Tìm thấy 20+ kết quả cho từ khóa "Cancer Cell Biology and Angiogenesis"
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Cancer Cell Biology and Angiogenesis. Cancer Cell Biology and Angiogenesis: Introduction. Two characteristic features define a cancer: unregulated cell growth and tissue invasion/metastasis. Unregulated cell growth without invasion is a feature of benign neoplasms, or new growths. Cancer is a synonym for malignant neoplasm.. Cancers of epithelial tissues are called carcinomas. cancers of nonepithelial (mesenchymal) tissues are called sarcomas.
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Cancer Cell Biology and Angiogenesis. types that must proliferate, migrate, invade, and differentiate in response to signals from the tumor microenvironment. Endothelial cells (ECs) sprout from host vessels in response to VEGF, bFGF, Ang2, and other proangiogenic stimuli.. Sprouting is stimulated by VEGF/VEGFR2, Ang2/Tie-2, and integrin/extracellular matrix (ECM) interactions.
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Cancer Cell Biology and Angiogenesis. Oncogene signaling pathways are activated during tumor progression and promote metastatic potential.. This figure shows a cancer cell that has undergone epithelial to mesenchymal transition (EMT) under the influence of several environmental signals.
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Cancer Cell Biology and Angiogenesis. Acetylation of the amino terminus of the core histones H3 and H4 induces an open chromatin conformation that promotes transcription initiation.
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Because these pathways regulate proliferation, survival, migration, and angiogenesis, they have been identified as important targets for cancer therapeutics.. Therapeutic targeting of signal transduction pathways in cancer cells.. Three major signal transduction pathways are activated by receptor tyrosine kinases (RTK).
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As discussed earlier in this chapter and outlined in Fig. 80-3, cancer cells become physiologically dependent upon signaling pathways containing activated oncogenes. this can effect proliferation (i.e., mutated Ras, BRAF, overexpressed Myc, or activated tyrosine kinases), survival (overexpression of Bcl-2 or NFκB), cell metabolism (as occurs when HIF-1α and Akt increase dependence on glycolysis), and perhaps angiogenesis (production of VEGF, e.g., renal cell cancer).
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VEGF and its receptors are required for vasculogenesis (the de novo formation of blood vessels from differentiating endothelial cells, as occurs during embryonic development) and angiogenesis under normal (wound healing, corpus luteum formation) and pathologic processes (tumor angiogenesis, inflammatory conditions such as rheumatoid arthritis).
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The dependency or addiction of the cancer cell to pathway A makes it highly vulnerable to inhibitors that target components of this pathway. makes the cell dependent on the function of the other gene. As shown in the figure, if an inhibitor of gene B can be identified, this can cause death of the cancer cell, without harming normal cells (which maintain wild-type function for gene A)
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Curr Opin Cell Biol PMID:. Kaelin Jr WG: The concept of synthetic lethality in the context of anticancer therapy. Nat Rev Cancer . Panares RL, Garcia AA: Bevacizumab in the management of solid tumors.. Sharma SV et al: Epidermal growth factor receptor mutations in lung cancer. Nat Rev Cancer PMID: 17318210]. Sherbenou DW, Drucker BJ: Applying the discovery of the Philadelphia. Nat Rev Mol Cell Biol PMID: 17380161]. Jones PA, Baylin SB: The epigenomics of cancer.
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If cancer stem cells can be identified and isolated, then aberrant signaling pathways that distinguish these cells from normal tissue stem cells can be identified and targeted.. Cancer stem cells play a critical role in the initiation, progression, and resistance to therapy of malignant neoplasms. In normal tissues (left), homeostasis is maintained by asymmetric division of stem cells leading to one progeny cell that will differentiate, and one cell that will maintain the stem cell pool.
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Therapeutic Approaches to Cell Cycle Abnormalities in Cancer. The cell cycle is divided into four phases. The other three phases of the cell cycle are called interphase: G 1 (gap 1), during which the cell determines its readiness to commit to DNA synthesis. Deregulation of the molecular mechanisms controlling cell cycle progression is a hallmark of cancer.
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These pathways can lead to programmed cell death (apoptosis) or irreversible growth arrest (senescence). Much as a panoply of intra- and extracellular signals impinge upon the core cell cycle machinery to regulate cell division, so too these signals are transmitted to a core enzymatic machinery that regulates cell death and survival.. Apoptosis is induced by two main pathways (Fig.
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No phase III trials have demonstrated single-agent activity for bevacizumab. colon and lung cancer trials have demonstrated a lack of activity when used alone. An exception may be renal cell cancer (RCC), a tumor that is specifically dependent upon VEGF as the result of deletion of the VHL tumor suppressor and activation of the HIF-1α transcription factor (see above).
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Acquired mutation in p53 is the most common genetic alteration found in human cancer (>50. germline mutation in p53 is the causative genetic lesion of the Li-Fraumeni familial cancer syndrome. The mutations often abrogate the DNA binding function of p53 that is required for its transcription factor activity and tumor-suppressor functions, and also result in high intracellular levels of p53 protein.
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Most tumors have hypoxic regions due to poor blood flow, and tumor cells in these areas stain positive for HIF-1α expression. tumor cells express high levels of HIF-1α, and VEGF-induced angiogenesis leads to high microvascular density (hence the term hypernephroma).
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Early clinical data indicate that tem has activity in renal cell cancer, perhaps by blocking the translation of the transcription factor hypoxia- inducible factor (HIF)-1α mRNA, a mediator of cellular responses to hypoxia, which requires mTOR activity for efficient translation..
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The three major features of tissue invasion are cell adhesion to the basement membrane, local proteolysis of the membrane, and movement of the cell through the rent in the membrane and the ECM. The rate-limiting step for metastasis is the ability for tumor cells to survive and expand in the novel microenvironment of the metastatic site, and multiple host-tumor interactions determine the ultimate outcome (Fig
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The wild-type EGFR is expressed by many other human cancers, and in colon cancer and head and neck cancers, targeting of the EGFR with a. The gene encoding HER2/neu, a member of the EGFR family, is amplified in ~20% of breast cancers.. Tumors that overexpress HER2/neu are less responsive to chemotherapy, and patients with these tumors have a reduced survival compared with patients with normal levels of HER2/neu.
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The protein product of the Philadelphia chromosome occurs in all patients with chronic myeloid leukemia (CML) and in ~30% of patients with adult acute lymphoid leukemia (ALL) and encodes the fusion protein Bcr-Abl.
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Incre ased OS (20.3 vs 15.6 months), PFS (10.6 vs 6.2 months),. (44.8 vs 34.8%). Incre ased OS (12.9 vs 10.8 months), PFS (7.2 vs. 4.8 months), RR (21.8 vs 9.2%).. Incre ased OS (12.5 vs 10.2 months), PFS (6.4 vs 4.5 months), RR (27.2 vs 10.0%).. Incre ased PFS (11.0 vs 6.2 months), RR (28 vs 14%).