Log In Sign up
The largest database of trusted experimental protocols

Pms2 clone a16 4

Manufactured by BD
Visit Supplier
Sourced in Japan, United States

The PMS2 (clone A16-4) is a laboratory equipment product manufactured by BD. It is a monoclonal antibody that is used in immunohistochemical and flow cytometric applications. The core function of this product is to detect the presence of the PMS2 protein, which is involved in DNA mismatch repair processes.

Automatically generated - may contain errors

Lab products found in correlation

Mlh1 clone g168 728, by BD (5 mentions) Msh6 clone epr3945, by GeneTex (2 mentions) Msh6 clone grbp p1 2 d4, by Bio-Rad (2 mentions) Msh6 clone 44, by BD (1 mentions) Benchmark xt, by Roche (1 mentions) Anti β catenin antibody, by Cell Marque (1 mentions) Msh6 clone 44, by Roche (1 mentions) Cell conditioning solution cc1, by Roche (1 mentions) Optiview dab detection kit, by Roche (1 mentions) Autostainer, by Agilent Technologies (1 mentions) Msh6 clone 44 msh6, by BD (1 mentions)

7 protocols using pms2 clone a16 4

1

Immunohistochemical Assessment of Mismatch Repair Proteins

Check if the same lab product or an alternative is used in the 5 most similar protocols
IHC for the assessment of mismatch repair protein expression was conducted by using the following primary monoclonal antibodies: mouse antihuman MLH1 (clone ES05, 1:100; Leica Biosystems, Newcastle, UK), mouse antihuman MSH2 (clone G219–1129, 1:500; BD Biosciences, Tokyo, Japan), MSH6 (clone EPR3945, 1:200; GeneTex, Tokyo, Japan), and PMS2 (clone A16–4, 1:100; BD Biosciences, Tokyo, Japan). The loss of a mismatch repair protein was defined as the absence of nuclear expression in the tumor cells with a positive nuclear expression of the lymphocytes or the epithelium. Three tissue cores per tumor were studied for each protein expression analysis. We considered a tumor to have lost its protein expression when all the three tissue cores did not express the protein. Deficient mismatch repair protein (dMMR) was defined as the expression loss of a tumor’s mismatch repair protein. Two pathologists (Y.S. and K.I.) independently evaluated the protein expression in this case.
Shigematsu Y., Inamura K., Yamamoto N., Mise Y., Saiura A., Ishikawa Y., Takahashi S, & Kanda H. (2018). Impact of CDX2 expression status on the survival of patients after curative resection for colorectal cancer liver metastasis. BMC Cancer, 18, 980.
+ Open protocol
+ Expand
2

Immunohistochemical Analysis of MMR Proteins

Check if the same lab product or an alternative is used in the 5 most similar protocols
Immunoperoxidase staining was performed on formalin-fixed tissue. Immunohistochemistry with MMR protein has performed by using the standard streptavidin–biotin–peroxidase procedure. Primary monoclonal antibodies against MLH1 (clone G168-728; BD PharMingen, San Diego, CA, USA; 1:200), MSH2 (clone FE11; Oncogene Research Products, Cambridge, MA, USA; 1:100), MSH6 (clone 44; BD Transduction, San Jose, CA, USA; 1:200), and PMS2 (clone A16-4, BD Biosciences, San Jose, CA, USA; 1:10) were applied to 5-μm-thick formalin-fixed, paraffin-embedded whole tumor sections.
Wu B., Ji W., Liang S., Ling C., You Y., Xu L., Zhong M.E., Xiao Y., Qiu H.Z., Lu J.Y, & Banerjee S. (2017). A novel heterozygous germline deletion in MSH2 gene in a five generation Chinese family with Lynch syndrome. Oncotarget, 8(33), 55194-55203.
+ Open protocol
+ Expand
3

