PhenoPath Laboratories

Seattle, WA, United States

PhenoPath Laboratories

Seattle, WA, United States
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News Article | March 1, 2017

SUNNYVALE, Calif.--(BUSINESS WIRE)--OptraSCAN, Inc. today announced the appointment of four new members to its Advisory Board, including Dr. Michael C. Montalto of Bristol-Myer Squibb, Dr. Jiaoti Huang of Duke University, Dr. Allen Gown of PhenoPath Laboratories, and Dr. Abul Abbas of University of California, San Francisco. OptraSCAN will be exhibiting at the upcoming USCAP Annual Conference in San Antonio, TX, March 4-10 at booth #513. Dr. Michael C. Montalto, PhD, is the Executive Director and Head of Translational Pathology and Biomarker Sciences in Translational Medicine at Bristol-Myer Squibb. Prior to this role, Dr. Montalto was a co-founder and executive of Omnyx, LLC, a joint venture of GE Healthcare and the University of Pittsburgh Medical Center that commercialized diagnostic pathology imaging and software products through GE Healthcare. He has patented and published on novel digital pathology-based multiplexing technology (MultiOmyx™, Clarient/Neogenomics) for oncology biomarker discovery. Dr. Jiaoti Huang, MD, PhD, is Professor and Chairman of Department of Pathology, Professor of Pharmacology and Cancer Biology at Duke University, as well as a member of the Duke Cancer Institute. His research laboratory is a leader in studying neuroendocrine differentiation of prostate cancer and molecular pathogenesis of prostatic small cell neuroendocrine carcinoma. Dr. Huang has published 200 research papers, review articles and book chapters. Dr. Allen Gown, MD, is Medical Director and Chief Pathologist at PhenoPath Laboratories. Dr. Gown founded PhenoPath, which has grown to become an internationally renowned specialty pathology reference laboratory. He is a pathologist-scientist recognized as one of the world’s leading experts in the diagnostic and research applications of IHC. He has developed numerous clinically important monoclonal antibodies employed in IHC laboratories around the world (HMB-45, OSCAR, etc.). Dr. Abul Abbas, MD, is Distinguished Professor and Chair, Department of Pathology, University of California San Francisco. His laboratory has used experimental models to analyze the generation and maintenance of regulatory T cells. He has published over 200 peer-reviewed papers and invited reviews, and is the author of four widely read textbooks, two in Immunology and two in Pathology. Dr. David L. Rimm, MD, PhD, is Professor in the Department of Pathology at Yale University School of Medicine, and has been a member of the OptraSCAN Advisory Board since 2016. Dr. Rimm’s lab group (15 researchers) focuses on quantitative pathology using the AQUA® technology invented in his lab with projects related to predicting response to therapy in breast cancer and predicting recurrence or metastasis in melanoma and lung cancer. “We are delighted to have such a diverse and distinguished team of pathology thought leaders joining our Advisory Board,” said Abhi Gholap, Founder and CEO of OptraSCAN. “We will be working closely with our advisors to broaden the reach of our On-Demand Digital Pathology solutions and enter new markets where molecular pathology, immunology and biomarker development are integral components to advancing cancer research.” For more information on the OptraSCAN Advisory Board, visit: OptraSCAN ( for research-use-only, is the first On-Demand Digital Pathology System to provide a comprehensive, affordable end-to-end Digital Pathology solution for both low and high throughput users. OptraSCAN serves as a perfect tool for the transition from conventional microscopy to Digital Pathology for the effective acquisition of Whole Slide images, viewing, sharing, analysis and management of digital slides and associated metadata. The On-Demand solutions include a small-footprint, high and low throughput WSI scanner OptraSCANTM, an integrated image viewer and image management system ImagePathTM and telepathology TELEPathTM, image analysis OptraASSAYSTM and CARDSTM (computer aided region detection system), as well as 10 TB of complimentary cloud storage. Focused on delivering fully integrated Digital Pathology solutions that maximize quality, efficiency and throughput of its customer’s pathology lab (at minimized cost), paired with a complementary Whole Slide image scanner and viewer—OptraSCAN provides a complete Whole Slide Image solution system via an On-Demand pay-per-use program. Follow OptraSCAN on Linkedin and Twitter.

