Combined Inactivation of MYC and K-Ras oncogenes reverses tumorigenesis in lung adenocarcinomas and lymphomas. - Wikidata - wikimedia - TriplyDB

Combined Inactivation of MYC and K-Ras oncogenes reverses tumorigenesis in lung adenocarcinomas and lymphomas.

Combined Inactivation of MYC and K-Ras oncogenes reverses tumorigenesis in lung adenocarcinomas and lymphomas.

http://www.wikidata.org/entity/Q33332189

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Weaknesses and Pitfalls of Using Mice and Rats in Cancer Chemoprevention Studies The other side of the coin: the tumor-suppressive aspect of oncogenes and the oncogenic aspect of tumor-suppressive genes, such as those along the CCND-CDK4/6-RB axis MYC is a metastasis gene for non-small-cell lung cancer Interaction between MYC and MCL1 in the genesis and outcome of non-small-cell lung cancer.Survival and death signals can predict tumor response to therapy after oncogene inactivation Clinicopathologic and prognostic significance of c-MYC copy number gain in lung adenocarcinomas.ERBB2 increases metastatic potentials specifically in androgen-insensitive prostate cancer cells.Alteration of the lipid profile in lymphomas induced by MYC overexpression.Twist1 suppresses senescence programs and thereby accelerates and maintains mutant Kras-induced lung tumorigenesis.PET imaging of tumor neovascularization in a transgenic mouse model with a novel 64Cu-DOTA-knottin peptide.Enabling online studies of conceptual relationships between medical terms: developing an efficient web platform miR-155: on the crosstalk between inflammation and cancer.Lymphomas that recur after MYC suppression continue to exhibit oncogene addiction.The metabolic profile of tumors depends on both the responsible genetic lesion and tissue type.Suppression of Ras/Mapk pathway signaling inhibits Myc-induced lymphomagenesis.Cervical cancers require the continuous expression of the human papillomavirus type 16 E7 oncoprotein even in the presence of the viral E6 oncoprotein Cancer prevention as biomodulation: targeting the initiating stimulus and secondary adaptations Cigarette smoke mediates epigenetic repression of miR-487b during pulmonary carcinogenesis Noncanonical roles of the immune system in eliciting oncogene addiction A quantitative PCR method to detect blood microRNAs associated with tumorigenesis in transgenic mice.N-myc alters the fate of preneoplastic cells in a mouse model of medulloblastoma.RARalpha2 expression is associated with disease progression and plays a crucial role in efficacy of ATRA treatment in myeloma.Differential effects on ARF stability by normal versus oncogenic levels of c-Myc expression.Mutational landscape of EGFR-, MYC-, and Kras-driven genetically engineered mouse models of lung adenocarcinoma.Reviewing once more the c-myc and Ras collaboration: converging at the cyclin D1-CDK4 complex and challenging basic concepts of cancer biology.Immunology in the clinic review series; focus on cancer: multiple roles for the immune system in oncogene addiction.Stat5-deficient hematopoiesis is permissive for Myc-induced B-cell leukemogenesis.Lineage factors and differentiation states in lung cancer progression.The twist box domain is required for Twist1-induced prostate cancer metastasis.Hypoxia in models of lung cancer: implications for targeted therapeutics.Investigation of the effects of treatment planning variables in small animal radiotherapy dose distributions Definition of an enhanced immune cell therapy in mice that can target stem-like lymphoma cells.Targeted overexpression of an activated N-ras gene results in B-cell and plasma cell lymphoproliferation and cooperates with c-myc to induce fatal B-cell neoplasia.Re-engineering the Pancreas Tumor Microenvironment: A "Regenerative Program" Hacked.Deletion of Pim kinases elevates the cellular levels of reactive oxygen species and sensitizes to K-Ras-induced cell killing.Just like the rest of evolution in Mother Nature, the evolution of cancers may be driven by natural selection, and not by haphazard mutations Tumor dormancy, oncogene addiction, cellular senescence, and self-renewal programs.Development of a micro-computed tomography-based image-guided conformal radiotherapy system for small animals.Combination Therapy Targeting BCL6 and Phospho-STAT3 Defeats Intratumor Heterogeneity in a Subset of Non-Small Cell Lung Cancers.Myc Cooperates with Ras by Programming Inflammation and Immune Suppression.

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Combined Inactivation of MYC and K-Ras oncogenes reverses tumorigenesis in lung adenocarcinomas and lymphomas.

http://www.wikidata.org/entity/Q33332189

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2008 nî lūn-bûn

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P2860

Mutations in the EGFR kinase domain mediate STAT3 activation via IL-6 production in human lung adenocarcinomas

Development of new mouse lung tumor models expressing EGFR T790M mutants associated with clinical resistance to kinase inhibitors

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

The impact of human EGFR kinase domain mutations on lung tumorigenesis and in vivo sensitivity to EGFR-targeted therapies.

MET amplification leads to gefitinib resistance in lung cancer by activating ERBB3 signaling.

The concept of synthetic lethality in the context of anticancer therapy

Gefitinib-sensitizing EGFR mutations in lung cancer activate anti-apoptotic pathways

Signal transducer and activator of transcription 3 is required for the oncogenic effects of non-small-cell lung cancer-associated mutations of the epidermal growth factor receptor

Induction and apoptotic regression of lung adenocarcinomas by regulation of a K-Ras transgene in the presence and absence of tumor suppressor genes

Cancer. Addiction to oncogenes--the Achilles heal of cancer

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