Lista de obras -

A preliminary study of apoptosis induction in glioma cells via alteration of the Bax/Bcl-2-p53 axis by transformed and non-transformed root extracts of Leonurus sibiricus L.

artículo científico publicado en 2016

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

artículo científico publicado en 2006

Advances in the biology and therapy of chronic myeloid leukemia: proceedings from the 6th Post-ASH International Chronic Myeloid Leukemia and Myeloproliferative Neoplasms Workshop

artículo científico

Amifostine differentially modulates DNA damage evoked by idarubicin in normal and leukemic cells

artículo científico publicado en 2002

BCR-ABL1 Kinase: Hunting an Elusive Target with New Weapons ⬇️

artículo científico publicado el 23 de noviembre de 2011

BCR-ABL1 kinase facilitates localization of acetylated histones 3 and 4 on DNA double-strand breaks

artículo científico publicado en 2011

BCR/ABL and other kinases from chronic myeloproliferative disorders stimulate single-strand annealing, an unfaithful DNA double-strand break repair

artículo científico publicado en 2008

BCR/ABL inhibits mismatch repair to protect from apoptosis and induce point mutations

artículo científico publicado en 2008

BCR/ABL kinase induces self-mutagenesis via reactive oxygen species to encode imatinib resistance

artículo científico publicado en 2006

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

artículo científico publicado en 2005

BCR/ABL oncogenic kinase promotes unfaithful repair of the reactive oxygen species-dependent DNA double-strand breaks

scientific article published on 10 August 2004

BCR/ABL recruits p53 tumor suppressor protein to induce drug resistance

artículo científico publicado en 2004

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

artículo científico publicado en 2002

BCR/ABL stimulates WRN to promote survival and genomic instability.

artículo científico publicado en 2010

BCR/ABL, DNA damage and DNA repair: implications for new treatment concepts

artículo científico publicado en 2008

BLM helicase is activated in BCR/ABL leukemia cells to modulate responses to cisplatin.

artículo científico publicado en 2005

Chronic myeloid leukemia cells refractory/resistant to tyrosine kinase inhibitors are genetically unstable and may cause relapse and malignant progression to the terminal disease state ⬇️

artículo científico publicado el 1 de febrero de 2011

Chronic myeloid leukemia: mechanisms of blastic transformation

artículo científico publicado en 2010

Complementary functions of the antiapoptotic protein A1 and serine/threonine kinase pim-1 in the BCR/ABL-mediated leukemogenesis

artículo científico publicado en 2002

Downregulation of BRCA1 protein in BCR-ABL1 leukemia cells depends on stress-triggered TIAR-mediated suppression of translation

artículo científico publicado en 2014

Doxorubicin Differentially Induces Apoptosis, Expression of Mitochondrial Apoptosis-Related Genes, and Mitochondrial Potential in BCR-ABL1-Expressing Cells Sensitive and Resistant to Imatinib

artículo científico publicado en 2015

Enhanced phosphorylation of Nbs1, a member of DNA repair/checkpoint complex Mre11-RAD50-Nbs1, can be targeted to increase the efficacy of imatinib mesylate against BCR/ABL-positive leukemia cells

artículo científico publicado en 2007

Free radical scavengers can differentially modulate the genotoxicity of amsacrine in normal and cancer cells

artículo científico publicado en 2003

Fusion oncogenic tyrosine kinases alter DNA damage and repair after genotoxic treatment: role in drug resistance?

artículo científico publicado en 2003

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

artículo científico publicado en 2002

Gadd45a deficiency accelerates BCR-ABL driven chronic myelogenous leukemia.

scientific article published on 10 January 2017

Genetic mechanisms of chronic myeloid leukemia blastic transformation

artículo científico

Genomic instability may originate from imatinib-refractory chronic myeloid leukemia stem cells

artículo científico publicado en 2013

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

artículo científico publicado en 2007

HIV-1 Tat increases cell survival in response to cisplatin by stimulating Rad51 gene expression

scientific journal article

Identification of a Small Molecule Inhibitor of RAD52 by Structure-Based Selection

artículo científico publicado en 2016

Imatinib mesylate (STI571) abrogates the resistance to doxorubicin in human K562 chronic myeloid leukemia cells by inhibition of BCR/ABL kinase-mediated DNA repair.

