Results 71 to 80 of about 77,245 (318)

Visualizing and exploring patterns of large mutational events with SigProfilerMatrixGenerator

open access: yesBMC Genomics, 2023
Background All cancers harbor somatic mutations in their genomes. In principle, mutations affecting between one and fifty base pairs are generally classified as small mutational events.
Azhar Khandekar   +8 more
doaj   +1 more source

The Caenorhabditis elegans DPF‐3 and human DPP4 have tripeptidyl peptidase activity

open access: yesFEBS Letters, EarlyView.
The dipeptidyl peptidase IV (DPPIV) family comprises serine proteases classically defined by their ability to remove dipeptides from the N‐termini of substrates, a feature that gave the family its name. Here, we report the discovery of a previously unrecognized tripeptidyl peptidase activity in DPPIV family members from two different species.
Aditya Trivedi, Rajani Kanth Gudipati
wiley   +1 more source

Pan-squamous genomic profiling stratified by anatomic tumor site and viral association [PDF]

open access: yes, 2018
Background: Squamous cell carcinomas (SCC) have diverse anatomic etiologies but may share common genomic biomarkers. We profiled 7,871 unique SCCs across nine anatomic sites to investigate commonality in genomic alterations (GA), tumor mutational burden (
Albacker, L. A.   +10 more
core   +1 more source

The newfound relationship between extrachromosomal DNAs and excised signal circles

open access: yesFEBS Letters, EarlyView.
Extrachromosomal DNAs (ecDNAs) contribute to the progression of many human cancers. In addition, circular DNA by‐products of V(D)J recombination, excised signal circles (ESCs), have roles in cancer progression but have largely been overlooked. In this Review, we explore the roles of ecDNAs and ESCs in cancer development, and highlight why these ...
Dylan Casey, Zeqian Gao, Joan Boyes
wiley   +1 more source

Using CRISPR to understand how cancer mutations happen

open access: yesCommunications Biology, 2021
Somatic mutations in cancer genomes can be caused by many different mutational processes, each of which produce distinctive patterns termed “mutational signatures”.
Eve H. Rogers
doaj   +1 more source

Somatic mutations render human exome and pathogen DNA more similar

open access: yes, 2019
Immunotherapy has recently shown important clinical successes in a substantial number of oncology indications. Additionally, the tumor somatic mutation load has been shown to associate with response to these therapeutic agents, and specific mutational ...
Cristescu, Razvan   +4 more
core   +1 more source

Interpreting the dependence of mutation rates on age and time [PDF]

open access: yes, 2015
Mutations can arise from the chance misincorporation of nucleotides during DNA replication or from DNA lesions that are not repaired correctly. We introduce a model that relates the source of mutations to their accumulation with cell divisions, providing
Gao, Ziyue   +3 more
core   +5 more sources

Investigating the cell of origin and novel molecular targets in Merkel cell carcinoma: a historic misnomer

open access: yesMolecular Oncology, EarlyView.
This study indicates that Merkel cell carcinoma (MCC) does not originate from Merkel cells, and identifies gene, protein & cellular expression of immune‐linked and neuroendocrine markers in primary and metastatic Merkel cell carcinoma (MCC) tumor samples, linked to Merkel cell polyomavirus (MCPyV) status, with enrichment of B‐cell and other immune cell
Richie Jeremian   +10 more
wiley   +1 more source

Integrated genomic and proteomic profiling reveals insights into chemoradiation resistance in cervical cancer

open access: yesMolecular Oncology, EarlyView.
A comprehensive genomic and proteomic analysis of cervical cancer revealed STK11 and STX3 as a potential biomarkers of chemoradiation resistance. Our study demonstrated EGFR as a therapeutic target, paving the way for precision strategies to overcome treatment failure and the DNA repair pathway as a critical mechanism of resistance.
Janani Sambath   +13 more
wiley   +1 more source

YAP1::TFE3 mediates endothelial‐to‐mesenchymal plasticity in epithelioid hemangioendothelioma

open access: yesMolecular Oncology, EarlyView.
The YAP1::TFE3 fusion protein drives endothelial‐to‐mesenchymal transition (EndMT) plasticity, resulting in the loss of endothelial characteristics and gain of mesenchymal‐like properties, including resistance to anoikis, increased migratory capacity, and loss of contact growth inhibition in endothelial cells.
Ant Murphy   +9 more
wiley   +1 more source

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