scholarly journals The BRUCE-ATR Signaling Axis Is Required for Accurate DNA Replication and Suppression of Liver Cancer Development

Hepatology ◽  
2019 ◽  
Vol 69 (6) ◽  
pp. 2608-2622 ◽  
Author(s):  
Chunmin Ge ◽  
Chrystelle L. Vilfranc ◽  
Lixiao Che ◽  
Raj K. Pandita ◽  
Shashank Hambarde ◽  
...  
Keyword(s):  
Dna Replication ◽  
Liver Cancer ◽  
Cancer Development ◽  
Signaling Axis

scholarly journals Atractylenolide III predisposes miR‐195‐5p/FGFR1 signaling axis to exert tumor‐suppressive functions in liver cancer

2021 ◽  
Author(s):  
Langqing Sheng ◽  
Jiarong Li ◽  
Nianfeng Li ◽  
Liansheng Gong ◽  
Ling Liu ◽  
...  
Keyword(s):  
Liver Cancer ◽  
Signaling Axis ◽  
Atractylenolide Iii

scholarly journals Hepatic carboxylesterase 3 (Ces3/Tgh) is downregulated in the early stages of liver cancer development in the rat

2016 ◽  
Vol 1862 (11) ◽  
pp. 2043-2053 ◽  
Author(s):  
Ariel D. Quiroga ◽  
María P. Ceballos ◽  
Juan P. Parody ◽  
Carla G. Comanzo ◽  
Florencia Lorenzetti ◽  
...  
Keyword(s):  
Liver Cancer ◽  
Cancer Development ◽  
Early Stages

scholarly journals Association between expression of Carboxypeptidase 4 and stem cell markers and their clinical significance in liver cancer development

2017 ◽  
Vol 8 (1) ◽  
pp. 111-116 ◽  
Author(s):  
Lichao Sun ◽  
Chunguang Guo ◽  
Joseph Burnett ◽  
Jian Pan ◽  
Zhihua Yang ◽  
...  
Keyword(s):  
Stem Cell ◽  
Liver Cancer ◽  
Clinical Significance ◽  
Cancer Development ◽  
Stem Cell Markers ◽  
Cell Markers

scholarly journals Detours to Replication: Functions of Specialized DNA Polymerases during Oncogene-induced Replication Stress

2018 ◽  
Vol 19 (10) ◽  
pp. 3255 ◽  
Author(s):  
Wei-Chung Tsao ◽  
Kristin Eckert
Keyword(s):  
Dna Replication ◽  
Stress Responses ◽  
Dna Polymerases ◽  
Repetitive Sequences ◽  
Replication Stress ◽  
Fragile Sites ◽  
Cancer Development ◽  
Cycle Arrest ◽  
Chromosomal Fragile Sites ◽  
Dna Secondary Structures

Incomplete and low-fidelity genome duplication contribute to genomic instability and cancer development. Difficult-to-Replicate Sequences, or DiToRS, are natural impediments in the genome that require specialized DNA polymerases and repair pathways to complete and maintain faithful DNA synthesis. DiToRS include non B-DNA secondary structures formed by repetitive sequences, for example within chromosomal fragile sites and telomeres, which inhibit DNA replication under endogenous stress conditions. Oncogene activation alters DNA replication dynamics and creates oncogenic replication stress, resulting in persistent activation of the DNA damage and replication stress responses, cell cycle arrest, and cell death. The response to oncogenic replication stress is highly complex and must be tightly regulated to prevent mutations and tumorigenesis. In this review, we summarize types of known DiToRS and the experimental evidence supporting replication inhibition, with a focus on the specialized DNA polymerases utilized to cope with these obstacles. In addition, we discuss different causes of oncogenic replication stress and its impact on DiToRS stability. We highlight recent findings regarding the regulation of DNA polymerases during oncogenic replication stress and the implications for cancer development.

scholarly journals Cellular and Molecular Mechanisms Underlying Prostate Cancer Development: Therapeutic Implications

Medicines ◽  
2019 ◽  
Vol 6 (3) ◽  
pp. 82 ◽  
Author(s):  
Ugo Testa ◽  
Germana Castelli ◽  
Elvira Pelosi
Keyword(s):  
Prostate Cancer ◽  
Molecular Mechanisms ◽  
Intraepithelial Neoplasia ◽  
Cancer Development ◽  
Initial Development ◽  
Therapeutic Implications ◽  
Cancer Pathways ◽  
Signaling Axis ◽  
Prostate Cancer Development ◽  
Prostate Cancers

Prostate cancer is the most frequent nonskin cancer and second most common cause of cancer-related deaths in man. Prostate cancer is a clinically heterogeneous disease with many patients exhibiting an aggressive disease with progression, metastasis, and other patients showing an indolent disease with low tendency to progression. Three stages of development of human prostate tumors have been identified: intraepithelial neoplasia, adenocarcinoma androgen-dependent, and adenocarcinoma androgen-independent or castration-resistant. Advances in molecular technologies have provided a very rapid progress in our understanding of the genomic events responsible for the initial development and progression of prostate cancer. These studies have shown that prostate cancer genome displays a relatively low mutation rate compared with other cancers and few chromosomal loss or gains. The ensemble of these molecular studies has led to suggest the existence of two main molecular groups of prostate cancers: one characterized by the presence of ERG rearrangements (~50% of prostate cancers harbor recurrent gene fusions involving ETS transcription factors, fusing the 5′ untranslated region of the androgen-regulated gene TMPRSS2 to nearly the coding sequence of the ETS family transcription factor ERG) and features of chemoplexy (complex gene rearrangements developing from a coordinated and simultaneous molecular event), and a second one characterized by the absence of ERG rearrangements and by the frequent mutations in the E3 ubiquitin ligase adapter SPOP and/or deletion of CDH1, a chromatin remodeling factor, and interchromosomal rearrangements and SPOP mutations are early events during prostate cancer development. During disease progression, genomic and epigenomic abnormalities accrued and converged on prostate cancer pathways, leading to a highly heterogeneous transcriptomic landscape, characterized by a hyperactive androgen receptor signaling axis.

Remodeling Collapsed DNA Replication Forks for Cancer Development

2019 ◽  
Vol 79 (7) ◽  
pp. 1297-1298 ◽  
Author(s):  
Sotirios K. Sotiriou ◽  
Thanos D. Halazonetis
Keyword(s):  
Dna Replication ◽  
Cancer Development ◽  
Replication Forks
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