecular features that resemble the heterogeneity seen in endometrial carcinomas, with some showing endometrioid carcinoma-like and others showing serous carcinoma-like mutation profiles. While patients with serous-like tumors presented more frequently with advanced-stage disease compared to patients with endometrioid-like tumors, there was no statistical difference in outcome between the two groups. Our results provide insights into the oncogenesis of uterine carcinosarcoma and identify targetable mutations that represent early oncogenic events. The findings of the different molecular types of uterine carcinosarcoma that parallel the different molecular types in endometrial carcinoma may have future treatment implications with targeted therapies. This article is protected by copyright. All rights reserved.
    03/2015; DOI:10.1002/cjp2.18
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    ABSTRACT: A proportion of endometrial carcinomas (ECs) are associated with deficient DNA mismatch repair (MMR). These tumors are characterized by high levels of microsatellite instability (MSI). Identification of MSI is important in identifying women who should be tested for Lynch syndrome and identifying a phenotype that may have specific prognostic and predictive implications. Genomic characterization of ECs has shown that MSI tumors form a distinct subgroup. The two most common methodologies for MSI assessment have not been compared in EC.
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    ABSTRACT: AimsEvidence indicates that most non-uterine high-grade serous carcinomas (HGSC) arise from the fallopian tube, but approaches to primary site assignment have not evolved to reflect this. This study aimed to assess application of recently proposed criteria for site assignment.Methods and Results151 HGSCs from four centres were reviewed retrospectively. 63/80 (79%) chemo-naïve (CN) and 45/71 (68%) post-neoadjuvant chemotherapy (NACT) cases were assigned as fallopian tube (FT) primaries with the new criteria, while 58/80 (73%) and 45/71 (63%) were considered ovarian primaries using traditional criteria (p<0.0001). In 111 prospectively collected HGSC's, with consistent detailed fimbrial examination, 44/53 (83%) CN and 44/58 (76%) NACT cases were assigned as FT primaries. Reproducibility of site assignment was tested in a subset of 50 cases: 4/4 reviewing pathologists agreed on primary site in 48/50 (96%), and 3/4 in 49/50 (98%) cases. Of the 53 prospectively studied CN cases, bilateral ovarian involvement (62%) was significantly more frequent than bilateral tubal involvement (12%, p<0.0001), further supporting tubal origin and ovarian metastasis in most cases.Conclusions With currently accepted protocols, the proposed guidelines are easy to apply and result in consistent site assignment in non-uterine HGSC. Most cases of non-uterine HGSC were considered primary FT neoplasms.This article is protected by copyright. All rights reserved.
    Histopathology 01/2015; DOI:10.1111/his.12651 · 3.30 Impact Factor
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    ABSTRACT: Uterine tumors resembling ovarian sex cord tumors (UTROSCTs) are rare uterine neoplasms characterized by pure or predominant epithelial-like patterns that share morphologic, immunohistochemical, and ultrastructural features with ovarian sex cord tumors. FOXL2 immunoexpression has recently been found in sex cord stromal tumors of the ovary, including granulosa cell tumors, Sertoli-Leydig cell tumors, thecomas, and fibromas, but mutations have been identified mostly in adult granulosa cell tumors. In this study, we investigated FOXL2 mutation status and protein expression in UTROSCTs. Mutational analysis using a TaqMan real-time polymerase chain reaction-based allelic discrimination assay was performed on formalin-fixed, paraffin-embedded tissue from 15 UTROSCTs. FOXL2 mutation was absent in all tumors. FOXL2 immunoexpression was tested in all 15 tumors. Intensity of staining was scored as weak, moderate, or strong. Percentage of tumor cells with nuclear staining was recorded as follows: 0 (negative); 1+ (1% to 25%); 2+ (26% to 50%); 3+ (51% to 75%); and 4+ (76% to 100%). Nuclear expression of FOXL2 was present in 6 of 15 (40%) UTROSCTs. One tumor demonstrated strong 4+ staining. Moderate expression was seen in 3 cases, including 2 and 1 showing 2+ and 1+ staining, respectively. Weak expression was observed in 2 tumors demonstrating 3+ and 1+ staining. Although UTROSCTs show overlapping morphologic, immunohistochemical, and ultrastructural features with sex cord stromal tumors of the ovary, they do not harbor FOXL2 mutation despite focal immunoreactivity in a subset of these tumors.