Robens J.,Beth Israel Deaconess Medical Center | Goldstein L.,PhenoPath Laboratories | Gown A.M.,PhenoPath Laboratories | Schnitt S.J.,Beth Israel Deaconess Medical Center
American Journal of Surgical Pathology | Year: 2010

Immunostaining for thyroid transcription factor-1 (TTF-1) is frequently used to help assess the site of origin of metastatic carcinomas. TTF-1 expression is most frequently seen in carcinomas of thyroid and lung origin. Furthermore, it has been assumed that the expression of TTF-1 in a carcinoma excludes the possibility of a breast origin. We have recently encountered in our consultation practice 4 cases of invasive breast carcinoma (confirmed by clinical findings and other immunophenotypic features) that showed unequivocal tumor cell expression of TTF-1. However, the frequency with which TTF-1 expression is observed in breast carcinomas is unknown. To address this, we carried out immunostaining for TTF-1 on 546 primary breast carcinomas submitted for routine estrogen receptor, progesterone receptor, and/or HER2 testing. Cases were considered TTF-1 positive if they showed any nuclear staining for this marker. TTF-1 expression was identified in 13 cases (2.4%). Expression varied from focal and weak to diffuse and strong and was seen in both invasive and in situ components. We conclude that a small proportion of breast carcinomas show TTF-1 expression. Therefore, the presence of TTF-1 immunoreactivity in a carcinoma cannot by itself be used to exclude the possibility of a breast origin. © 2010 by Lippincott Williams & Wilkins.

Dewar R.,Beth Israel Deaconess Medical Center | Fadare O.,Vanderbilt University | Gilmore H.,Beth Israel Deaconess Medical Center | Gown A.M.,University of British Columbia | Gown A.M.,PhenoPath Laboratories
Archives of Pathology and Laboratory Medicine | Year: 2011

Context.-Numerous immunohistochemical stains have been shown to exhibit exclusive or preferential positivity in breast myoepithelial cells relative to their luminal/epithelial counterparts. These myoepithelial markers provide invaluable assistance in accurately classifying breast proliferations, especially in core biopsies. Although numerous myoepithelial markers are available, they differ in their sensitivity, specificity, and ease of interpretation, which may be attributed, to a large extent, to the variable immunoreactivity of these markers in stromal cells including myofibroblasts, vessels, luminal/epithelial cells, and tumor cells. Objective.-To review commonly used myoepithelial markers in breast pathology and a selection of diagnostic scenarios where they may be useful. Data Sources.-The information outlined in this review article is based on our experiences with routine cases and a review of English-language articles published between 1987 and 2008. Conclusions.-To demonstrate the presence or absence of myoepithelial cells, a panel-based approach of 2 or more markers is recommended. Markers that most effectively combine sensitivity, specificity, and ease of interpretation include smooth muscle myosin heavy chains, calponin, p75, p63, P-cadherin, basal cytokeratins, maspin, and CD10. These markers, however, display varying crossreactivity patterns and variably reduced expression in the myoepithelial cells bordering in situ carcinomas. The choice of a myoepithelial marker should be dependent on a combination of factors, including published evidence on its diagnostic utility, its availability, performance characteristics that have been achieved in a given laboratory, and the specific diagnostic scenario. When its use is deemed necessary, immunohistochemistry for myoepithelial cells in breast pathology is most effective when conceptualized as supplemental, rather than central to routine morphologic interpretation.

