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Author: Dmitry I. Gabrilovich
Publisher: Springer Science & Business Media
ISBN: 1489980563
Category : Medical
Languages : en
Pages : 471
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Book Description
Tumor-Induced Immune Suppression - Prospects and Progress in Mechanisms and Therapeutic Reversal presents a comprehensive overview of large number of different mechanisms of immune dysfunction in cancer and therapeutic approaches to their correction. This includes the number of novel mechanisms that has never before been discussed in previous monographs. The last decades were characterized by substantial progress in the understanding of the role of the immune system in tumor progression. Researchers have learned how to manipulate the immune system to generate tumor specific immune response, which raises high expectations for immunotherapy to provide breakthroughs in cancer treatment. It is increasingly clear that tumor-induced abnormalities in the immune system not only hampers natural tumor immune surveillance, but also limits the effect of cancer immunotherapy. Therefore, it is critically important to understand the mechanisms of tumor-induced immune suppression to make any progress in the field and this monograph provides these important insights.
Author: Dmitry I. Gabrilovich
Publisher: Springer Science & Business Media
ISBN: 1489980563
Category : Medical
Languages : en
Pages : 471
Get Book Here
Book Description
Tumor-Induced Immune Suppression - Prospects and Progress in Mechanisms and Therapeutic Reversal presents a comprehensive overview of large number of different mechanisms of immune dysfunction in cancer and therapeutic approaches to their correction. This includes the number of novel mechanisms that has never before been discussed in previous monographs. The last decades were characterized by substantial progress in the understanding of the role of the immune system in tumor progression. Researchers have learned how to manipulate the immune system to generate tumor specific immune response, which raises high expectations for immunotherapy to provide breakthroughs in cancer treatment. It is increasingly clear that tumor-induced abnormalities in the immune system not only hampers natural tumor immune surveillance, but also limits the effect of cancer immunotherapy. Therefore, it is critically important to understand the mechanisms of tumor-induced immune suppression to make any progress in the field and this monograph provides these important insights.
Author: Dmitry I. Gabrilovich
Publisher: Springer Science & Business Media
ISBN: 0387691189
Category : Medical
Languages : en
Pages : 304
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Book Description
This monograph, for the first time, presents a comprehensive overview of different mechanisms of immune dysfunction in cancer as well as therapeutic approaches to their correction. It discusses a number of new mechanisms that have never been discussed in a monograph before: T-cell inhibitory molecules, regulatory tolerogenic DCs, and signaling pathways in antigen-presenting cells involved in T-cell tolerance. There is now a pressing need to discuss the already described and newly emerging mechanisms to see how they can be put together in a more or less cohesive structure and how they can help to improve immune response to tumors.
Author: Craig Anthony Mullen
Publisher:
ISBN:
Category : Immunosuppression
Languages : en
Pages : 244
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Book Description
Author: Suzanne Ostrand-Rosenberg
Publisher: Elsevier Inc. Chapters
ISBN: 0128059249
Category : Medical
Languages : en
Pages : 50
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Book Description
Immune escape and inflammation are now recognized as hallmarks of tumor onset and progression. Myeloid-derived suppressor cells (MDSC), a heterogeneous population of immature myeloid cells that are present in virtually all patients and mice with advanced cancer, are a major contributor to immune escape through their inhibition of innate and adaptive antitumor immunity. Immature myeloid cells with the phenotype of MDSC are present in low levels in healthy individuals; however, chronic inflammation perturbs normal myelopoiesis and mobilizes MDSC, thereby facilitating tumor growth. This chapter reviews the experimental and patient findings that identified MDSC as an immune suppressive cell population mediating tumor immune escape, the phenotypic characteristics and heterogeneity of MDSC from cancer patients and mice, the diversity of mechanisms used by MDSC to facilitate tumor progression and metastasis, the pro-inflammatory mediators that drive the induction and accumulation of MDSC, and therapeutic approaches that have been developed to reduce MDSC levels and/or impair MDSC function.
Author: Robert C. Bast, Jr.
Publisher: John Wiley & Sons
ISBN: 111900084X
Category : Medical
Languages : en
Pages : 2008
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Book Description
Holland-Frei Cancer Medicine, Ninth Edition, offers a balanced view of the most current knowledge of cancer science and clinical oncology practice. This all-new edition is the consummate reference source for medical oncologists, radiation oncologists, internists, surgical oncologists, and others who treat cancer patients. A translational perspective throughout, integrating cancer biology with cancer management providing an in depth understanding of the disease An emphasis on multidisciplinary, research-driven patient care to improve outcomes and optimal use of all appropriate therapies Cutting-edge coverage of personalized cancer care, including molecular diagnostics and therapeutics Concise, readable, clinically relevant text with algorithms, guidelines and insight into the use of both conventional and novel drugs Includes free access to the Wiley Digital Edition providing search across the book, the full reference list with web links, illustrations and photographs, and post-publication updates
Author: Angus G. Dalgleish
Publisher: Springer Science & Business Media
ISBN: 0387262830
Category : Medical
Languages : en
Pages : 260
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Book Description
A link between inflammation and cancer has been established many years ago, yet it is only recently that the potential significance of this connection has become apparent. Although several examples of chronic inflammatory conditions, often induced by persistent irritation and/or infection, developing into cancer have been known for some time, there has been a notable resistance to contemplate the possibility that this association may apply in a causative way to other cancers. Examples for such progression from chronic inflammation to cancer are colon carcinoma developing with increased frequency in patients with ulcerative colitis, and the increased incidence of bladder cancer in patients suffering from chronic Schistosoma infection. Inflammation and cancer have been recognized to be linked in another context for many years, i.e., with regards to pathologies resembling chronic lacerations or 'wounds that do not heal.' More recently, the immunology of wound healing has given us clues as to the mechanistic link between inflammation and cancer, in as much as wounds and chronic inflammation turn off local cell-mediated immune responses and switch on growth factor release as well the growth of new blood vessels - angiogenesis. Both of these are features of most types of tumours, which suggest that tumours may require an immunologically shielded milieu and a growth factor-rich environment.
