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Polyguanine microsatellites are robust replication clocks in cancer.
Nat Genet
February 2025
Department of Medicine, Division of Hematology/Oncology, Vagelos College of Physicians and Surgeons, Columbia University Irving Medical Center, New York, NY, USA.
[Poly-G for tumor matched samples chronicles the evolution of human colorectal cancer].
Zhonghua Zhong Liu Za Zhi
May 2023
Department of General Surgery, Tianjin Medical University General Hospital, Tianjin 300052, China.
To analyze poly-guanine (poly-G) genotypes and construct the phylogenetic tree of colorectal cancer (CRC) and provide an efficient and convenient method for the study of intra-tumor heterogeneity and tumor metastasis pathway. The clinicopathological information of patients with primary colorectal cancer resection with regional lymph node metastases were retrospectively collected in the Department of General Surgery, General Hospital of Tianjin Medical University from January 2017 to December 2017. The paraffin sections of the paired tumor samples were performed consecutively, and multi-region microdissection was performed after histogene staining.
View Article and Find Full Text PDFHypermutable DNA chronicles the evolution of human colon cancer.
Proc Natl Acad Sci U S A
May 2014
Edwin L. Steele Laboratory for Tumor Biology, Department of Radiation Oncology, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114.
Intratumor genetic heterogeneity reflects the evolutionary history of a cancer and is thought to influence treatment outcomes. Here we report that a simple PCR-based assay interrogating somatic variation in hypermutable polyguanine (poly-G) repeats can provide a rapid and reliable assessment of mitotic history and clonal architecture in human cancer. We use poly-G repeat genotyping to study the evolution of colon carcinoma.
View Article and Find Full Text PDFChemotherapy of MMR-deficient colorectal cancer.
Fam Cancer
June 2013
Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Ontario, Canada.
Colorectal cancer (CRC) continues to rank as the third most common cancer in Western society and the second leading cause of cancer death in North America. There are at least three distinct, and relatively discreet, molecular pathways associated with this disease: chromosomal instability (CIN), microsatellite instability (MSI) and the cytosine polyguanine island methylator phenotype. Defects in the DNA mismatch repair system (MMR) account for the MSI phenotype and genotype of about 15 % of CRC.
View Article and Find Full Text PDFBAX frameshift mutations in cell lines derived from human haemopoietic malignancies are associated with resistance to apoptosis and microsatellite instability.
Oncogene
April 1998
Ludwig Institute for Cancer Research, Imperial College School of Medicine at St Mary's, London.
Bax suppresses tumorigenesis in a mouse model system and Bax-deficient mice exhibit lymphoid hyperplasia suggesting that BAX functions as a tumour suppressor in human haemopoietic cells. We examined BAX expression in 20 cell lines derived from human haemopoietic malignancies and consistent with a potential tumour suppressor function, identified two cell lines, DG75 (a Burkitt lymphoma cell line) and Jurkat (a T-cell leukaemia line), which lacked detectable BAX expression. Apoptosis of DG75 cells induced by low serum or ionomycin was significantly delayed relative to similar Burkitt lymphoma cell lines with normal BAX levels.
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