Terry J.,BC Cancer Agency | Leung S.,BC Cancer Agency | Laskin J.,BC Cancer Agency | Leslie K.O.,Mayo Medical School | And 2 more authors.
American Journal of Surgical Pathology | Year: 2010

The histologic subtype of non-small cell lung carcinoma is important in selecting appropriate chemotherapy for patients with advanced disease. As many of these patients are not operative candidates, they are treated medically after biopsy for diagnosis. Inherent limitations of small biopsy samples can make distinguishing poorly differentiated lung adenocarcinoma (ADC) from squamous cell carcinoma (SCC) difficult. The value of histochemical and immunohistochemical markers to help separate poorly differentiated ADC from SCC in resection specimens is well established; however, the optimal use of markers in small tissue samples has only recently been examined and the correlation of marker expression in small tissue samples with histologic subtype determined on resection specimens has not been well documented. We address this issue by examining the expression of 9 markers (p63, TTF1, CK5/6, CK7, 34βE12, Napsin A, mucicarmine, NTRK1, and NTRK2) on 200 cases of ADC and 225 cases of SCC in tissue microarray format to mimic small tissue specimens. The single best marker to separate ADC from SCC is p63 (for SCC: sensitivity 84%, specificity 85%). Logistic regression analysis identifies p63, TTF1, CK5/6, CK7, Napsin A, and mucicarmine as the optimal panel to separate ADC from SCC. Reduction of the panel to p63, TTF1, CK5/6, and CK7 is marginally less effective but may be the best compromise when tissue is limited. We present an algorithm for the stepwise application of p63, TTF1, CK5/6, CK7, Napsin A, and mucicarmine in situations in which separation of ADC from SCC in small specimens cannot be accomplished by morphology alone. © 2010 by Lippincott Williams & Wilkins.

Allison K.H.,University of Washington | Kandalaft P.L.,PhenoPath Laboratories | Sitlani C.M.,University of Washington | Dintzis S.M.,University of Washington | Gown A.M.,PhenoPath Laboratories
Breast Cancer Research and Treatment | Year: 2012

Oncotype DXTM is an RT-PCR-based assay used to predict chemotherapy benefit in patients with estrogen receptor (ER) positive breast cancers. We were interested if routinely available pathologic parameters could predict Oncotype DXTM Recurrence Scores (RS) in subsets of patients. We identified 173 breast cancers with available RSs and used 104 of these as a test set and 69 cases as a validation set. Pathologic characteristics including size, histologic type, Nottingham grade, and lymphatic invasion were recorded. Test set cases were stained for ER, progesterone receptor (PR), HER2, Ki67, CyclinD1, BCL2, D2-40, and P53. Statistical correlations with RS and regression tree analysis were performed. The validation set was subjected to analysis on the basis of grade, PR, and Ki67. In the test set, grade, PR levels and Ki67 had the strongest correlation with RS (P = 0.0002-0.0007). Regression tree analysis showed grade and PR as factors that could segregate cases into RS categories, with Ki67 adding value in certain subsets. A subset of cancers with a high likelihood of having a low RS (0-18) was identified with the following characteristics: grade 1, strong PR expression (Allred score ≥5) and Ki67 ≤ 10%. No cases with these characteristics had a high RS (≥31) and 73% had a low RS. Cancers highly likely to have a high RS were grade 3, low to absent PR expression (Allred score <5) and Ki67 > 10%. 80% of cases with these characteristics had a high RS and no cases had a low RS. Our validation set had similar findings in these two subsets. In conclusion, When cost and time are a consideration and the added value of Oncotype DXTM testing is in question, it may be reasonable to assume the results of this test in two specific subsets of breast cancers: (1) grade 1, high PR, low Ki67 cancers (low RS), and (2) grade 3, low PR, high Ki67 cancers (high RS). © 2011 Springer Science+Business Media, LLC.

Lee A.F.,Vancouver General Hospital | Lee A.F.,University of British Columbia | Gown A.M.,University of British Columbia | Gown A.M.,PhenoPath Laboratories | And 2 more authors.
American Journal of Surgical Pathology | Year: 2013