Immunohistochemical Assessment of MMR Proteins

Check if the same lab product or an alternative is used in the 5 most similar protocols
MMR status was assessed by immunohistochemistry (IHC) for MLH1, MSH2, MSH6, and PMS2 proteins using standard protocols [21] (link). Primary monoclonal antibodies were MLH1 (clone G168–728, diluted 1:250; BD Biosciences Pharmingen, San Diego, CA), MSH2 (clone FE11, diluted 1:50; Oncogene Research Products, Cambridge, MA), MSH6 (clone GRBP.P1/2.D4, diluted 1:200; AbD Serotec, Raleigh, NC), and PMS2 (clone A16-4, diluted 1:200; BD Biosciences Pharmingen). Non-neoplastic colonic mucosa and colorectal tumors known to be deficient of MLH1, MSH2, MSH6, and PMS2 were used as external positive and negative controls, respectively. Tumors showing loss of expression in one or more of these proteins were considered dMMR, and those showing normal expression of the proteins were mismatch repair-proficient (pMMR).
Li L., Zhou W., Li Q., Li P., Yang L., Xia X., Yi X, & Wan D. (2020). Tumor-derived mutations in postoperative plasma of colorectal cancer with microsatellite instability. Translational Oncology, 14(1), 100945.
+ Open protocol
+ Expand
4

Immunohistochemical Analysis of MMR Proteins

Check if the same lab product or an alternative is used in the 5 most similar protocols
Analysis of IHC expression of MMR proteins was performed by using a
clinically validated standard streptavidin-biotin-peroxidase procedure. Primary
monoclonal antibodies used were MLH1 (clone G168–728, diluted 1:250; BD
Biosciences Pharmingen, San Diego, CA), MSH2 (clone FE11, diluted 1:50; Oncogene
Research Products, Cambridge, MA), MSH6 (clone GRBP.P1/2.D4, diluted 1:200; AbD
Serotec, Raleigh, NC), and PMS2 (clone A16–4, diluted 1:200; BD
Biosciences Pharmingen). Non-neoplastic colonic mucosa and colorectal tumors
known to be deficient of MLH1, MSH2, MSH6, and PMS2 were used as external
positive and negative controls, respectively. Retained expression of each
protein was defined by nuclear IHC reactivity of tumor cells, whereas loss of
expression for each protein was defined by the complete absence of nuclear IHC
reactivity of tumor cells. Tumors were MMR proficient if all four proteins were
expressed (retained) by IHC and MMR deficient (MMR-D) if any of the four
proteins was not expressed (lost) by IHC.
Middha S., Zhang L., Nafa K., Jayakumaran G., Wong D., Kim H.R., Sadowska J., Berger M.F., Delair D.F., Shia J., Stadler Z., Klimstra D.S., Ladanyi M., Zehir A, & Hechtman J.F. (2017). Reliable Pan-Cancer Microsatellite Instability Assessment by Using Targeted Next-Generation Sequencing Data. JCO Precision Oncology, 1, PO.17.00084.
+ Open protocol
+ Expand
5

Immunohistochemical Analysis of Mismatch Repair Proteins

Check if the same lab product or an alternative is used in the 5 most similar protocols
Four-micrometer-thick sections were cut from FFPE tumor blocks for IHC. IHC for β-catenin was performed on a BenchMark XT automated immunostainer (Ventana Medical Systems Inc., Tucson, AZ). Sections were incubated with anti-β-catenin antibody (Cell Marque, catalog #760-4242) at a concentration of 1.73 ug/mL. Antigen retrieval was performed with Cell Conditioning Solution (CC1, Ventana Medical Systems Inc.) for 24 hours, and primary antibody incubation was for 24 hours. Antigen detection was performed using the Optiview DAB Detection kit (Ventana Medical Systems Inc.). For analysis of mismatch repair protein expression, primary monoclonal antibodies against MLH1 (clone G168-728, diluted 1:250, BD PharMingen, San Diego, CA), MSH2 (clone FE11, diluted 1:50, Oncogene Research Products, La Jolla, CA), MSH6 (clone 44, ready to use, Ventana Medical Systems Inc.), and PMS2 (clone A16-4, diluted 1:200, BD PharMingen) were used. Non-neoplastic colonic mucosa and colorectal tumors known to be deficient of MLH1, MSH2, MSH6, and PMS2 were used as external positive and negative controls, respectively. Retained expression of each protein was defined by nuclear IHC reactivity of tumor cells, whereas loss of expression for each protein was defined by the total absence of nuclear staining.
Yaeger R., Chatila W.K., Lipsyc M.D., Hechtman J.F., Cercek A., Sanchez-Vega F., Jayakumaran G., Middha S., Zehir A., Donoghue M.T., You D., Viale A., Kemeny N., Segal N.H., Stadler Z.K., Varghese A.M., Kundra R., Gao J., Syed A., Hyman D.M., Vakiani E., Rosen N., Taylor B.S., Ladanyi M., Berger M.F., Solit D.B., Shia J., Saltz L, & Schultz N. (2018). Clinical sequencing defines the genomic landscape of metastatic colorectal cancer. Cancer cell, 33(1), 125-136.e3.
+ Open protocol
+ Expand
6

