Pms2 clone epr3947

Manufactured by Roche

Sourced in Switzerland, United States

PMS2 (clone EPR3947) is an antibody used in laboratory applications for the detection of the PMS2 protein. PMS2 is a DNA mismatch repair protein that plays a role in the repair of DNA replication errors. This antibody can be used in various immunoassay techniques, such as immunohistochemistry, to identify the presence and localization of the PMS2 protein within biological samples.

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Lab products found in correlation

Msh2 clone g219 1129, by Roche (4 mentions) Msh6 clone 44, by Roche (4 mentions) Anti mlh1 clone g168 728, by Roche (3 mentions) Arid1a clone d2a8u, by Roche (3 mentions) Benchmark xt platform, by Roche (3 mentions) Mlh1 clone m1, by Roche (1 mentions) Benchmark autostainer, by Roche (1 mentions) Pan keratin, by Roche (1 mentions)

Spelling variants of this product

Clone EPR3947 (6 citations) EPR3947 (6 citations) Anti-PMS2 rabbit mAb clone EPR3947 (2 citations)

6 protocols using pms2 clone epr3947

Evaluating Mismatch Repair and ARID1A Deficiency

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Immunohistochemical staining was performed on TMAs with the Ventana Benchmark XT platform. The following panel of antibodies was used: anti-MLH1 (clone G168-728, Roche), -PMS2 (clone EPR3947, Roche), -MSH2 (clone G219-1129, Roche), -MSH6 (clone 44, Roche), and -ARID1A (clone D2A8U, Roche). According to the published criteria of abnormal expression of MMR and ARID1A [15 , 23 ], both markers were interpreted as loss of expression, whereas no tumor cells were stained.
We chose the recommended guidelines that the immunohistochemistry results be reported in a binary manner, either positive (indicating intact mismatch repair, showing intact nuclear expression in tumor cells) or negative (indicating deficient mismatch repair, showing nuclear expression completely lost in tumor cells) [24 , 25 ] Nuclei of lymphocytes and ovarian stromal cells served as positive internal controls. All staining results were reviewed by the above 2 pathologists. Because immunohistochemical examination was performed using a tissue microarray, when deficient mismatch repair (dMMR) was observed, the immunohistochemistry procedure was repeated on whole-slide sections to avoid heterogeneous expression, such as for MSH6 [26 ]. Ultimately, MMR protein restaining was performed in 51 instances involving 27 of 176 cases; ARID1A restaining was performed in 15 instances involving 3 cases of dMMR among 135 cases.

Ge H., Xiao Y., Qin G., Gu Y., Cai X., Jiang W., Tu X., Yang W, & Bi R. (2021). Mismatch repair deficiency is associated with specific morphologic features and frequent loss of ARID1A expression in ovarian clear cell carcinoma. Diagnostic Pathology, 16, 12.

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Mismatch Repair Protein Immunohistochemistry

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Immunohistochemical staining was performed on TMAs with the Ventana Benchmark XT platform. The following panel of antibodies was used: anti-MLH1 (clone G168-728, Roche), -PMS2 (clone EPR3947, Roche), -MSH2 (clone G219-1129, Roche), -MSH6 (clone 44, Roche), and -ARID1A (clone D2A8U, Roche).
According to the published criteria of abnormal expression of MMR and ARID1A [15] [23], both markers were interpreted as loss of expression, whereas no tumor cells were stained.
We chose the recommended guidelines that the immunohistochemistry results be reported in a binary manner, either positive (indicating intact mismatch repair, showing intact nuclear expression in tumor cells) or negative (indicating de cient mismatch repair, showing nuclear expression completely lost in tumor cells) [ Nuclei of lymphocytes and ovarian stromal cells served as positive internal controls. All staining results were reviewed by the above 2 pathologists. Because immunohistochemical examination was performed using a tissue microarray, when de cient mismatch repair (dMMR) was observed, the immunohistochemistry procedure was repeated on whole-slide sections to avoid heterogeneous expression, such as for MSH6 [26] . Ultimately, MMR protein restaining was performed in 51 instances involving 27 of 176 cases; ARID1A restaining was performed in 15 instances involving 3 cases of dMMR among 135 cases.

Ge H., Xiao Y., Qin G., Gu Y., Xu C., Jiang W., Tu X., Yang W., & Bi R. (2021). Mismatch repair deficiency is associated with specific morphologic features and frequent loss of ARID1A expression in ovarian clear cell carcinoma.