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    ABSTRACT: To conduct a cost-effectiveness analysis of opportunistic salpingectomy (elective salpingectomy at hysterectomy or instead of tubal ligation). A Markov Monte Carlo simulation model estimated the costs and benefits of opportunistic salpingectomy in a hypothetical cohort of women undergoing hysterectomy for benign gynecologic conditions or surgical sterilization. The primary outcome measure was the incremental cost-effectiveness ratio. Effectiveness was measured in terms of life expectancy gain. Sensitivity analyses accounted for uncertainty around various parameters. Monte Carlo simulation estimated the number of ovarian cancer cases associated with each strategy in the Canadian population. Salpingectomy with hysterectomy was less costly ($11,044.32±$1.56) than hysterectomy alone ($11,206.52±$29.81) or with bilateral salpingo-oophorectomy ($12,626.84±$13.11) but more effective at 21.12±0.02 years compared with 21.10±0.03 and 20.94±0.03 years, representing average gains of 1 week and 2 months, respectively. For surgical sterilization, salpingectomy was more costly ($9,719.52±$3.74) than tubal ligation ($9,339.48±$26.74) but more effective at 22.45±0.02 years compared with 22.43±0.02 years (average gain of 1 week) with an incremental cost-effectiveness ratio of $27,278 per year of life gained. Our results were stable over a wide range of costs and risk estimates. Monte Carlo simulation predicted that salpingectomy would reduce ovarian cancer risk by 38.1% (95% confidence interval [CI] 36.5-41.3%) and 29.2% (95% CI 28.0-31.4%) compared with hysterectomy alone or tubal ligation, respectively. Salpingectomy with hysterectomy for benign conditions will reduce ovarian cancer risk at acceptable cost and is a cost-effective alternative to tubal ligation for sterilization. Opportunistic salpingectomy should be considered for all women undergoing these surgical procedures.
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    ABSTRACT: Sprouty (SPRY) proteins are well-characterized factors that inhibit receptor tyrosine kinase signaling. Our Human Exonic Evidence-Based Oligonucleotide (HEEBO) microarray results showed that the mRNA levels of SPRY2, but not of SPRY1 or SPRY4, are down-regulated in high-grade serous ovarian carcinoma (HGSC) tissues and epithelial ovarian cancer (EOC) cell lines. Molecular inversion probe (MIP) copy number analysis showed the deletion of the SPRY2 locus in HGSC. Overexpression of SPRY2 reduced EGF-induced cell invasion by attenuating EGF-induced E-cadherin down-regulation. Moreover, a positive correlation between SPRY2 and E-cadherin protein levels was observed in HGSC tissues. This study reveals the loss of SPRY2 in HGSC and indicates an important tumor-suppressive role for SPRY2 in mediating the stimulatory effect of EGF on human EOC progression. Copyright © 2014. Published by Elsevier B.V.
    FEBS Letters 12/2014; DOI:10.1016/j.febslet.2014.12.012 · 3.34 Impact Factor
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    ABSTRACT: Most nonuterine high-grade serous carcinomas (HGSCs) in women with hereditary breast and ovarian cancer syndrome, due to germline BRCA1/2 mutation, arise in the fimbria of the fallopian tube. However, the site of origin of sporadic HGSC, which is usually widely disseminated at presentation, is not well established. We sought to characterize cases of HGSC discovered incidentally in patients not known to be at high risk, in order to determine the site distribution and possible origin of sporadic HGSC. Incidental microscopic, non-mass-forming cases of serous tubal intraepithelial carcinoma or HGSC in salpingo-oophorectomy specimens in which the tubes and ovaries had been extensively examined were identified. No patients were known or suspected BRCA1/2 mutation carriers. Twenty-one cases were identified (mean age: 57 y). Surgery was for benign disease (n=15), uterine endometrioid adenocarcinoma or atypical hyperplasia (n=3), bladder carcinoma (n=1), or ovarian serous borderline tumor (n=2). In 16 of 21 cases, the lesion was confined to the fallopian tube (unilateral in 14 cases, bilateral in 2). There was serous tubal intraepithelial carcinoma in all cases and invasive HGSC into the underlying lamina propria in 8 of these 16 cases; the invasive focus measured 1.3 cm or less in every case. In the remaining 5 cases, there was fallopian tube mucosal and ovarian involvement; in 2 of these cases, there was also microscopic peritoneal involvement. Sporadic cases of nonuterine HGSC arise in the fallopian tube fimbria in a large majority of cases, providing further evidence for the tubal origin of these neoplasms.