Tumor Mismatch Repair Status Assessment

Check if the same lab product or an alternative is used in the 5 most similar protocols
Tumor MMR status was determined by immunohistochemistry. A dMMR status was defined as the loss of tumor MSH2, MSH6, PMS2, or MLH1 protein expression. A proficient MMR status was defined by normal tumor MSH2, MSH6, PMS2, and MLH1 protein expression. Sections (5 μm thick) from paraffin‐embedded tissues were stained using an Autostainer (Dako, Glostrup, Denmark). Staining was carried out using antibodies to MSH2 (clone FE11, 1/200; Calbiochem, Tokyo, Japan), MSH6 (clone EPR3945, 1/200; GeneTex, Hsinchu City, Taiwan), PMS2 (clone A16‐4, 1/200; BD Biosciences Pharmingen, Tokyo, Japan) and MLH1 (clone G168‐278, 1/200; BD Biosciences Pharmingen). Mismatch repair protein loss was defined as abnormal (or absent) when nuclear staining of tumor cells was absent in the presence of positive staining in surrounding cells.
Sasaki Y., Akasu T., Saito N., Kojima H., Matsuda K., Nakamori S., Komori K., Amagai K., Yamaguchi T., Ohue M., Nagashima K, & Yamada Y. (2016). Prognostic and predictive value of extended RAS mutation and mismatch repair status in stage III colorectal cancer. Cancer Science, 107(7), 1006-1012.
+ Open protocol
+ Expand
7

Evaluating Mismatch Repair Protein Expression

Check if the same lab product or an alternative is used in the 5 most similar protocols
Immunohistochemical stains were performed to evaluate MLH1 (clone G168-728, BD Biosciences, San Jose, CA), PMS2 (clone A16-4, BD Biosciences, San Jose, CA), MSH2 (clone FE11, Calbiochem, Burlington, MA), and MSH6 (clone 44/MSH6, BD Biosciences, San Jose, CA) using standard techniques. Loss of staining was defined as complete loss of nuclear staining in all of the tumor nuclei with preserved staining of lymphocytes and/or nonneoplastic crypt epithelium. Decreased staining intensity of tumor cells was noted when the internal control showed strong nuclear staining.
Hissong E., Crowe E.P., Yantiss R.K, & Chen Y.T. (2018). Assessing colorectal cancer mismatch repair status in the modern era: a survey of current practices and re-evaluation of the role of microsatellite instability testing. Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc, 31(11).
+ Open protocol
+ Expand

About PubCompare

Our mission is to provide scientists with the largest repository of trustworthy protocols and intelligent analytical tools, thereby offering them extensive information to design robust protocols aimed at minimizing the risk of failures.

We believe that the most crucial aspect is to grant scientists access to a wide range of reliable sources and new useful tools that surpass human capabilities.

However, we trust in allowing scientists to determine how to construct their own protocols based on this information, as they are the experts in their field.

Ready to get started?

Sign up for free.
Registration takes 20 seconds.
Available from any computer
No download required

Sign up now

Revolutionizing how scientists
search and build protocols!