Tumor angiogenesis

Xem 1-20 trên 32 kết quả Tumor angiogenesis
  • Publishing Process Manager Iva Lipovic Technical Editor InTech DTP team Cover InTech Design team First published January, 2013 Printed in Croatia A free online edition of this book is available at www.intechopen.com Additional hard copies can be obtained from orders@intechopen.com Research Directions in Tumor Angiogenesis, Edited by Jianyuan Chai p. cm. ISBN 978-953-51-0963-1

    pdf300p xumxaxumxit 09-04-2013 26 12   Download

  • Angiogenesis is an extension process of the cardiovascular network within human body. It is usually triggered by the demand of oxygen and nutrients from the fast growing tissue and uncontrollably dividing cells, as seen during wound healing and tumor progression. This book focuses on tumor angiogenesis and includes 8 chapters written by highly experienced scholars from five different countries.

    pdf300p phoebe75 19-02-2013 23 5   Download

  • Tham khảo sách 'tumor angiogenesis edited by sophia ran', y tế - sức khoẻ, y học thường thức phục vụ nhu cầu học tập, nghiên cứu và làm việc hiệu quả

    pdf306p bachtuocpaul 15-04-2013 19 4   Download

  • Tumor angiogenesis is a complex process involving many different cell 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.

    pdf6p konheokonmummim 03-12-2010 37 6   Download

  • 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).

    pdf5p konheokonmummim 03-12-2010 36 5   Download

  • Antiangiogenic Therapy Understanding the molecular mechanisms that regulate tumor angiogenesis may provide unique opportunities for cancer treatment. Acquired drug resistance of tumor cells due to their high intrinsic mutation rate is a major cause of treatment failure in human cancers. ECs comprising the tumor vasculature are genetically stable and do not share genetic changes with tumor cells; the EC apoptosis pathways are therefore intact.

    pdf5p konheokonmummim 03-12-2010 30 5   Download

  • Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành y học dành cho các bạn tham khảo đề tài: Expression of Ets-1, Ang-2 and maspin in ovarian cancer and their role in tumor angiogenesis

    pdf6p toshiba22 21-11-2011 23 3   Download

  • Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học quốc tế cung cấp cho các bạn kiến thức về ngành y đề tài: Stanniocalcin-1 promotes tumor angiogenesis through up-regulation of VEGF in gastric cancer cells

    pdf9p toshiba23 18-11-2011 12 1   Download

  • Although technical advances have resulted in marked improvements in the ability to diag‐ nose and surgically treat primary and metastatic brain tumors, the incidence and mortality rates of these tumors is increasing. Particularly affected are young adults and the elderly. The present standard treatment modalities following surgical resection including cranial irradia‐ tion and systemic or local chemotherapy each have limited efficacy and serious adverse side effects.

    pdf648p lyly_5 22-03-2013 20 5   Download

  • Cancer Cell Biology The treatment of most human cancers with conventional cytoreductive agents has been unsuccessful due to the Gompertzian-like growth kinetics of solid tumors (i.e., tumor growth is exponential in small tumors, with increasing doubling times as tumors expand; since conventional chemotherapeutic agents target proliferating cells, noncycling cells in large tumors are relatively resistant). Genetic instability is inherent in most cancer cells and predisposes to the development of intrinsic and acquired drug resistance. Thus, although tumors arise from a single cell (i.e.

    pdf5p konheokonmummim 03-12-2010 47 4   Download

  • Imatinib has also demonstrated targeted activity in other diseases, including gastrointestinal stromal tumors (GIST), rare mesenchymal tumors of the GI tract (stomach and small intestine). The pathogenic molecular event for most patients with this disease is mutation of the proto-oncogene c-Kit, leading to the constitutive activation of this receptor tyrosine kinase without the binding of its physiologic ligand, stem cell factor. About 10% of GISTs encode activating mutations of the PDGFRα instead of c-Kit.