artículo científico publicado en 2006

Imatinib sensitivity in BCR-ABL1-positive chronic myeloid leukemia cells is regulated by the remaining normal ABL1 allele

artículo científico publicado en 2011

Increased phosphorylation of eIF2α in chronic myeloid leukemia cells stimulates secretion of matrix modifying enzymes

artículo científico publicado en 2016

Intrinsic regulation of the interactions between the SH3 domain of p85 subunit of phosphatidylinositol-3 kinase and the protein network of BCR/ABL oncogenic tyrosine kinase

artículo científico publicado en 2005

Mitochondrial mutagenesis in BCR-ABL1-expressing cells sensitive and resistant to imatinib

artículo científico publicado en 2016

Molecular basis of microhomology-mediated end-joining by purified full-length Polθ

scientific article published on 27 September 2019

Normal ABL1 is a tumor suppressor and therapeutic target in human and mouse leukemias expressing oncogenic ABL1 kinases

artículo científico publicado en 2016

Oncogenic tyrosine kinases and the DNA-damage response

artículo científico publicado en 2002

PARP1 inhibitor olaparib (Lynparza) exerts synthetic lethal effect against ligase 4-deficient melanomas.

artículo científico publicado en 2016

Personalized synthetic lethality induced by targeting RAD52 in leukemias identified by gene mutation and expression profile

artículo científico publicado en 2013

Phosphatidylinositol 3-kinase p85{alpha} subunit-dependent interaction with BCR/ABL-related fusion tyrosine kinases: molecular mechanisms and biological consequences

artículo científico publicado en 2005

Publisher Correction: Molecular basis of microhomology-mediated end-joining by purified full-length Polθ

scientific article published on 09 April 2020

Rac2-MRC-cIII-generated ROS cause genomic instability in chronic myeloid leukemia stem cells and primitive progenitors

artículo científico publicado en 2012

Reactive Oxygen Species and Mitochondrial DNA Damage and Repair in BCR-ABL1 Cells Resistant to Imatinib

artículo científico publicado en 2015

Role of the insulin-like growth factor I/insulin receptor substrate 1 axis in Rad51 trafficking and DNA repair by homologous recombination.

artículo científico publicado en 2003

STI571 reduces NER activity in BCR/ABL-expressing cells.

artículo científico publicado en 2008

Small-Molecule Disruption of RAD52 Rings as a Mechanism for Precision Medicine in BRCA-Deficient Cancers.

artículo científico publicado en 2015

Synthetic lethality as a functional tool in basic research and in anticancer therapy

artículo científico publicado en 2014

Targeting BRCA1- and BRCA2-deficient cells with RAD52 small molecule inhibitors

artículo científico publicado en 2016

Targeting RAD51 phosphotyrosine-315 to prevent unfaithful recombination repair in BCR-ABL1 leukemia ⬇️

artículo científico publicado el 7 de junio de 2011

The Src family kinase Hck couples BCR/ABL to STAT5 activation in myeloid leukemia cells.

artículo científico publicado en 2002

The role of focal adhesion kinase in the emigration of cells from confluent cultures.

artículo científico publicado en 2002

UV Differentially Induces Oxidative Stress, DNA Damage and Apoptosis in BCR-ABL1-Positive Cells Sensitive and Resistant to Imatinib

artículo científico publicado en 2015

Lista de obras de

A preliminary study of apoptosis induction in glioma cells via alteration of the Bax/Bcl-2-p53 axis by transformed and non-transformed root extracts of Leonurus sibiricus L.

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

Advances in the biology and therapy of chronic myeloid leukemia: proceedings from the 6th Post-ASH International Chronic Myeloid Leukemia and Myeloproliferative Neoplasms Workshop

Amifostine differentially modulates DNA damage evoked by idarubicin in normal and leukemic cells

BCR-ABL1 Kinase: Hunting an Elusive Target with New Weapons ⬇️

BCR-ABL1 kinase facilitates localization of acetylated histones 3 and 4 on DNA double-strand breaks

BCR/ABL and other kinases from chronic myeloproliferative disorders stimulate single-strand annealing, an unfaithful DNA double-strand break repair

BCR/ABL inhibits mismatch repair to protect from apoptosis and induce point mutations

BCR/ABL kinase induces self-mutagenesis via reactive oxygen species to encode imatinib resistance

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

BCR/ABL oncogenic kinase promotes unfaithful repair of the reactive oxygen species-dependent DNA double-strand breaks

BCR/ABL recruits p53 tumor suppressor protein to induce drug resistance

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

BCR/ABL stimulates WRN to promote survival and genomic instability.

