Neoplastic Transformation

Rubin, Harry

doi:10.1002/047120918x.emb0990

Cited by 1 publication

(1 citation statement)

References 17 publications

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“…Another were produced, and has been a lifetime interest for studies of the transformation process by H. Rubin [51]. In essence the methodology of their derivations was nutritional deficit, which also was used in our establishment of the marsupial to be normal cells [56], which certainly should be erased from cancer literature to come.…”

Section: Cells With Normal Karyotypes Are Not a Guarantee Of A Normalmentioning

confidence: 99%

Genomic Instability in Cancer II: 4N-Skewed (90°) Reductive Division via Fragile Sites to Fitness Increase for Solid and Hematological Cancer Beginnings

Walen¹

2019

JCT

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The objective herein was to connect the ontogeny process of diplochromosomal, amitotic, 4n-skewed division-system, to cytogenetic deficiency lesions in satellite, repetitive DNAs, especially in the chromosomal fragile sites, some 100 distributed over the genome. These latter studies had shown that chemical induced replication-stress led to un-replicated lesions in these fragile sites, which from inaccurate repair processes caused genomic instability. In the chain of events of the ontogeny process to the special tetraploidy, it was proposed that primary damaged human cells could undergo replication stress from repair-process present during cell replication, a suggestion verified by X-ray damaged cells producing the unstable fragile sites (see text). The cancer-importance for therapy is recognition of cell cycle change for the 4n derivative fitness-gained, diploid progeny cells. An open question is whether RB controlling G1 to S-period is mutated at this suggested tumorigenesis initiating phase, and if so, with what consequences for therapy. The fragile site studies further showed that repair of repetitive DNAs could produce two types of genomic changes: single gene mutations and CNVs, which were here shown to be chromosomally located on "borders" to repairing satellite lesions. This genomic placement was found to correspond to mutations identified in tumor sequencing (p53, Rb, MYC), favoring a bad luck location for their cancer "mutational nature". The CNVs in cancers, are here seen as molecular expressions of long-known cytogenetic HSRs and DMs also with demonstrated origin from amplifications of single genes. Over-expression of oncogenes was hinted of being from duplications, but Drosophila genetics demonstrated the opposite, gene inactivation. The reduced eye-size from dominant, BAR-Ultra-Bar-eye phenotypes, was caused by duplications, inactivating the How to cite this paper: Walen, K.H. (2019) Genomic Instability in Cancer II: 4N-Skewed (90˚) Reductive Division via Fragile Sites to Fitness Increase for Solid and Hematological Cancer Beginnings.

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Section: Cells With Normal Karyotypes Are Not a Guarantee Of A Normalmentioning

confidence: 99%

Genomic Instability in Cancer II: 4N-Skewed (90°) Reductive Division via Fragile Sites to Fitness Increase for Solid and Hematological Cancer Beginnings

Walen¹

2019

JCT

View full text Add to dashboard Cite

show abstract

Neoplastic Transformation

Cited by 1 publication

References 17 publications

Genomic Instability in Cancer II: 4N-Skewed (90°) Reductive Division via Fragile Sites to Fitness Increase for Solid and Hematological Cancer Beginnings

Genomic Instability in Cancer II: 4N-Skewed (90°) Reductive Division via Fragile Sites to Fitness Increase for Solid and Hematological Cancer Beginnings

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Neoplastic Transformation

Cited by 1 publication

References 17 publications

Genomic Instability in Cancer II: 4N-Skewed (90&#176;) Reductive Division via Fragile Sites to Fitness Increase for Solid and Hematological Cancer Beginnings

Genomic Instability in Cancer II: 4N-Skewed (90&#176;) Reductive Division via Fragile Sites to Fitness Increase for Solid and Hematological Cancer Beginnings

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Genomic Instability in Cancer II: 4N-Skewed (90°) Reductive Division via Fragile Sites to Fitness Increase for Solid and Hematological Cancer Beginnings

Genomic Instability in Cancer II: 4N-Skewed (90°) Reductive Division via Fragile Sites to Fitness Increase for Solid and Hematological Cancer Beginnings