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"Balkwill, Richard"
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Bridging the Gap: Some Perspectives from Yerevan, Armenia
The government of Armenia and the Next Page Foundation supported the Sixth International Forum of Translators and Publishers held in Yerevan from 5th to 8th November 2012. Antje Sorensen and Richard Balkwill from the International Publishers Association led a two-day workshop entitled ‘The Role of Copyright System in the Promotion of Publishing as a Cultural Industry’. Presentations on international perspectives on copyright and the mechanics of trading in translation and other rights were blended with discussion and debate. The international issues of digital open access and free information were of less concern to local publishers than the effective application of and compliance to recent copyright laws in the country. Piracy was still sapping publishers’ business and continuing to deter potential foreign collaboration and co-publishing deals. The forum was enriched with an extensive program of cultural events and social gatherings.
Journal Article
Supporting creativity in the supply chain: The role of creative teams in the authoring process
The publishing industry has changed out of all recognition in the last quarter of the twentieth century, but the book has not disappeared as many predicted it would. Technology created an environment in which self-publishing looks easy.
Journal Article
YOUR LETTERS: Write for help
Less well known is The Samaritans' national Correspondence Branch, which offers the same degree of confidential support through the written word.
Newspaper Article
Get it write with The Samaritans
EACH year at this time The Samaritans aim to encourage all those who may be passing through any form of emotional crisis or contemplating suicide to make contact with us via the national emergency telephone number listed in all phone books (08457 90 90 90).
Newspaper Article
Murine CD27⁽⁻⁾ Vγ6⁽⁺⁾ γδ T cells producing IL-17A promote ovarian cancer growth via mobilization of protumor small peritoneal macrophages
Cancer-associated inflammation mobilizes a variety of leukocyte populations that can inhibit or enhance tumor cell growth in situ. These subsets include γδ T cells, which can infiltrate tumors and typically provide large amounts of antitumor cytokines, such as IFN-γ. By contrast, we report here that in a well-established transplantable (ID8 cell line) model of peritoneal/ovarian cancer, γδ T cells promote tumor cell growth. γδ T cells accumulated in the peritoneal cavity in response to tumor challenge and could be visualized within solid tumor foci. Functional characterization of tumor-associated γδ T cells revealed preferential production of interleukin-17A (IL-17), rather than IFN-γ. Consistent with this finding, both T cell receptor (TCR)δ-deficient and IL-17–deficient mice displayed reduced ID8 tumor growth compared with wild-type animals. IL-17 production by γδ T cells in the tumor environment was essentially restricted to a highly proliferative CD27 ⁽⁻⁾ subset that expressed Vγ6 instead of the more common Vγ1 and Vγ4 TCR chains. The preferential expansion of IL-17–secreting CD27 ⁽⁻⁾ Vγ6 ⁽⁺⁾ γδ T cells associated with the selective mobilization of unconventional small peritoneal macrophages (SPMs) that, in comparison with large peritoneal macrophages, were enriched for IL-17 receptor A, and for protumor and proangiogenic molecular mediators, which were up-regulated by IL-17. Importantly, SPMs were uniquely and directly capable of promoting ovarian cancer cell proliferation. Collectively, this work identifies an IL-17–dependent lymphoid/myeloid cross-talk involving γδ T cells and SPMs that promotes tumor cell growth and thus counteracts cancer immunosurveillance.
Journal Article
A CCR4 antagonist reverses the tumor-promoting microenvironment of renal cancer
Elevated expression of the chemokine receptor CCR4 in tumors is associated with poor prognosis in several cancers. Here, we have determined that CCR4 was highly expressed in human renal cell carcinoma (RCC) biopsies and observed abnormal levels of CCR4 ligands in RCC patient plasma. An antagonistic anti-CCR4 antibody had antitumor activity in the RENCA mouse model of RCC. CCR4 inhibition did not reduce the proportion of infiltrating leukocytes in the tumor microenvironment but altered the phenotype of myeloid cells, increased NK cell and Th1 cytokine levels, and reduced immature myeloid cell infiltrate and blood chemokine levels. In spite of prominent changes in the myeloid compartment, the anti-CCR4 antibody did not affect RENCA tumors in T cell-deficient mice, and treatment with an anti-class II MHC antibody abrogated its antitumor activity. We concluded that the effects of the anti-CCR4 antibody required the adaptive immune system and CD4+ T cells. Moreover, CCL17-induced IFN-γ production was reduced when Th1-polarized normal CD4+ T cells were exposed to the CCR4 ligand, evidencing the involvement of CCR4 in Th1/Th2 regulation. The anti-CCR4 antibody, alone or in combination with other immune modulators, is a potential treatment approach to human solid cancers with high levels of CCR4-expressing tumor-infiltrating leukocytes and abnormal plasma CCR4 ligand levels.
