Results 61 to 70 of about 4,575,740 (255)

Breast Cancer Therapy by Small-Molecule Reactivation of Mutant p53

open access: yesCurrent Oncology
Tumor suppressor p53 is essential for maintaining DNA stability and preventing cancer. Under normal conditions, the p53 protein is either degraded or bound to a negative regulator, rendering it inactive, but when DNA damage occurs, p53 is activated ...
Simon H. Slight, Salman M. Hyder
doaj   +1 more source

New therapeutic strategies to treat human cancers expressing mutant p53 proteins

open access: yesJournal of Experimental & Clinical Cancer Research, 2018
The tumor suppressor p53 plays a critical role to preserve DNA fidelity from diverse insults through the regulation of cell-cycle checkpoints, DNA repair, senescence and apoptosis. The TP53 is the most frequently inactivated gene in human cancers.
Giovanni Blandino, Silvia Di Agostino
doaj   +1 more source

Cancer‐associated mutations in endometriosis reframe a benign disease through molecular oncology

open access: yesMolecular Oncology, EarlyView.
This review aims to comprehensively analyse cancer‐associated somatic mutations (CAMs) present in endometriotic lesions, emphasizing their biological roles, spatial distribution and implications for translational applications in medicine. By contextualizing a benign state within a genomic framework, this analysis seeks to establish its value as a ...
Clarissa Mujacic   +15 more
wiley   +1 more source

PANoptosis in the pathogenesis of myelodysplastic syndromes

open access: yesMolecular Oncology, EarlyView.
PANoptosis, a combination of three types of programmed cell death, is mediated by a large protein complex called a PANoptosome. In healthy bone marrow hematopoietic cells, PANoptosis is restricted by inhibitory signaling. In MDS, bone marrow cells become sensitive to the PANoptotic stimuli due to the aberrant inactivation of inhibitory signaling or ...
Rohit Thalla   +4 more
wiley   +1 more source

Correlation of cell cycle regulatory proteins (p53 and p16ink4a) and bcl-2 oncoprotein with mitotic index and thickness of primary cutaneous malignant melanoma

open access: yesBiomolecules & Biomedicine, 2010
The purpose of the study was to determine the frequency of expression p53 and p16INK4a proteins and bcl2- oncoprotein in malignant skin melanoma and to determine their correlation with the proliferative index and tumor thickness.
Miloš Kostov   +5 more
doaj   +1 more source

Equine sarcoids: Bovine Papillomavirus type 1 transformed fibroblasts are sensitive to cisplatin and UVB induced apoptosis and show aberrant expression of p53 [PDF]

open access: yes, 2012
Bovine papillomavirus type 1 infects not only cattle but also equids and is a causative factor in the pathogenesis of commonly occurring equine sarcoid tumours.
Finlay, M.   +14 more
core   +1 more source

Somatostatin receptor 4 (SSTR4) is a tumor suppressor in cutaneous and head & neck squamous cell carcinomas

open access: yesMolecular Oncology, EarlyView.
This study identifies somatostatin receptor 4 (Sstr4) as a critical tumor suppressor against skin and head/neck cancers (HNSCC, cSCC, and BCC). The loss of Sstr4 removes a check on cell growth, causing hyperactivation of the MAPK‐ERK signaling pathway (↑).
Ali Taqvi   +6 more
wiley   +1 more source

P53 mutations in human adrenocortical neoplasms [PDF]

open access: yes, 1994
The mechanisms of tumorigenesis of adrenocortical neoplasms have not been elucidated as yet. However, loss of heterozygosity at chromosomal locus 17p has been consistently observed in adrenocortical cancer.
Travis, W.   +6 more
core   +1 more source

p53 Genetics and Biology in Lung Carcinomas: Insights, Implications and Clinical Applications

open access: yesBiomedicines
The TP53 gene is renowned as a tumor suppressor, playing a pivotal role in overseeing the cell cycle, apoptosis, and maintaining genomic stability. Dysregulation of p53 often contributes to the initiation and progression of various cancers, including ...
Dixan A. Benitez   +7 more
doaj   +1 more source

Independent regulation of P53 stabilisation and activation after Rb deletion in primary epithelial cells [PDF]

open access: yes, 2010
We have previously reported that deletion of the retinoblastoma gene Rb leads to rapid but transient p53 stabilisation. We investigated here the pathways involved.
Bellamy, Christopher   +4 more
core   +1 more source

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