Special Issue "Cytokines in Cancer"

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A special issue of Cancers (ISSN 2072-6694).

Deadline for manuscript submissions: closed (20 January 2014)

Special Issue Editor

Guest Editor
Dr. Howard A. Young

Principal Investigator & Deputy Lab Chief, Laboratory of Experimental Immunology, Cancer and Inflammation Program, Center for Cancer Research, National Cancer Institute at Frederick, Bldg. 560/31-23, Chandler Street, Frederick, MD 21702-1201, USA
Website | E-Mail
Phone: 301-846-5743
Fax: +1 301 846 1673
Interests: interferon-gamma; cytokines, interferons, post transcriptional mRNA regulation; interleukins

Special Issue Information

Dear Colleagues,

Cancer is a complex disease that is regulated during its initiation, development, and progression by many different host factors. Cytokines play an important role in all aspects of cancer biology. Cytokines trigger specific signal transduction pathways within cancer cells and, in the tumor microenvironment, greatly impact the tumor cell itself as well as the host response to the malignancy. Furthermore, cytokines and interferons now play an important role in cancer immunotherapies, as they are being used to direct immune effector cells to directly attack and destroy the tumor cells. In this issue, "Cytokines and Cancer," authors are invited to contribute original research papers or review articles that will provide further insights on the direct impact of cytokines on cancer cells, the biological significance of cytokine production by tumor cells, the role of cytokines on the tumor microenvironment, and the use of cytokines to manipulate the host response as a treatment for the disease.

Dr. Howard A. Young (EBM of Pharmaceuticals)
Guest Editor

Submission

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. Papers will be published continuously (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are refereed through a peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cancers is an international peer-reviewed Open Access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 800 CHF (Swiss Francs).

Keywords

  • cytokines
  • interleukins
  • interferon
  • cancer
  • innate immunity
  • immunotherapy

Published Papers (5 papers)

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Research

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Open AccessArticle Effect of the Premalignant and Tumor Microenvironment on Immune Cell Cytokine Production in Head and Neck Cancer
Cancers 2014, 6(2), 756-770; doi:10.3390/cancers6020756
Received: 10 January 2014 / Revised: 12 March 2014 / Accepted: 14 March 2014 / Published: 2 April 2014
Cited by 10 | PDF Full-text (574 KB) | HTML Full-text | XML Full-text
Abstract
Head and neck squamous cell carcinoma (HNSCC) is marked by immunosuppression, a state in which the established tumor escapes immune attack. However, the impact of the premalignant and tumor microenvironments on immune reactivity has yet to be elucidated. The purpose of this study
[...] Read more.
Head and neck squamous cell carcinoma (HNSCC) is marked by immunosuppression, a state in which the established tumor escapes immune attack. However, the impact of the premalignant and tumor microenvironments on immune reactivity has yet to be elucidated. The purpose of this study was to determine how soluble mediators from cells established from carcinogen-induced oral premalignant lesions and HNSCC modulate immune cell cytokine production. It was found that premalignant cells secrete significantly increased levels of G-CSF, RANTES, MCP-1, and PGE2 compared to HNSCC cells. Splenocytes incubated with premalignant supernatant secreted significantly increased levels of Th1-, Th2-, and Th17-associated cytokines compared to splenocytes incubated with HNSCC supernatant. These studies demonstrate that whereas the premalignant microenvironment elicits proinflammatory cytokine production, the tumor microenvironment is significantly less immune stimulatory and may contribute to immunosuppression in established HNSCC. Full article
(This article belongs to the Special Issue Cytokines in Cancer)

