Results 131 to 140 of about 342,913 (296)

Genetics (Tumor Suppressor Genes) and Breast Cancer Risk Bibliography

open access: yes, 2003
Bibliography on tumor suppressor genes and breast cancer riskBibliography on tumor suppressor genes and breast cancer risk. Includes review articles, commentaries, studies on p53 and BRCA genes, commentaries on genetic testing, emerging tumor suppressor ...
Snedeker, Suzanne M.
core  

METHYLATION PROFILING OF TUMOR SUPPRESSOR GENES INVOLVED IN LUNG CANCER

open access: yes, 2012
The causes of cancer are due to mutations of key proteins involved in cell cycle regulation, DNA repair enzymes and in some cases inactivation of tumor suppressor genes leads to the growth of tumors.
Amajala, Krishna Chaitanya
core   +1 more source

Loss of IGF‐1R impairs DNA‐PKcs recruitment to chromatin leading to defective end‐joining

open access: yesMolecular Oncology, EarlyView.
IGF‐1R promotes radioresistance by facilitating DNA‐PKcs recruitment to chromatin, enabling non‐homologous end‐joining (NHEJ) repair of double‐strand breaks. Inhibition or loss of IGF‐1R disrupts this recruitment to damage sites, driving compensatory reliance on microhomology‐mediated end‐joining (MMEJ) repair.
Matthew O. Ellis   +3 more
wiley   +1 more source

USP29‐regulated noncanonical stabilization of the hypoxia‐inducible factor‐α in aggressive prostate cancer

open access: yesMolecular Oncology, EarlyView.
We identify USP29 as the only DUB mirroring CA9 expression, a marker of hypoxia and HIF pathway activation associated with PCA aggressiveness. USP29 stabilizes HIF‐1α and HIF‐2α via a noncanonical mechanism that is independent of PHD/pVHL activity yet relies on proteasomal regulation, establishing USP29 as a previously unrecognized regulator of hypoxic
Amelie S Schober   +16 more
wiley   +1 more source

Tumor suppressor genes in breast cancer [PDF]

open access: yes, 2017
Rak dojke je najčešća zloćudna bolest u žena u razvijenim zemljama svijeta. Iako mehanizam nastajanja raka dojke još uvijek nije u potpunosti razjašnjen, epidemiološka istraživanja utvrdila su razne rizične čimbenike za obolijevanje od ove bolesti, među ...
Franić, Ivana
core   +1 more source

Finding novel vulnerabilities of hypomorphic BRCA1 alleles

open access: yesMolecular Oncology, EarlyView.
Synthetic lethality screens performed to identify novel vulnerabilities often model complete gene loss, thereby overlooking patient‐derived hypomorphic mutations. In this study, we have performed genome‐wide CRISPR screens on BRCA1 hypomorphic mutations, showing BRCA1I26A behaves like wild‐type, while BRCA1R1699Q mimics deficiency. Furthermore, we have
Anne Schreuder   +10 more
wiley   +1 more source

Elucidating the role of the tumor suppressor Protein Phoshatase 2A in Chronic Myeloid Leukemia.

open access: yes, 2010
Protein phosphatase-2A (PP2A) is one of the major cellular serine-threonine phosphatases and is involved in the regulation of cell homeostasis through the negative regulation of signaling pathways initiated by protein kinases.
Neviani, Paolo
core  

MITF maintains genome stability in nonmelanocyte lineages

open access: yesMolecular Oncology, EarlyView.
MITF is essential for melanocyte survival and acts as an oncogene in 10%–20% of melanomas. We show that MITF depletion causes genome instability in nonmelanocytic cells, leading to LATS2‐mediated P53 activation, cell cycle arrest, and apoptosis. This study highlights the role of MITF as a genome maintenance factor beyond the melanocyte lineage. Created
Drifa H. Gudmundsdottir   +13 more
wiley   +1 more source

Studies of Tumor Suppressor Genes via Chromosome Engineering

open access: yes, 2015
The development and progression of malignant tumors likely result from consecutive accumulation of genetic alterations, including dysfunctional tumor suppressor genes. However, the signaling mechanisms that underlie the development of tumors have not yet
Hiroyuki Kugoh   +2 more
core   +1 more source

A novel quinazolinone insulin receptor inhibitor and its synergy with an EGFR inhibitor in glucose‐driven glioblastoma

open access: yesMolecular Oncology, EarlyView.
The novel styrylquinazolinone‐based molecule W1B effectively suppresses glioblastoma by inhibiting IGF1R and EGFR. In high‐glucose microenvironments driving tumor resistance, W1B acts synergistically with the EGFR inhibitor dacomitinib. This combination safely blocks compensatory survival signaling in zebrafish xenograft models. Showcasing promising in
Patryk Rurka   +9 more
wiley   +1 more source

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