Reversibility of acute B-cell leukaemia induced by BCR-ABL1.
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EGF receptor gene mutations are common in lung cancers from "never smokers" and are associated with sensitivity of tumors to gefitinib and erlotinibKnockdown of c-Myc expression by RNAi inhibits MCF-7 breast tumor cells growth in vitro and in vivo.Inducible transgenics. New lessons on events governing the induction and commitment in mammary tumorigenesis.Brief inactivation of c-Myc is not sufficient for sustained regression of c-Myc-induced tumours of pancreatic islets and skin epidermisConditional mouse models demonstrate oncogene-dependent differences in tumor maintenance and recurrenceChildhood leukemia: electric and magnetic fields as possible risk factorsMYC activation is a hallmark of cancer initiation and maintenanceAnimal models of leukemia: any closer to the real thing?Modeling of Chronic Myeloid Leukemia: An Overview of In Vivo Murine and Human Xenograft ModelsCharacterization of a Steroid Receptor Coactivator Small Molecule Stimulator that Overstimulates Cancer Cells and Leads to Cell Stress and DeathCooperation of BCR-ABL and AML1/MDS1/EVI1 in blocking myeloid differentiation and rapid induction of an acute myelogenous leukemiaMolecular cloning and characterization of TPP36 and its isoform TPP32, novel substrates of Abl tyrosine kinasePrinciples of cancer therapy: oncogene and non-oncogene addictionAbelson kinase acts as a robust, multifunctional scaffold in regulating embryonic morphogenesis.Peptide aptamers: recent developments for cancer therapy.The B cell antigen receptor and overexpression of MYC can cooperate in the genesis of B cell lymphomasReciprocal t(9;22) ABL/BCR fusion proteins: leukemogenic potential and effects on B cell commitment.Murine models of acute leukemia: important tools in current pediatric leukemia research.Sustained Hedgehog signaling is required for basal cell carcinoma proliferation and survival: conditional skin tumorigenesis recapitulates the hair growth cycleAML1-ETO expression is directly involved in the development of acute myeloid leukemia in the presence of additional mutationsThe NH(2)-terminal coiled-coil domain and tyrosine 177 play important roles in induction of a myeloproliferative disease in mice by Bcr-AblIRF4 is a suppressor of c-Myc induced B cell leukemia.Oncogene withdrawal engages the immune system to induce sustained cancer regression.A neoplastic gene fusion mimics trans-splicing of RNAs in normal human cells.A murine model of CML blast crisis induced by cooperation between BCR/ABL and NUP98/HOXA9Enhanced paracrine FGF10 expression promotes formation of multifocal prostate adenocarcinoma and an increase in epithelial androgen receptorOncogene-targeting T cells reject large tumors while oncogene inactivation selects escape variants in mouse models of cancer.Tumor reversion: correction of malignant behavior by microenvironmental cuesSystems biology modeling reveals a possible mechanism of the tumor cell death upon oncogene inactivation in EGFR addicted cancers.Abl-kinase-sensitive levels of ERK5 and its intrinsic basal activity contribute to leukaemia cell survivalRecent advances in the molecular and cellular biology of chronic myeloid leukaemia: lessons to be learned from the laboratory.MYC Inactivation Elicits Oncogene Addiction through Both Tumor Cell-Intrinsic and Host-Dependent Mechanisms.MYC through miR-17-92 suppresses specific target genes to maintain survival, autonomous proliferation, and a neoplastic state.PROBING CANCER SIGNALING WITH RESONANT WAVEGUIDE GRATING BIOSENSORSCD4(+) T cells contribute to the remodeling of the microenvironment required for sustained tumor regression upon oncogene inactivationβ-catenin contributes to lung tumor development induced by EGFR mutationsAn essential role for the immune system in the mechanism of tumor regression following targeted oncogene inactivation.Modeling Philadelphia chromosome positive leukemias.Persistence of high-grade cervical dysplasia and cervical cancer requires the continuous expression of the human papillomavirus type 16 E7 oncogene.Minimal residual disease in soft-tissue sarcomas.
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P2860
Reversibility of acute B-cell leukaemia induced by BCR-ABL1.
description
2000 nî lūn-bûn
@nan
2000年の論文
@ja
2000年学术文章
@wuu
2000年学术文章
@zh
2000年学术文章
@zh-cn
2000年学术文章
@zh-hans
2000年学术文章
@zh-my
2000年学术文章
@zh-sg
2000年學術文章
@yue
2000年學術文章
@zh-hant
name
Reversibility of acute B-cell leukaemia induced by BCR-ABL1.
@en
Reversibility of acute B-cell leukaemia induced by BCR-ABL1.
@nl
type
label
Reversibility of acute B-cell leukaemia induced by BCR-ABL1.
@en
Reversibility of acute B-cell leukaemia induced by BCR-ABL1.
@nl
prefLabel
Reversibility of acute B-cell leukaemia induced by BCR-ABL1.
@en
Reversibility of acute B-cell leukaemia induced by BCR-ABL1.
@nl
P2093
P2860
P356
P1433
P1476
Reversibility of acute B-cell leukaemia induced by BCR-ABL1.
@en
P2093
Huettner CS
Van Etten RA
P2860
P2888
P356
10.1038/71691
P407
P577
2000-01-01T00:00:00Z
P5875
P6179
1040950884