Distinguishing malignant mesotheliomas from benign mesothelial proliferations on hematoxylin and eosin-stained sections can be extremely challenging. Various immunohistochemical stains have been suggested to help in making this distinction, but all are controversial. Recently, IMP3 (insulin-like growth factor II mRNA binding protein 3) and GLUT-1 (glucose transporter protein 1) have been proposed as immunohistochemical markers that are positive in mesotheliomas but not in benign proliferations. We evaluated the performance of these markers on a tissue microarray containing 30 malignant mesotheliomas and 48 benign thoracic or abdominal mesothelial proliferations. IMP3 was positive in 53% of malignant and 27% of benign cases (P=0.03), whereas GLUT-1 was positive in 60% of malignant and 13% of benign cases (P=0.0003). Forty-three percent of malignant cases, but only 4% of benign cases, were positive for both IMP3 and GLUT-1 (P=0.00003). We conclude that, statistically, both IMP3 and GLUT-1 are more frequently positive in malignant compared with benign mesothelial processes; however, the frequency of positive staining in benign cases is too high to allow their diagnostic use as single stains. The combination of both markers may be of greater diagnostic value, but this hypothesis should be confirmed in further studies. Copyright © 2013 by Lippincott Williams & Wilkins.

Hwang H.,PhenoPath Laboratories | Tse C.,PhenoPath Laboratories | Rodriguez S.,PhenoPath Laboratories | Gown A.,PhenoPath Laboratories | Churg A.,University of British Columbia
American Journal of Surgical Pathology | Year: 2014

An atypical mesothelial proliferation along the pleural or peritoneal surface without evidence of invasive tumor poses a diagnostic challenge. Homozygous deletion of p16 (CDKN2A) by fluorescence in situ hybridization (FISH) has been shown to be a good marker of malignancy in mesothelial proliferations, but correlations of p16 status between atypical surface proliferations and underlying mesothelioma have not been described. We used p16 FISH to investigate 11 pleural and 7 peritoneal mesotheliomas that had both an invasive component and a separate surface mesothelial proliferation. In 5/11 pleural samples and 1/7 peritoneal samples, the invasive mesotheliomas showed homozygous deletion of p16 (all cases in excess of 90% of cells deleted); the surface proliferation in all 6 cases with deletion in the invasive tumor was also p16 deleted. Conversely, the 12 tumors that did not show p16 deletion in the invasive compartment also did not have deletion in the surface component. We conclude that (1) surface mesothelial proliferations near invasive mesotheliomas show the same pattern of p16 by FISH as the underlying tumor and may represent in situ disease or growth of the underlying mesothelioma along the serosal surface; (2) p16 deletion in mesothelial surface proliferations is strongly associated with p16 deletion in underlying mesotheliomas, and biopsies consisting of pure surface mesothelial proliferations that are p16 deleted allow a diagnosis of mesothelioma without an additional biopsy if there is clinical (thoracosopic/laparoscopic) or radiologic evidence of diffuse pleural or peritoneal tumor; (3) however, the absence of p16 deletion in surface proliferations does not rule out underlying invasive mesothelioma. © 2014 by Lippincott Williams and Wilkins.

Hwang H.C.,PhenoPath Laboratories | Sheffield B.S.,Vancouver General Hospital | Sheffield B.S.,University of British Columbia | Rodriguez S.,PhenoPath Laboratories | And 5 more authors.
American Journal of Surgical Pathology | Year: 2016

The diagnosis of malignant mesothelioma in effusion cytology specimens is controversial. BAP1 immunohistochemistry and p16 fluorescence in situ hybridization (FISH) have recently been reported as reliable markers of malignancy in biopsies of mesothelioma. To determine whether these markers, singly or in combination, might also be useful in effusion cytology specimens, we examined 15 biopsies of epithelial mesotheliomas and 3 benign mesothelial reactions and corresponding effusion cytology paraffin-embedded cell blocks. Four cytology specimens were too scanty for p16 FISH analysis but were interpretable for BAP1 immunohistochemistry. Overall, loss of BAP1 and/or deletion of p16 was seen in 11/11 (100%) of matched cytology and tissue biopsy specimens. BAP1 loss alone was seen in 10/15 (67%) biopsies and 10/15 (67%) cytology specimens. Homozygous deletion of p16 by FISH was found in 12/15 (80%) biopsy specimens and 8/11 (73%) evaluable cytology specimens. Seven of 15 (47%) biopsies and 5/11 (42%) cytology specimens showed loss of both markers. All mesothelioma biopsy/cytology pairs showed exactly the same pattern of BAP1 or p16 retention or loss in the biopsy and cytology specimens. The 2 peritoneal mesothelioma cases demonstrated loss of BAP1 but not p16. None of the benign mesothelial reactions or corresponding cytology specimens showed loss of either marker. We conclude that both BAP1 immunohistochemistry and p16 FISH analysis provide reliable markers of mesothelial malignancy in effusion cytology specimens, especially where the atypical mesothelial proliferation is well sampled. BAP1 is easier to interpret with scanty specimens. On the basis of small numbers of cases, use of both markers appears to increase sensitivity. © 2015 Wolters Kluwer Health, Inc.