Review

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Open AccessReview CCL21 Cancer Immunotherapy
Cancers 2014, 6(2), 1098-1110; doi:10.3390/cancers6021098
Received: 1 March 2014 / Revised: 22 March 2014 / Accepted: 28 April 2014 / Published: 7 May 2014
Cited by 7 | PDF Full-text (503 KB) | HTML Full-text | XML Full-text
Abstract
Cancer, a major health problem, affects 12 million people worldwide every year. With surgery and chemo-radiation the long term survival rate for the majority of cancer patients is dismal. Thus novel treatments are urgently needed. Immunotherapy, the harnessing of the immune system to
[...] Read more.
Cancer, a major health problem, affects 12 million people worldwide every year. With surgery and chemo-radiation the long term survival rate for the majority of cancer patients is dismal. Thus novel treatments are urgently needed. Immunotherapy, the harnessing of the immune system to destroy cancer cells is an attractive option with potential for long term anti-tumor benefit. Cytokines are biological response modifiers that stimulate anti-tumor immune responses. In this review, we discuss the anti-tumor efficacy of the chemotactic cytokine CCL21 and its pre-clinical and clinical application in cancer. Full article
(This article belongs to the Special Issue Cytokines in Cancer)
Open AccessReview Role of Tertiary Lymphoid Structures (TLS) in Anti-Tumor Immunity: Potential Tumor-Induced Cytokines/Chemokines that Regulate TLS Formation in Epithelial-Derived Cancers
Cancers 2014, 6(2), 969-997; doi:10.3390/cancers6020969
Received: 20 January 2014 / Revised: 19 March 2014 / Accepted: 31 March 2014 / Published: 23 April 2014
Cited by 7 | PDF Full-text (405 KB) | HTML Full-text | XML Full-text
Abstract
Following the successes of monoclonal antibody immunotherapies (trastuzumab (Herceptin®) and rituximab (Rituxan®)) and the first approved cancer vaccine, Provenge® (sipuleucel-T), investigations into the immune system and how it can be modified by a tumor has become an exciting
[...] Read more.
Following the successes of monoclonal antibody immunotherapies (trastuzumab (Herceptin®) and rituximab (Rituxan®)) and the first approved cancer vaccine, Provenge® (sipuleucel-T), investigations into the immune system and how it can be modified by a tumor has become an exciting and promising new field of cancer research. Dozens of clinical trials for new antibodies, cancer and adjuvant vaccines, and autologous T and dendritic cell transfers are ongoing in hopes of identifying ways to re-awaken the immune system and force an anti-tumor response. To date, however, few consistent, reproducible, or clinically-relevant effects have been shown using vaccine or autologous cell transfers due in part to the fact that the immunosuppressive mechanisms of the tumor have not been overcome. Much of the research focus has been on re-activating or priming cytotoxic T cells to recognize tumor, in some cases completely disregarding the potential roles that B cells play in immune surveillance or how a solid tumor should be treated to maximize immunogenicity. Here, we will summarize what is currently known about the induction or evasion of humoral immunity via tumor-induced cytokine/chemokine expression and how formation of tertiary lymphoid structures (TLS) within the tumor microenvironment may be used to enhance immunotherapy response. Full article
(This article belongs to the Special Issue Cytokines in Cancer)
Open AccessReview HiJAK’d Signaling; the STAT3 Paradox in Senescence and Cancer Progression
Cancers 2014, 6(2), 741-755; doi:10.3390/cancers6020741
Received: 8 February 2014 / Revised: 8 March 2014 / Accepted: 11 March 2014 / Published: 26 March 2014
Cited by 9 | PDF Full-text (978 KB) | HTML Full-text | XML Full-text
Abstract
Clinical and epidemiological data have associated chronic inflammation with cancer progression. Most tumors show evidence of infiltrating immune and inflammatory cells, and chronic inflammatory disorders are known to increase the overall risk of cancer development. While immune cells are often observed in early
[...] Read more.
Clinical and epidemiological data have associated chronic inflammation with cancer progression. Most tumors show evidence of infiltrating immune and inflammatory cells, and chronic inflammatory disorders are known to increase the overall risk of cancer development. While immune cells are often observed in early hyperplastic lesions in vivo, there remains debate over whether these immune cells and the cytokines they produce in the developing hyperplastic microenvironment act to inhibit or facilitate tumor development. The interleukin-6 (IL-6) family of cytokines, which includes IL-6 and oncostatin M (OSM), among others (LIF, CT-1, CNTF, and CLC), are secreted by immune cells, stromal cells, and epithelial cells, and regulate diverse biological processes. Each of the IL-6 family cytokines signals through a distinct receptor complex, yet each receptor complex uses a shared gp130 subunit, which is critical for signal transduction following cytokine binding. Activation of gp130 results in the activation of Signal Transducer and Activator of Transcription 3 (STAT3), and the Mitogen-Activated Protein Kinase (MAPK) and Phosphatidylinositol 3-Kinase (PI3K) signaling cascades. Tumor suppressive signaling can often be observed in normal cells following prolonged STAT3 activation. However, there is mounting evidence that the IL-6 family cytokines can contribute to later stages of tumor progression in many ways. Here we will review how the microenvironmental IL-6 family cytokine OSM influences each stage of the transformation process. We discuss the intrinsic adaptations a developing cancer cell must make in order to tolerate and circumvent OSM-mediated growth suppression, as well as the OSM effectors that are hijacked during tumor expansion and metastasis. We propose that combining current therapies with new ones that suppress the signals generated from the tumor microenvironment will significantly impact an oncologist’s ability to treat cancer. Full article
(This article belongs to the Special Issue Cytokines in Cancer)
Open AccessReview Structural Pathways of Cytokines May Illuminate Their Roles in Regulation of Cancer Development and Immunotherapy
Cancers 2014, 6(2), 663-683; doi:10.3390/cancers6020663
Received: 26 February 2014 / Revised: 11 March 2014 / Accepted: 12 March 2014 / Published: 25 March 2014
Cited by 7 | PDF Full-text (5474 KB) | HTML Full-text | XML Full-text
Abstract
Cytokines are messengers between tissues and the immune system. They play essential roles in cancer initiation, promotion, metastasis, and immunotherapy. Structural pathways of cytokine signaling which contain their interactions can help understand their action in the tumor microenvironment. Here, our aim is to
[...] Read more.
Cytokines are messengers between tissues and the immune system. They play essential roles in cancer initiation, promotion, metastasis, and immunotherapy. Structural pathways of cytokine signaling which contain their interactions can help understand their action in the tumor microenvironment. Here, our aim is to provide an overview of the role of cytokines in tumor development from a structural perspective. Atomic details of protein-protein interactions can help in understanding how an upstream signal is transduced; how higher-order oligomerization modes of proteins can influence their function; how mutations, inhibitors or antagonists can change cellular consequences; why the same protein can lead to distinct outcomes, and which alternative parallel pathways can take over. They also help to design drugs/inhibitors against proteins de novo or by mimicking natural antagonists as in the case of interferon-γ. Since the structural database (PDB) is limited, structural pathways are largely built from a series of predicted binary protein-protein interactions. Below, to illustrate how protein-protein interactions can help illuminate roles played by cytokines, we model some cytokine interaction complexes exploiting a powerful algorithm (PRotein Interactions by Structural Matching—PRISM). Full article
(This article belongs to the Special Issue Cytokines in Cancer)

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