The Journal for ImmunoTherapy of Cancer (JITC) is the official journal of the Society for Immunotherapy of Cancer (SITC). This open access, peer-reviewed journal not only serves as the global voice of the society, but also a targeted outlet for the publication of original research articles, literature reviews, position papers and discussion on all aspects of tumor immunology and cancer immunotherapy—from basic research to clinical application.
Today, more than ever before, the tremendous excitement in the field and the increased momentum brought about by the latest approvals of immunotherapy-based treatments in various cancer types has shown the clear need for the Journal for ImmunoTherapy of Cancer, an outlet devoted to and created by today's leaders in the field.
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JITC is indexed in six major indexing sources, including PubMed, PubMed Central, MEDLINE, the Directory of Open Access journals, Scopus, and Thomson Reuters’ Emerging Sources Citation Index (ESCI). The ESCI is part of the robust Web and Science collection, the world’s largest compilation of research data, books, journals, proceedings, publications, and patents.
As a way to say thank you to the dedicated society members who tirelessly work to advance the science and ultimately to improve the lives of patients with cancer, SITC is pleased to offer society members waived article processing charges for manuscripts accepted through 2017. To take advantage of this member benefit, contact SITC at +1 414-271-2456 or firstname.lastname@example.org for your member code.
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Cancer immunotherapy and in particular monoclonal antibodies blocking the inhibitory programed cell death 1 pathway (PD-1/PD-L1) have made a significant impact on the treatment of cancer patients in recent years. However, despite the remarkable clinical efficacy of these agents in a number of malignancies, it has become clear that they are not sufficiently active for many patients. Initial evidence, for example with combined inhibition of PD-1 and CTLA-4 in melanoma and non-small cell lung cancer (NSCLC), has highlighted the potential to further enhance the clinical benefits of monotherapies by combining agents with synergistic mechanisms of action...
Assays of the abundance of immune cell populations in the tumor microenvironment promise to inform immune oncology research and the choice of immunotherapy for individual patients. We propose to measure the intratumoral abundance of various immune cell populations with gene expression. In contrast to IHC and flow cytometry, gene expression assays yield high information content from a clinically practical workflow. Previous studies of gene expression in purified immune cells have reported hundreds of genes showing enrichment in a single cell type, but the utility of these genes in tumor samples is unknown. We use co-expression patterns in large tumor gene expression datasets to evaluate previously reported candidate cell type marker genes lists, eliminate numerous false positives and identify a subset of high confidence marker genes...
Multiple anti-PD-L1/PD-1 checkpoint monoclonal antibodies (MAb) have shown clear evidence of clinical benefit. All except one have been designed or engineered to omit the possibility to mediate antibody-dependent cell-mediated cytotoxicity (ADCC) as a second potential mode of anti-tumor activity; the reason for this is the concern of lysis of PD-L1 positive immune cells. Avelumab is a fully human IgG1 MAb which has been shown in prior in vitro studies to mediate ADCC versus a range of human tumor cells, and clinical studies have demonstrated anti-tumor activity versus a range of human cancers. This study was designed to investigate the effect on immune cell subsets in the peripheral blood of cancer patients prior to and following multiple administrations of avelumab...
This may be due to an alternate immune checkpoint, CD200 (OX2) checkpoint blockade. The immuneosuppressive CD200 protein shuts down the immune system through multiple mechanisms (Xiong et al, 2016). We demonstrated that human glioblastoma in the top ...
While I agree with Stephanie's detailed account, simply put checkpoint molecules are a signature of exhausted/ chronically stimulated lymphocytes and therefore serves as a feedback mechanism to mitigate the immune activation from entering an overdrive ...
Hi Stephanie many thanks for your ample reply. It makes sense indeed in order to secure self-antigens. However, is immune system evasion by means of immune checkpoint a matter of quality or quantity? I mean is there a cutoff for "normal"CTLA4, PD1 levels ...
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