Gown A.M.,PhenoPath Laboratories | Gown A.M.,University of British Columbia
Archives of Pathology and Laboratory Medicine | Year: 2016

Context: There are a number of critical factors that can lead to incorrect results if the diagnostic pathologist performing immunohistochemistry is unaware of, or not vigilant about, their influence. Objective: To highlight 3 arenas in which errors may be introduced. Data Sources: For choosing the correct primary antibody, selection of the most appropriate antibodies for a given clinical application can be aided by obtaining information from the vendor; however, this can yield incomplete information. There are a number of online databases that have comparisons of antibodies from different vendors, particularly with respect to their use and properties. Reading the published literature can assist in this process, particularly with respect to determining antibody sensitivity and specificity, but it is a daunting task to keep up with all of the immunohistochemistry-related papers published. Finally, Web sites of a number of quality assurance organizations are accessible and can provide a wealth of information comparing the "real world" performance characteristics of different antibodies to the same target protein. False-positive signals can result from a number of factors, including the use of inappropriately high antibody concentration, and "pseudospecific" signal that is in the wrong compartment of the cell. Falsenegative signal can result from factors such as use of a nonoptimized epitope retrieval method. It is critical that epitope retrieval methods be optimized for each antibody employed in the laboratory. Conclusions: By paying attention to these potential problems, the "black box" of diagnostic immunohistochemistry can be made more transparent.

Sheffield B.S.,Vancouver General Hospital | Hwang H.C.,PhenoPath Laboratories | Lee A.F.,Childrens and Womens Hospital of British Columbia | Thompson K.,PhenoPath Laboratories | And 4 more authors.
American Journal of Surgical Pathology | Year: 2015

A variety of immunohistochemical (IHC) stains have been proposed to mark either benign or malignant mesothelial proliferations. Loss of the p16 tumor suppressor (CDKN2A), through homozygous deletions of 9p21, is a good marker of mesotheliomas but lacks sensitivity. Recent reports indicate that some mesotheliomas are associated with loss of BRCA-associated protein 1 (BAP1) expression. Here we investigate BAP1 and p16 as potential markers of malignancy and compare test characteristics with previously proposed markers using a well-characterized tissue microarray. BAP1 protein expression was interrogated by IHC. The p16 locus was examined by fluorescence in situ hybridization (FISH) directed toward chromosome 9p21. Loss of BAP1 was identified in 7/26 mesotheliomas and 0/49 benign proliferations. Loss of p16 was identified in 14/27 mesotheliomas and 0/40 benign proliferations, yielding 100% specificity and positive predictive value for each marker. Together, BAP1 IHC and p16 FISH were 58% sensitive for detecting malignancy. Various combinations of p53, EMA, IMP3, and GLUT1 showed reasonably high specificity (96% to 98%) but poor to extremely poor sensitivity. Combined BAP1 IHC/p16 FISH testing is a highly specific method of diagnosing malignant mesotheliomas when the question is whether a mesothelial proliferation is benign or malignant and is particularly useful when tissue invasion by mesothelial cells cannot be demonstrated. However, combined BAP1/p16 FISH testing is not highly sensitive, and negative results do not rule out a mesothelioma. The test characteristics of previously proposed markers EMA, p53, GLUT1, IMP3 suggest that, even in combination, these markers are not useful tools in this clinical setting. © 2015 Wolters Kluwer Health, Inc. All rights reserved.

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