    pdf5p konheokonmummim 03-12-2010 40 4   Download

  • PI3K is a heterodimeric lipid kinase that catalyses the conversion of phosphatidylinositol bisphosphate (PIP2) to phosphatidylinositol trisphosphate (PIP3), which acts as a plasma membrane docking site for proteins that contain a pleckstrin homology (PH) domain. These include the serine/threonine kinases Akt and PDK1 that are key downstream effectors of PI3K action (Fig. 80-2). The PI3K pathway is activated in 30–40% of human cancers and is thought to play a critical role in tumor cell survival, proliferation, growth, and glucose utilization.

    pdf5p konheokonmummim 03-12-2010 39 4   Download

  • Estrogen receptors (ERs) and androgen receptors, members of the steroid hormone family of nuclear receptors, are targets of inhibition by drugs used to treat breast and prostate cancers, respectively. Tamoxifen, a partial agonist and antagonist of ER function, can mediate tumor regression in metastatic breast cancer and can prevent disease recurrence in the adjuvant setting, saving thousands of lives each year. Tamoxifen binds to the ER and modulates its transcriptional activity, inhibiting activity in the breast but promoting activity in bone and uterine epithelium.

    pdf5p konheokonmummim 03-12-2010 34 4   Download

  • Figure 80-6 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. Critical components include activated transforming growth factor beta (TGF-β) and the hepatocyte growth factor (HGF)/c-Met pathways, as well as changes in the expression of adhesion molecules that mediate cell-cell and cellextracellular matrix interactions.

    pdf5p konheokonmummim 03-12-2010 33 4   Download

  • New Concepts in the Development of Cancer Therapeutics Cancer Stem Cells It has long been recognized that only a small proportion of the cells within a tumor are capable of initiating colonies in vitro or of forming tumors at high efficiency when injected into immunocompromised NOD/SCID mice. Current work indicates that human acute and chronic myeloid leukemias (AML and CML) have a small population of cells (

    pdf5p konheokonmummim 03-12-2010 32 4   Download

  • The bevacizumab experience suggests that inhibition of the VEGF pathway will be most efficacious when combined with agents that directly target tumor cells. This also appears to be the case in the development of small-molecule inhibitors (SMI) that target VEGF receptor tyrosine kinase activity but are also inhibitory to other kinases that are expressed by tumor cells and important for their proliferation and survival.

    pdf6p konheokonmummim 03-12-2010 35 4   Download

  • Signaling Pathways Downstream of Rtks: Ras and PI3K Several oncogene and tumor-suppressor gene products are components of signal transduction pathways that emanate from RTK activation (Fig. 80-2). The most extensively studied are the Ras/mitogen-activated protein (MAP) kinase pathway and the phosphatidylinositol-3-kinase (PI3K) pathway, both of which regulate multiple processes in cancer cells, including cell cycle progression, resistance to apoptotic signals, angiogenesis, and cell motility.

    pdf5p konheokonmummim 03-12-2010 28 3   Download

  • Oncogene Addiction and Synthetic Lethality The concepts of oncogene addiction and synthetic lethality have spurred new drug development targeting oncogene and tumor-suppressor pathways. 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.

    pdf5p konheokonmummim 03-12-2010 31 3   Download

  • Normalization of tumor blood vessels due to inhibition of VEGF signaling. A. Blood vessels in normal tissues exhibit a regular hierarchical branching pattern that delivers blood to tissues in a spatially and temporally efficient manner to meet the metabolic needs of the tissue (top). At the microscopic level, tight junctions are maintained between endothelial cells (EC), which are adherent to a thick and evenly distributed basement membrane (BM). Pericytes form a surrounding layer that provides trophic signals to the EC and helps maintain proper vessel tone.

    pdf5p konheokonmummim 03-12-2010 31 3   Download

  • Several general principles have arisen from these studies. Bevacizumab appears to potentiate the effects of many different types of active chemotherapeutic regimens used to treat a variety of different tumor types. 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).

    pdf5p konheokonmummim 03-12-2010 28 3   Download

CHỦ ĐỀ BẠN MUỐN TÌM

Đồng bộ tài khoản