(Q37738460)

22 August 2017

1 reference

title

Genomic instability: The cause and effect of BCR/ABL tyrosine kinase (English)

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22 August 2017

1

Tomasz Skorski

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PubMed ID

20425353

22 August 2017

language of work or name

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1 May 2007

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Current hematologic malignancy reports

22 August 2017

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22 August 2017

2

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22 August 2017

2

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22 August 2017

69-74

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https://scigraph.springernature.com/pub.10.1007/s11899-007-0010-6

22 August 2017

0 references

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ATR-Chk1 axis protects BCR/ABL leukemia cells from the lethal effect of DNA double-strand breaks.

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Homologous recombinational repair of DNA ensures mammalian chromosome stability

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Treatment of Chronic Myeloid Leukemia Cells with Imatinib (STI571) Impairs p53 Accumulation in Response to DNA Damage

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Common chromatin structures at breakpoint cluster regions may lead to chromosomal translocations found in chronic and acute leukemias

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BCR-ABL-mediated inhibition of apoptosis with delay of G2/M transition after DNA damage: a mechanism of resistance to multiple anticancer agents.

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Increased error-prone NHEJ activity in myeloid leukemias is associated with DNA damage at sites that recruit key nonhomologous end-joining proteins

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DNA damage response as a candidate anti-cancer barrier in early human tumorigenesis

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Persistent oxidative stress in chromosomally unstable cells

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Oncogenic kinase signalling

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Activation of the DNA damage checkpoint and genomic instability in human precancerous lesions

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BCR/ABL translocates to the nucleus and disrupts an ATR-dependent intra-S phase checkpoint

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Frequent chromosomal translocations induced by DNA double-strand breaks

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p210 BCR/ABL kinase regulates nucleotide excision repair (NER) and resistance to UV radiation

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Treatment of chronic myeloid leukemia cells with imatinib (STI571) impairs p53 accumulation in response to DNA damage

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Oxygen metabolism causes chromosome breaks and is associated with the neuronal apoptosis observed in DNA double-strand break repair mutants

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BCR/ABL modifies the kinetics and fidelity of DNA double-strand breaks repair in hematopoietic cells

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Rad51 overexpression promotes alternative double-strand break repair pathways and genome instability

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Fusion tyrosine kinases induce drug resistance by stimulation of homology-dependent recombination repair, prolongation of G(2)/M phase, and protection from apoptosis

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BCR/ABL regulates response to DNA damage: the role in resistance to genotoxic treatment and in genomic instability

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c-Myc can induce DNA damage, increase reactive oxygen species, and mitigate p53 function: a mechanism for oncogene-induced genetic instability

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Alu and translisin recognition site sequences flanking translocation sites in a novel type of chimeric bcr-abl transcript suggest a possible general mechanism for bcr-abl breakpoints

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12 December 2020

10.1007/S11899-007-0010-6

Identifiers

DOI

1 reference

22 August 2017

1 reference

PubMed ID

20425353