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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 11/2014; DOI:10.1200/JCO.2014.55.6092 · 17.88 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. DOI:10.5858/arpa.2013-0604-OA · 2.88 Impact Factor
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    ABSTRACT: Objectives: Formalin-fixed, paraffin-embedded unstained archived diagnostic tissue sections are frequently exchanged between clinical laboratories for iminunohistochemical 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. Methods: Recommendatio. ns were derived from review of the literature and expert consensus of the Canadian Association of Pathologists Association canadienne des pathologists National Standards Committee for High Complexity Testing/ Immunohistochemistry. Results: Relevant considerations include the type of glass slide on which to mount the unstained sections; the thickness of the tissue sections; the time from slide preparation to testing; the environment, particularly the temperature at which the unstained sections will be maintained prior to testing; the inclusion of on-slide positive control tissue where possible; and whether patient identifier(s) should be included on slide labels. Conclusions: Clear communication between requesting and releasing laboratories will facilitate the proper preparation of unstained sections and also ensure that applicable privacy considerations are addressed
    American Journal of Clinical Pathology 11/2014; 142(5):629-33. DOI:10.1309/AJCP77GXYVEQXMXT · 2.88 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.
    International Journal of Gynecological Pathology 09/2014; 33(6). DOI:10.1097/PGP.0000000000000091 · 1.63 Impact Factor
  • Geburtshilfe und Frauenheilkunde 09/2014; 74(S 01). DOI:10.1055/s-0034-1388327 · 0.96 Impact Factor
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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.
    International Journal of Gynecological Pathology 07/2014; DOI:10.1097/PGP.0b013e31829ff239 · 1.63 Impact Factor
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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; 24(11). DOI:10.1101/gr.180281.114 · 13.85 Impact Factor
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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. DOI:10.1371/journal.pone.0102370 · 3.53 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.
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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; 39(1). DOI:10.1097/PAS.0000000000000291 · 4.59 Impact Factor
  • C. Blake Gilks
    Gynecologic Oncology 07/2014; 134(1):1–2. DOI:10.1016/j.ygyno.2014.05.023 · 3.69 Impact Factor
  • Clinical Cancer Research 05/2014; 19(19_Supplement):A13-A13. DOI:10.1158/1078-0432.OVCA13-A13 · 8.19 Impact Factor
  • Clinical Cancer Research 05/2014; 19(19_Supplement):A17-A17. DOI:10.1158/1078-0432.OVCA13-A17 · 8.19 Impact Factor

Publication Stats

8k Citations
1,175.58 Total Impact Points


  • 1989–2015
    • Vancouver General Hospital
      • Department of Pathology and Laboratory Medicine (UBC)
      Vancouver, British Columbia, Canada
  • 1987–2015
    • University of British Columbia - Vancouver
      • • Department of Pathology and Laboratory Medicine
      • • Department of Obstetrics and Gynaecology
      • • Genetic Pathology Evaluation Center (GPEC)
      Vancouver, British Columbia, Canada
  • 2013
    • Memorial Sloan-Kettering Cancer Center
      • Department of Pathology
      New York City, NY, United States
  • 2011
    • Memorial University of Newfoundland
      St. John's, Newfoundland and Labrador, Canada
  • 2008–2011
    • Vancouver Coastal Health
      Vancouver, British Columbia, Canada
    • BC Cancer Agency
      Vancouver, British Columbia, Canada
  • 2010
    • Tabriz University of Medical Sciences
      • Department of Pathology
      Tabrīz, East Azarbaijan, Iran
    • King Fahad Hospital Medina La Munawarah Kingdom Of Saudi Arabia
      Al Madīnah al Munawwarah, Al Madīnah, Saudi Arabia
  • 2005–2010
    • The University of Calgary
      • Department of Pathology and Laboratory Medicine
      Calgary, Alberta, Canada
  • 2004
    • Stanford Medicine
      Stanford, California, United States
  • 2003
    • Howard Hughes Medical Institute
      Ashburn, Virginia, United States
  • 2002–2003
    • Stanford University
      • • Department of Pathology
      • • Department of Biochemistry
      Palo Alto, California, United States
  • 1991–1995
    • Fox Chase Cancer Center
      • • Department of Medical Oncology
      • • Department of Pathology
      Filadelfia, Pennsylvania, United States