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This article was published in the following journal.
Name: Journal of clinical oncology : official journal of the American Society of Clinical Oncology
Despite the tissue-agnostic approval of pembrolizumab in mismatch repair deficient (MMRD) solid tumors, important unanswered questions remain about the role of immune checkpoint blockade in mismatch r...
The National Cancer Institute Molecular Analysis for Therapy Choice (NCI-MATCH) trial, the largest national precision oncology study to date (> 1,100 sites) of patients with relapsed or refractory mal...
Alterations to mismatch repair (MMR) pathways are a known cause of cancer, particularly colorectal and endometrial carcinomas. Recently, checkpoint inhibitors have been approved for use in MMR-deficie...
Genomes of tumors that are deficient in DNA mismatch repair (dMMR) have high microsatellite instability (MSI-H) and harbor hundreds to thousands of somatic mutations that encode potential neoantigens....
Lynch syndrome (LS) and constitutional mismatch repair deficiency (CMMRD) are hereditary cancer syndromes associated with mismatch repair (MMR) deficiency. Tumours show microsatellite instability (MSI...
This phase II trial studies how well pembrolizumab works before surgery in treating patients with mismatch repair deficient solid cancers that have spread to nearby tissue or lymph nodes (...
Single Center, open label, Phase I-II trial designed to test the safety and efficacy of the combination of Ataluren and Pembrolizumab for the treatment of metastatic mismatch repair defici...
A Study of Nivolumab, Nivolumab Plus Ipilimumab, or Investigator's Choice Chemotherapy for the Treatment of Patients With Deficient Mismatch Repair (dMMR)/Microsatellite Instability High (MSI-H) Metastatic Colorectal Cancer (mCRC)
The main purpose of this study is to compare the clinical benefit, as measured by Progression-Free Survival (PFS), Objective Response Rate (ORR), and Overall Survival (OS), achieved by niv...
This randomized phase III trial studies combination chemotherapy and atezolizumab to see how well it works compared with combination chemotherapy alone in treating patients with stage III ...
This phase II trial studies how well pembrolizumab works with capecitabine and radiation therapy in treating patients with mismatch repair deficient and Epstein-Barr virus positive gastric...
Eukaryotic homolog of the bacterial MutL DNA MISMATCH REPAIR protein. It heterodimerizes with MISMATCH REPAIR ENDONUCLEASE PMS2 to form MutL alpha, which is recruited to DNA mismatch sites by the MUTS DNA MISMATCH-BINDING PROTEIN. Mutations in the human MLH1 gene are associated with COLORECTAL NEOPLASMS, HEREDITARY NONPOLYPOSIS.
A MutL protein and component of the DNA MISMATCH REPAIR system. Its ENDONUCLEASE activity introduces SINGLE-STRAND DNA BREAKS which create entry points for EXO1 exonuclease to remove the strand containing the mismatch. It may also function in DNA DAMAGE signaling.
DNA repair proteins that include the bacterial MutL protein and its eukaryotic homologs. They consist of a conserved N-terminal region with weak ATPase activity, an endonuclease motif, and a C-terminal domain that forms MutL homodimers or heterodimers between MLH1 and the PMS1, MISMATCH REPAIR ENDONUCLEASE PMS2; or MLH3 proteins. These complexes function in DNA repair pathways, primarily DNA MISMATCH REPAIR, where MutL/MLH1 and the MUTS DNA MISMATCH-BINDING PROTEIN are targeted to damaged DNA.
DNA repair proteins that include the bacterial MutS DNA mismatch-binding protein and its eukaryotic homologs that function in DNA MISMATCH REPAIR and recombination of DNA during MEIOSIS. MutS has a conserved mismatch recognition domain characterized by GxFxE, or similar AMINO ACID MOTIFS that also occur in eukaryotic homologs such as MSH1, MSH6, and MSH8. All MutS proteins also contain a highly-conserved ATP-binding domain and most have weak ATPase activity.
A DNA repair pathway involved in correction of errors introduced during DNA replication when an incorrect base, which cannot form hydrogen bonds with the corresponding base in the parent strand, is incorporated into the daughter strand. Excinucleases recognize the BASE PAIR MISMATCH and cause a segment of polynucleotide chain to be excised from the daughter strand, thereby removing the mismatched base. (from Oxford Dictionary of Biochemistry and Molecular Biology, 2001)
Cancer is not just one disease but many diseases. There are more than 100 different types of cancer. Most cancers are named for the organ or type of cell in which they start - for example, cancer that begins in the colon is called colon cancer; cancer th...