(Q38187388)

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Concise review: cancer cells escape from oncogene addiction: understanding the mechanisms behind treatment failure for more effective targeting

scientific article published on June 2014

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scholarly article

1 reference

Europe PubMed Central

PubMed publication ID

30 August 2017

Concise review: cancer cells escape from oncogene addiction: understanding the mechanisms behind treatment failure for more effective targeting (English)

1 reference

Europe PubMed Central

PubMed publication ID

30 August 2017

object named as

Tessa L Holyoake

3

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author name string

Francesca Pellicano

1

1 reference

Europe PubMed Central

PubMed publication ID

30 August 2017

Leena Mukherjee

2

1 reference

Europe PubMed Central

PubMed publication ID

30 August 2017

publication date

1 June 2014

1 reference

Europe PubMed Central

PubMed publication ID

30 August 2017

1 reference

Europe PubMed Central

PubMed publication ID

30 August 2017

32

1 reference

Europe PubMed Central

PubMed publication ID

30 August 2017

6

1 reference

Europe PubMed Central

PubMed publication ID

30 August 2017

1373-1379

1 reference

Europe PubMed Central

PubMed publication ID

30 August 2017

Oncogene addiction

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Disorders in cell circuitry during multistage carcinogenesis: the role of homeostasis

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Oncogene addiction as a foundational rationale for targeted anti-cancer therapy: promises and perils

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Kinase mutations and imatinib response in patients with metastatic gastrointestinal stromal tumor

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Improved survival with vemurafenib in melanoma with BRAF V600E mutation

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Mutations of the BRAF gene in human cancer

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RAF inhibitor resistance is mediated by dimerization of aberrantly spliced BRAF(V600E)

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Trastuzumab: mechanism of action, resistance and future perspectives in HER2-overexpressing breast cancer.

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EGFR tyrosine kinase inhibitors in lung cancer: an evolving story

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Rational, biologically based treatment of EGFR-mutant non-small-cell lung cancer

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EGFR exon 20 insertion mutations in non-small-cell lung cancer: preclinical data and clinical implications

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EML4-ALK mutations in lung cancer that confer resistance to ALK inhibitors.

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Crizotinib versus chemotherapy in advanced ALK-positive lung cancer.

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Targeted therapy for cancer using PARP inhibitors

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Inhibition of poly(ADP-ribose) polymerase in tumors from BRCA mutation carriers

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Iniparib plus chemotherapy in metastatic triple-negative breast cancer

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Oncogene addiction: setting the stage for molecularly targeted cancer therapy

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Seeking the causes and solutions to imatinib-resistance in chronic myeloid leukemia

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Persistence of malignant hematopoietic progenitors in chronic myelogenous leukemia patients in complete cytogenetic remission following imatinib mesylate treatment

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Primitive, quiescent, Philadelphia-positive stem cells from patients with chronic myeloid leukemia are insensitive to STI571 in vitro

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Enhanced BCR-ABL kinase inhibition does not result in increased inhibition of downstream signaling pathways or increased growth suppression in CML progenitors

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Dasatinib (BMS-354825) targets an earlier progenitor population than imatinib in primary CML but does not eliminate the quiescent fraction

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Effects of dasatinib on SRC kinase activity and downstream intracellular signaling in primitive chronic myelogenous leukemia hematopoietic cells

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Effective and selective inhibition of chronic myeloid leukemia primitive hematopoietic progenitors by the dual Src/Abl kinase inhibitor SKI-606.

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Evolving concepts in the management of chronic myeloid leukemia: recommendations from an expert panel on behalf of the European LeukemiaNet

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Mechanisms of BCR-ABL in the pathogenesis of chronic myelogenous leukaemia

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Induction of chronic myelogenous leukemia in mice by the P210bcr/abl gene of the Philadelphia chromosome

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Reversibility of acute B-cell leukaemia induced by BCR-ABL1.

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Inducible chronic phase of myeloid leukemia with expansion of hematopoietic stem cells in a transgenic model of BCR-ABL leukemogenesis.

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BCR-ABL enhances differentiation of long-term repopulating hematopoietic stem cells

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Cancer induction by restriction of oncogene expression to the stem cell compartment

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Chronic myeloid leukemia stem cells are not dependent on Bcr-Abl kinase activity for their survival

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Human chronic myeloid leukemia stem cells are insensitive to imatinib despite inhibition of BCR-ABL activity

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Five-year follow-up of patients receiving imatinib for chronic myeloid leukemia

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Leukemic stem cell persistence in chronic myeloid leukemia patients with sustained undetectable molecular residual disease

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Frequency of major molecular responses to imatinib or interferon alfa plus cytarabine in newly diagnosed chronic myeloid leukemia

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Divergent clinical outcome in two CML patients who discontinued imatinib therapy after achieving a molecular remission

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Persistence of leukemia stem cells in chronic myelogenous leukemia patients in prolonged remission with imatinib treatment

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Discontinuation of imatinib in patients with chronic myeloid leukaemia who have maintained complete molecular remission for at least 2 years: the prospective, multicentre Stop Imatinib (STIM) trial

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

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Instability of BCR-ABL gene in primary and cultured chronic myeloid leukemia stem cells.

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TGF-beta-FOXO signalling maintains leukaemia-initiating cells in chronic myeloid leukaemia

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Assembling defenses against therapy-resistant leukemic stem cells: Bcl6 joins the ranks

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BCL6-mediated repression of p53 is critical for leukemia stem cell survival in chronic myeloid leukemia

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Bcr-Abl with an SH3 deletion retains the ability To induce a myeloproliferative disease in mice, yet c-Abl activated by an SH3 deletion induces only lymphoid malignancy

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A BCR-ABL mutant lacking direct binding sites for the GRB2, CBL and CRKL adapter proteins fails to induce leukemia in mice

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Targeting primitive chronic myeloid leukemia cells by effective inhibition of a new AHI-1-BCR-ABL-JAK2 complex

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Loss of the Alox5 gene impairs leukemia stem cells and prevents chronic myeloid leukemia

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PP2A-activating drugs selectively eradicate TKI-resistant chronic myeloid leukemic stem cells

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BMS-214662 induces mitochondrial apoptosis in chronic myeloid leukemia (CML) stem/progenitor cells, including CD34+38- cells, through activation of protein kinase Cbeta.

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The tumor suppressor PP2A is functionally inactivated in blast crisis CML through the inhibitory activity of the BCR/ABL-regulated SET protein

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PML targeting eradicates quiescent leukaemia-initiating cells

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Targeting autophagy potentiates tyrosine kinase inhibitor-induced cell death in Philadelphia chromosome-positive cells, including primary CML stem cells

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Low BCR-ABL expression levels in hematopoietic precursor cells enable persistence of chronic myeloid leukemia under imatinib

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Role of epigenetics in chronic myeloid leukemia

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Gene sets identified with oncogene cooperativity analysis regulate in vivo growth and survival of leukemia stem cells.

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Synergistic response to oncogenic mutations defines gene class critical to cancer phenotype.

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Evolutionary dynamics of carcinogenesis and why targeted therapy does not work.

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A deep-sequencing study of chronic myeloid leukemia patients in blast crisis (BC-CML) detects mutations in 76.9% of cases

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Identifiers

10.1002/STEM.1678

1 reference

Europe PubMed Central

PubMed publication ID

30 August 2017

PubMed publication ID

1 reference

Europe PubMed Central

PubMed publication ID

30 August 2017

ResearchGate publication ID

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