Large-scale mitochondrial DNA deletion mutations and nuclear genome instability in human breast cancer

2004 ◽  
Vol 28 (2) ◽  
pp. 119-126 ◽  
Author(s):  
Weizhu Zhu ◽  
Wenyi Qin ◽  
Edward R. Sauter
2020 ◽  
Vol 48 (20) ◽  
pp. 11244-11258
Author(s):  
Gabriele A Fontana ◽  
Hailey L Gahlon

Abstract Deletions in mitochondrial DNA (mtDNA) are associated with diverse human pathologies including cancer, aging and mitochondrial disorders. Large-scale deletions span kilobases in length and the loss of these associated genes contributes to crippled oxidative phosphorylation and overall decline in mitochondrial fitness. There is not a united view for how mtDNA deletions are generated and the molecular mechanisms underlying this process are poorly understood. This review discusses the role of replication and repair in mtDNA deletion formation as well as nucleic acid motifs such as repeats, secondary structures, and DNA damage associated with deletion formation in the mitochondrial genome. We propose that while erroneous replication and repair can separately contribute to deletion formation, crosstalk between these pathways is also involved in generating deletions.


2012 ◽  
Vol 11 (11) ◽  
pp. 5311-5322 ◽  
Author(s):  
Ryohei Narumi ◽  
Tatsuo Murakami ◽  
Takahisa Kuga ◽  
Jun Adachi ◽  
Takashi Shiromizu ◽  
...  

Genes ◽  
2019 ◽  
Vol 10 (12) ◽  
pp. 961 ◽  
Author(s):  
Rohan Kar ◽  
Niraj Kumar Jha ◽  
Saurabh Kumar Jha ◽  
Ankur Sharma ◽  
Sunny Dholpuria ◽  
...  

Notch signaling is a primitive signaling pathway having various roles in the normal origin and development of each multicellular organisms. Therefore, any aberration in the pathway will inevitably lead to deadly outcomes such as cancer. It has now been more than two decades since Notch was acknowledged as an oncogene in mouse mammary tumor virus-infected mice. Since that discovery, activated Notch signaling and consequent up-regulation of tumor-promoting Notch target genes have been observed in human breast cancer. Moreover, consistent over-expression of Notch ligands and receptors has been shown to correlate with poor prognosis in human breast cancer. Notch regulates a number of key processes during breast carcinogenesis, of which, one key phenomenon is epithelial–mesenchymal transition (EMT). EMT is a key process for large-scale cell movement during morphogenesis at the time of embryonic development. Cancer cells aided by transcription factors usurp this developmental program to execute the multi-step process of tumorigenesis and metastasis. In this review, we recapitulate recent progress in breast cancer research that has provided new perceptions into the molecular mechanisms behind Notch-mediated EMT regulation during breast tumorigenesis.


Author(s):  
Entela B. Lushaj ◽  
Lucian Lozonschi ◽  
Maria Barnes ◽  
Emily Anstadt ◽  
Takushi Kohmoto

Sign in / Sign up

Export Citation Format

Share Document