Author: George C. Prendergast
Publisher: Academic Press
ISBN: 0123946336
Category : Medical
Languages : en
Pages : 679
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Book Description
There has been major growth in understanding immune suppression mechanisms and its relationship to cancer progression and therapy. This book highlights emerging new principles of immune suppression that drive cancer, and it offers radically new ideas about how therapy can be improved by attacking these principles. Following work that firmly establishes immune escape as an essential trait of cancer, recent studies have now defined specific mechanisms of tumor immune suppression. It also demonstrates how attacking tumors with molecular targeted therapeutics or traditional chemotherapeutic drugs can produce potent anti-tumor effects in preclinical models. This book provides basic, translational, and clinical cancer researchers with an indispensable overview of immune escape as a critical trait in cancer and how applying specific combinations of immunotherapy and chemotherapy to attack this trait may radically improve the treatment of advanced disease. Offers a synthesis of concepts that are useful to cancer immunologists and pharmacologists, who tend to work in disparate fields with little cross-communication Drs. Prendergast and Jaffee are internationally recognized leaders in cancer biology and immunology who have created a unique synthesis of fundamental and applied concepts in this important new area of cancer research Summarizes the latest insights into how immune escape defines an essential trait of cancer Includes numerous illustrations, including how molecular-targeted therapeutic drugs or traditional chemotherapy can be combined with immunotherapy to improve anti-tumor efficacy and how reversing immune suppression by the tumor can cause tumor regression
Author: James H. Finke
Publisher: Springer Science & Business Media
ISBN: 1592597432
Category : Medical
Languages : en
Pages : 392
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Book Description
Leading investigators and clinicians detail the different mechanisms used by tumors to escape and impair the immune system and then spell out possible clinical strategies to prevent or reverse tumor-induced immune dysfunction. The authors review the mechanisms of immune dysfunction and evasion mechanisms in histologically diverse human tumors, focusing on tumor-induced molecular defects in T cells and antigen-presenting cells (dendritic cells and tumors), that may serve as biomarkers for patient prognosis. They discuss the means by which these immune functions may be protected or restored in order to more effectively support the process of tumor rejection in situ. Cutting-edge techniques are outlined with the capacity to monitor the strength and quality of patients' immune responses using immunocytometry, MHC-peptide tetramers combined with apoptosis assay, ELISPOT assay, and detection of MHC-TAA peptide complexes on tumor cells.
Author:
Publisher:
ISBN:
Category :
Languages : en
Pages : 14
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Book Description
Chemokines play a pivotal role in the maturation of the immune system, and in the initiation, and maintenance of an immune response. Because of their key role in the immune response, the aberrant expression of chemokines can have a profound effect on the ability of T cells to respond to antigen. We have found that several breast cancer cell lines produced chemokines capable of recruiting T cells. However, instead of increasing anti-tumor immunity, the tumor-derived chemokines may have prevented an effective immune response by desensitizing T-cell chemokine receptors. Our hypothesis is that disrupting the synthesis of tumor-derived chemokines (using anti-sense technology) will remove tumor-induced immune suppression and enhance the immunogenicity of the tumor. In order to test this hypothesis we have generated stable clones that lack MCP-l and RANTES production compared to the parental tumor cell line. Using these tumors we will determine whether the T cells are better able to elicit an anti-tumor immune response by comparing the immunogenicity of the tumors that do and do not express chemokines. These tumor cells will be evaluated by immunization/challenge experiments and by the ability to generate tumor-specific T cells in vaccine draining lymph nodes.
Author: David H. Munn
Publisher: Elsevier Inc. Chapters
ISBN: 012805929X
Category : Medical
Languages : en
Pages : 31
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Book Description
Indoleamine 2,3-dioxygenase (IDO) is a metabolic pathway implicated in a number of settings that lead to acquired peripheral tolerance. IDO may also participate in the functional tolerance of the immune system towards tumors. Foxp3+ Tregs are major contributors to tumor-induced immune suppression, and emerging evidence links the IDO pathway with Treg activation. IDO-expressing dendritic cells (DCs) can drive the differentiation of naive CD4+ T cells into Foxp3+ Tregs. IDO+ DCs can also directly activate mature, preformed Tregs to mediate enhanced suppression. In experimental models, IDO also stabilizes the suppressive Treg phenotype and prevents inflammation-induced reprogramming of Tregs into pro-inflammatory (T-helper-like) cells. IDO may thus represent an important regulatory checkpoint that enhances Treg activity in tumor-bearing hosts. Drugs that target the IDO pathway may assist in reducing Treg-mediated suppression during antitumor immunotherapy.
