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BackgroundHuman acellular dermal matrices (HADMs) are used in a variety of settings. AlloMax is a new HADM currently being used for breast reconstruction and hernia repair. We compared the in vivo tissue integration of AlloMax to AlloDerm, a well-studied HADM, in rats.MethodsWe implanted AlloDerm and AlloMax patches into subcutaneous pockets on the backs of 32 male Sprague-Dawley rats. The animals were killed after either 4 or 8 weeks, and the patches were recovered and stained for histopathologic analyses. Microscopic end points included patch thickness, vascularization, tissue in-growth, fibroblast proliferation, and inflammation.ResultsAll animals completed the study without complications or infection. There were no significant differences in graft thicknesses at 4 and 8 weeks. Microscopically, at 4 weeks, AlloDerm sections had significantly more microvessels than AlloMax (P = 0.02). This disparity increased by 8 weeks (P < 0.01). Similarly, we found greater tissue in-growth and fibroblast proliferation in AlloDerm than AlloMax sections at 4 (P < 0.01) and at 8 (P < 0.01) weeks. Inflammatory infiltrates consisted of lymphocytes, histiocytes, eosinophils, and plasma cells. Deep graft infiltration by predominately lymphocytic inflammatory cells was significantly higher in AlloDerm than AlloMax grafts at 4 (P = 0.01) and 8 (P = 0.02) weeks. Graft necrosis was uncommon, but marginal fibrosis was similar in both.ConclusionsAlloDerm grafts had greater neovascularization, tissue infiltration, fibroblast proliferation, and inflammatory reaction than AlloMax grafts when placed subcutaneously in rats. AlloDerm may be better incorporated than AlloMax when placed in vivo.

Objectives Our aim was to explore the performance of TRPS1 as an immunohistochemical diagnostic marker; find the optimal conditions for its use in breast carcinomas, especially triple-negative breast cancers (TNBCs); and compare its results in carcinomas of a select few organ sites, with an emphasis on gynecologic tumors. Methods Tissue microarrays from breast carcinomas (n = 197), endometrial adenocarcinomas (n = 69), ovarian tumors (n = 250), vulvar squamous cell carcinomas (n = 97), pancreatic ductal adenocarcinomas (n = 20), and gastric adenocarcinomas (n = 12) were stained with TRPS1 using 2 different conditions (protocol 1: high pH; protocol 2: low pH). Breast carcinomas consisted of hormone receptor (HR)–positive/ERBB2 (formerly HER2 or HER2/neu)–negative (n = 53) samples, HR-positive/ERBB2-positive (n = 6) samples, and TNBCs (n = 138). Results Comparing TRPS1 results in breast carcinomas vs tumors from other organ sites, the sensitivity of TRPS1 was 91% and 87%, respectively, while the specificity was 66% and 74% for protocol 1 and 2, respectively. For TNBCs vs gynecologic tumors, the sensitivity of TRPS1 was 89% and 85%, respectively, while the specificity was 65% and 73%, respectively. Conclusions TRPS1 stains approximately 90% of breast carcinomas but also up to 71% of endometrial carcinomas, albeit with a weaker median expression. Our data show that although TRPS1 is a highly sensitive marker for TNBCs, it is not as highly specific as previously reported. [ABSTRACT FROM AUTHOR]

Mural nodules are rarely identified in cystic ovarian neoplasms, and have been categorized into sarcoma-like, sarcomatous, and anaplastic carcinomatous types. Most reports of these mural nodules have been described in mucinous ovarian tumors. In this case report, we describe an ovarian serous borderline tumor with mural nodules composed of high-grade carcinoma with anaplastic features and necrosis, including the morphologic features, immunoprofile, and results of tumor DNA sequencing. Omental involvement was also identified. Recognition of this phenomenon in serous tumors is important, so that thickened areas of cyst wall in ovarian serous tumors will be thoroughly examined. [ABSTRACT FROM AUTHOR]

Aims: Pathologists provide expert tissue assessment of breast cancer, yet their value to guide the appropriate use of breast cancer gene expression profile tests (GEPT) is underutilised. The specific aims of this study are to report morpho‐immunohistological characteristics of breast tumours with Oncotype DX® (ODx) recurrence scores (RS) of 10 or fewer (ultra‐low risk) and 25 or fewer (low risk) in order to determine if pathologists can identify prospectively patient tumours that do not require ODx testing. Methods and results: Oncotype DX® cases with RS < 10 from 2005 to 2010 comprised 441 of 2594 (17%) of clinical cases; this cohort had 5 years’ follow‐up and was treated with endocrine therapy alone. Tumours were analysed for tumour type, Nottingham grade, mitosis score (MS) semi‐quantitative (H‐score) hormone receptor content and Magee equation 3. Knowledge derived from this data set was used to develop algorithms in order to identify prospectively tumours with RS of 10 or fewer or 25 or fewer. Thirty‐four per cent of tumours were low‐grade special types, while the remainder were enriched with high hormone receptor content with MS of 1. These algorithmic selection criteria identified correctly all patient cases below the chemotherapy cut‐point, i.e. RS < 25, indicating that these oncotype test orders were an unnecessary cost. Conclusions: This unique study demonstrates that (i) pathologists add great value to triage breast cancer for GEPT; and (ii) can identify prospectively low‐grade tumour biology with high sensitivity and high specificity for those cases which do not require chemotherapy (RS < 25) using MS and hormone receptor content. [ABSTRACT FROM AUTHOR]

Purpose: Inspired by the hypothesis that heterogeneity in the biology of breast cancers at the cellular level may account for cognitive dysfunction symptom variability in survivors, the current study explored relationships between host single-nucleotide polymorphisms (SNPs) in 25 breast cancer-related candidate genes (AURKA, BAG1, BCL2, BIRC5, CCNB1, CD68, CENPA, CMC2, CTSL2, DIAPH3, ERBB2, ESR1, GRB7, GSTM1, MELK, MKI67, MMP11, MYBL2, NDC80, ORC6, PGR, RACGAP1, RFC4, RRM2, and SCUBE2), identified from clinically relevant prognostic multigene-expression profiles for breast cancer, and pretreatment cognitive performance. Patients and methods: The sample (n=220) was comprised of 138 postmenopausal women newly diagnosed with early stage breast cancer and 82 postmenopausal age- and educationmatched healthy controls without breast cancer. Cognitive performance was assessed after primary surgery but prior to initiation of adjuvant chemotherapy and/or hormonal therapy using a comprehensive battery of neuropsychological tests encompassing eight cognitive function composite domains: attention, concentration, executive function, mental flexibility, psychomotor speed, verbal memory, visual memory, and visual working memory. In total, 131 SNPs were included in the analysis. Standard and robust multiple linear regression modeling was used to examine relationships between each domain and the presence or absence of one or more minor alleles for each SNP. Genetic risk/protection scores (GRSs) were calculated for each domain to evaluate the collective effect of possession of multiple risk/protective alleles. Results: With the exception of CMC2, MMP11, and RACGAP1, significant (P<0.05) SNP main effect and/or SNP by future prescribed treatment group interactions were observed for every gene between at least one domain and one or more SNPs. All GRSs were found to be significantly (P<0.001) associated with each respective domain score. Conclusion: Associations between host SNPs and computed GRSs and variability in pretreatment cognitive function performance support the study hypothesis, and warrant further investigations to identify biomarkers for breast cancer-related cognitive dysfunction. [ABSTRACT FROM AUTHOR]