BCR/ABL, DNA damage and DNA repair: implications for new treatment concepts

BLM helicase is activated in BCR/ABL leukemia cells to modulate responses to cisplatin.

Chronic myeloid leukemia cells refractory/resistant to tyrosine kinase inhibitors are genetically unstable and may cause relapse and malignant progression to the terminal disease state ⬇️

Chronic myeloid leukemia: mechanisms of blastic transformation

Complementary functions of the antiapoptotic protein A1 and serine/threonine kinase pim-1 in the BCR/ABL-mediated leukemogenesis

Downregulation of BRCA1 protein in BCR-ABL1 leukemia cells depends on stress-triggered TIAR-mediated suppression of translation

Doxorubicin Differentially Induces Apoptosis, Expression of Mitochondrial Apoptosis-Related Genes, and Mitochondrial Potential in BCR-ABL1-Expressing Cells Sensitive and Resistant to Imatinib

Enhanced phosphorylation of Nbs1, a member of DNA repair/checkpoint complex Mre11-RAD50-Nbs1, can be targeted to increase the efficacy of imatinib mesylate against BCR/ABL-positive leukemia cells

Free radical scavengers can differentially modulate the genotoxicity of amsacrine in normal and cancer cells

Fusion oncogenic tyrosine kinases alter DNA damage and repair after genotoxic treatment: role in drug resistance?

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

Gadd45a deficiency accelerates BCR-ABL driven chronic myelogenous leukemia.

Genetic mechanisms of chronic myeloid leukemia blastic transformation

Genomic instability may originate from imatinib-refractory chronic myeloid leukemia stem cells

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

HIV-1 Tat increases cell survival in response to cisplatin by stimulating Rad51 gene expression

Identification of a Small Molecule Inhibitor of RAD52 by Structure-Based Selection

Imatinib mesylate (STI571) abrogates the resistance to doxorubicin in human K562 chronic myeloid leukemia cells by inhibition of BCR/ABL kinase-mediated DNA repair.

Imatinib sensitivity in BCR-ABL1-positive chronic myeloid leukemia cells is regulated by the remaining normal ABL1 allele

Increased phosphorylation of eIF2α in chronic myeloid leukemia cells stimulates secretion of matrix modifying enzymes

Intrinsic regulation of the interactions between the SH3 domain of p85 subunit of phosphatidylinositol-3 kinase and the protein network of BCR/ABL oncogenic tyrosine kinase

Mitochondrial mutagenesis in BCR-ABL1-expressing cells sensitive and resistant to imatinib

Molecular basis of microhomology-mediated end-joining by purified full-length Polθ

Normal ABL1 is a tumor suppressor and therapeutic target in human and mouse leukemias expressing oncogenic ABL1 kinases

Oncogenic tyrosine kinases and the DNA-damage response

PARP1 inhibitor olaparib (Lynparza) exerts synthetic lethal effect against ligase 4-deficient melanomas.

Personalized synthetic lethality induced by targeting RAD52 in leukemias identified by gene mutation and expression profile

Phosphatidylinositol 3-kinase p85{alpha} subunit-dependent interaction with BCR/ABL-related fusion tyrosine kinases: molecular mechanisms and biological consequences

Publisher Correction: Molecular basis of microhomology-mediated end-joining by purified full-length Polθ

Rac2-MRC-cIII-generated ROS cause genomic instability in chronic myeloid leukemia stem cells and primitive progenitors

Reactive Oxygen Species and Mitochondrial DNA Damage and Repair in BCR-ABL1 Cells Resistant to Imatinib

Role of the insulin-like growth factor I/insulin receptor substrate 1 axis in Rad51 trafficking and DNA repair by homologous recombination.

STI571 reduces NER activity in BCR/ABL-expressing cells.

Small-Molecule Disruption of RAD52 Rings as a Mechanism for Precision Medicine in BRCA-Deficient Cancers.

Synthetic lethality as a functional tool in basic research and in anticancer therapy

Targeting BRCA1- and BRCA2-deficient cells with RAD52 small molecule inhibitors

Targeting RAD51 phosphotyrosine-315 to prevent unfaithful recombination repair in BCR-ABL1 leukemia ⬇️

The Src family kinase Hck couples BCR/ABL to STAT5 activation in myeloid leukemia cells.

The role of focal adhesion kinase in the emigration of cells from confluent cultures.

UV Differentially Induces Oxidative Stress, DNA Damage and Apoptosis in BCR-ABL1-Positive Cells Sensitive and Resistant to Imatinib