Results 51 to 60 of about 2,151,650 (259)

Distinct promoter elements mediate the co-operative effect of Brn-3a and p53 on the p21 promoter and their antagonism on the Bax promoter [PDF]

open access: yes, 2002
Although the promoters of both the Bax and p21 genes are activated by p53, they differ in the effect on this activation of the POU family transcription factor Brn-3a. Thus, Brn-3a inhibits activation of the Bax promoter by p53 but enhances the ability of
Budhram-Mahadeo, VS   +2 more
core  

Tumour–host interactions in Drosophila: mechanisms in the tumour micro‐ and macroenvironment

open access: yesMolecular Oncology, EarlyView.
This review examines how tumour–host crosstalk takes place at multiple levels of biological organisation, from local cell competition and immune crosstalk to organism‐wide metabolic and physiological collapse. Here, we integrate findings from Drosophila melanogaster studies that reveal conserved mechanisms through which tumours hijack host systems to ...
José Teles‐Reis, Tor Erik Rusten
wiley   +1 more source

KDM7A and KDM1A inhibition suppresses tumour promoting pathways in prostate cancer

open access: yesMolecular Oncology, EarlyView.
Treatment resistance is a major challenge for patients with advanced prostate cancer. This study examined an alternative approach to target the major prostate cancer‐promoting pathway by targeting epigenetic factors, whose levels are higher in tumours.
Jennie N Jeyapalan   +16 more
wiley   +1 more source

Cell cycle control and its modulation in HPV infected cells [PDF]

open access: yes, 2010
A key effect of human papillomavirus (HPV) infection is to disrupt the normal cell cycle in order to subvert the cellular DNA replication machinery. Morphologically, condylomata induced by high and low risk HPV types cannot be distinguished and many ...
Lyman, Rachel C.
core   +2 more sources

p63 is an alternative p53 repressor in melanoma that confers chemoresistance and a poor prognosis [PDF]

open access: yes, 2013
The role of apoptosis in melanoma pathogenesis and chemoresistance is poorly characterized. Mutations in TP53 occur infrequently, yet the TP53 apoptotic pathway is often abrogated.
Graf, M   +47 more
core   +1 more source

Developmental programmes drive cellular plasticity, disease progression and therapy resistance in lung adenocarcinoma

open access: yesMolecular Oncology, EarlyView.
This study shows that lung adenocarcinomas exploit developmental branching morphogenesis to acquire a therapy resistant basal‐like tumour cell state. This process was found to be regulated by combined TP53 loss‐of‐function and type‐I interferon signalling, identifying a novel axis for biomarker and therapeutic target discovery.
Kamila J Bienkowska   +13 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

A Chromatin-Focused siRNA Screen for Regulators of p53-Dependent Transcription

open access: yesG3: Genes, Genomes, Genetics, 2016
The protein product of the Homo sapiens TP53 gene is a transcription factor (p53) that regulates the expression of genes critical for the response to DNA damage and tumor suppression, including genes involved in cell cycle arrest, apoptosis, DNA repair ...
Morgan A. Sammons   +2 more
doaj   +1 more source

Prognostic significance and gene expression profiles of p53 mutations in microsatellite-stable stage III colorectal adenocarcinomas. [PDF]

open access: yesPLoS ONE, 2012
Although the prognostic value of p53 abnormalities in Stage III microsatellite stable (MSS) colorectal cancers (CRCs) is known, the gene expression profiles specific to the p53 status in the MSS background are not known.
Venkat R Katkoori   +11 more
doaj   +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

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