Journal Article
B regulatory cells and the tumor-promoting actions of TNF-α during squamous carcinogenesis
The inflammatory cytokine TNF-α has been recognized as a critical tumor promoter, but the effector cells that mediate its action have not been fully characterized. Because B cells regulate squamous and prostate carcinogenesis, and Tnf-/- mice harbor B-cell defects, we investigated the hypothesis that B cells are important effector cells for TNF-α—mediated promotion of cancer development. Using an adoptive transfer strategy and the 7,12-dimethylbenz[α]anthracene/terephthalic acid (DMBA/TPA) two-stage model of skin carcinogenesis, we found that both B cells and TNF-α are critical for the development of DMBA/TPA-induced papilloma. Transfer of B cells from DMBA/TPA-treated wild-type mice to Tnf-/- mice rescued papilloma development to a wild-type level, a result not observed when B cells from Tnf-/- mice were transferred to Rag2-/- mice or when TNF-α was eliminated selectively in B cells. Resistance to papilloma development in Tnf-/- mice was associated with increased IFN-γ and CD8+ T cells in skin and a significant reduction in IL-10—producing B regulatory cells alongside an increase in IFN-γ—producing CD8+ T cells in the spleen. These data indicate that during DMBA/TPA-induced squamous carcinogenesis TNF-α mediates tumor-promoting activity via regulatory B cells that repress antitumor immunity.
Journal Article
Rethinking ovarian cancer II: reducing mortality from high-grade serous ovarian cancer
This Opinion article outlines a set of research priorities, based on discussions held at the 2015 Helene Harris Memorial Trust Ovarian Cancer Action meeting, that the authors believe will reduce incidence and improve outcomes for women with high-grade serous ovarian cancer.
High-grade serous ovarian cancer (HGSOC) accounts for 70–80% of ovarian cancer deaths, and overall survival has not changed significantly for several decades. In this Opinion article, we outline a set of research priorities that we believe will reduce incidence and improve outcomes for women with this disease. This 'roadmap' for HGSOC was determined after extensive discussions at an Ovarian Cancer Action meeting in January 2015.
Journal Article
The tumor-promoting actions of TNF-α involve TNFR1 and IL-17 in ovarian cancer in mice and humans
Cytokines orchestrate the tumor-promoting interplay between malignant cells and the immune system. In many experimental and human cancers, the cytokine TNF-alpha is an important component of this interplay, but its effects are pleiotropic and therefore remain to be completely defined. Using a mouse model of ovarian cancer in which either TNF receptor 1 (TNFR1) signaling was manipulated in different leukocyte populations or TNF-alpha was neutralized by antibody treatment, we found that this inflammatory cytokine maintained TNFR1-dependent IL-17 production by CD4+ cells and that this led to myeloid cell recruitment into the tumor microenvironment and enhanced tumor growth. Consistent with this, in patients with advanced cancer, treatment with the TNF-alpha-specific antibody infliximab substantially reduced plasma IL-17 levels. Furthermore, expression of IL-1R and IL-23R was downregulated in CD4+CD25- cells isolated from ascites of ovarian cancer patients treated with infliximab. We have also shown that genes ascribed to the Th17 pathway map closely with the TNF-alpha signaling pathway in ovarian cancer biopsy samples, showing particularly high levels of expression of genes encoding IL-23, components of the NF-kappaB system, TGF-beta1, and proteins involved in neutrophil activation. We conclude that chronic production of TNF-alpha in the tumor microenvironment increases myeloid cell recruitment in an IL-17-dependent manner that contributes to the tumor-promoting action of this proinflammatory cytokine.
Journal Article