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Immunohistochemistry for MMR and ARID1A

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Immunohistochemical staining was performed on TMAs with the Ventana Benchmark XT platform. The following panel of antibodies was used: anti-MLH1 (clone G168-728, Roche), -PMS2 (clone EPR3947, Roche), -MSH2 (clone G219-1129, Roche), -MSH6 (clone 44, Roche), and -ARID1A (clone D2A8U, Roche). As the published criteria of abnormal expression of MMR and ARID1A [15] [23], both markers were interpreted as loss of expression, whereas any tumor cells not staining.
Nuclei of lymphocytes and ovarian stromal cells served as positive internal controls. All staining results were reviewed by the above 2 pathologists. Because immunohistochemical examination was performed using a tissue microarray, when negative staining was observed, the immunohistochemistry procedure was repeated on whole-slide sections to avoid heterogeneous expression, such as for MSH6 [24] . Ultimately, MMR protein restaining was performed in 51 instances involving 27 of 176 cases; ARID1A restaining was performed in 15 instances involving 3 cases of dMMR among 135 cases.

Ge H., Xiao Y., Qin G., Gu Y., Cai X., Jiang W., Tu X., Yang W., & Bi R. (2020). Mismatch repair deficiency is associated with specific morphologic features and frequent loss of ARID1A expression in ovarian clear cell carcinoma.

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Immunohistochemical Analysis of DNA Mismatch Repair Proteins

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The formalin-fixed paraffin-embedded (FFPE) tumor samples were stained with MLH1, MSH2, MSH6, and PMS2 proteins. The loss of MMR proteins was defined as the absence of staining in the nuclei of tumor cells while the nuclei of lymphocytes and adjacent normal colonic epithelial cells were positive. MLH1 (clone M1, prediluted, Ventana, Roche, Basel, Switzerland), MSH2 (clone G219-1129, prediluted, Ventana), MSH6 (clone 44, prediluted, Ventana), and PMS2 (clone EPR3947, prediluted, Ventana) monoclonal primary antibodies were used.

Zhang Y., Wu Z., Zhang B., Hu H., Zhang J., Chen Y., Ding M., Cao Y, & Deng Y. (2022). Prognostic impact of high-risk factors and KRAS mutation in patients with stage II deficient mismatch repair colon cancer: a retrospective cohort study. Annals of Translational Medicine, 10(12), 702.

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Immunohistochemistry for MMR Protein Detection

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Immunohistochemical analysis for MMR proteins was used for the detection of MMR deficiency, and was performed on formalin-fixed paraffin-embedded tissue using 4-μm whole tissue sections. mAbs were used against MutS homolog 2, MSH2 (clone G219-1129, prediluted; Ventana), MutL Homolog 1, MLH1 (clone M1, prediluted; Ventana), MutS homolog 6, MSH6 (clone 44, prediluted; Ventana), and Postmeiotic Segregation Increased 2, PMS2 (clone EPR3947, prediluted; Ventana), following standard protocols recommended by the manufacturers. Control tissues included benign colorectal tissue and colorectal tumors with known Lynch syndrome by genetic analysis and a corresponding loss of MMR protein expression. Positive internal controls included nuclear staining in stromal or inflammatory cells. All stains were reviewed by a pathologist (C. Sigel). Tumors with positive nuclear reactivity were considered "normal," whereas complete absence of nuclear reactivity was considered "abnormal." Testing for MMR protein expression was not repeated for patients with results on record. Molecular analysis was not performed to correlate MMR abnormalities with genetic status but prior molecular testing results were noted if on record.

Sigel C., Cavalcanti M.S., Daniel T., Vakiani E., Shia J, & Sigel K. (2016). Clinicopathologic Features of Colorectal Carcinoma in HIV-Positive Patients. Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology, 25(7), 1098-1104.

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Immunohistochemical Profiling of Tumor Samples

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Immunohistochemistry was performed on a BenchMark autostainer (Ventana Medical Systems, Tucson, Arizona, USA) according to the manufacturer's protocol. The following monoclonal antibodies were used in the study: MT1-MMP (catalytic domain, clone 114-6G6), 1 : 100, mouse (from Merck Millipore, Darmstadt, Germany); Pan-Keratin (clone AE1/AE3/PCK26), mouse; MLH1 (clone G168–728), mouse; MSH2 (clone G219–1129), mouse; MSH6 (clone 44), mouse; PMS-2 (clone EPR3947), rabbit (prediluted; obtained from Ventana Medical Systems, Tucson, Arizona, USA). For MT1-MMP, cases with weak to strong cytoplasmic and/or membranous immunostaining at the leading edge of the tumor were classified as MT1-MMP positive (Figure 1). Loss of MMR protein expression required lack of nuclear immunostaining for MLH1, MSH2, MSH6, or PMS-2 in tumor cells with retained positivity in nonneoplastic epithelium, stromal and immune cells [27 (link)].

Arndt A., Kraft K., Wardelmann E, & Steinestel K. (2015). Lack of Association between Membrane-Type 1 Matrix Metalloproteinase Expression and Clinically Relevant Molecular or Morphologic Tumor Characteristics at the Leading Edge of Invasive Colorectal Carcinoma. BioMed Research International, 2015, 185404.

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