Immunosuppressive networks in the tumour environment and their therapeutic relevance

By W. Zou. Nature Reviews. Cancer, 2005

2,174 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/db09fef13891cc56c5dc09ce3e074060dc8e2754

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Citations in the corpus

Role of chemokines in tumor growth. (2007, background): “There is also immunosuppression through the release of IL-10 and TGF-β from type II tumor-associated macrophages, tumor cells, and fibroblasts [17-20].”
Cancer metastasis: building a framework. (2006, background): “However, this potent response is frequently blunted during the progression of neoplasms by the tumor-derived overexpression of immunosuppressive cytokines such as TGF-β, interleukin-10, and interleukin-23 (Gorelik and Flavell, 2002; Langowski et al., 2006; Zou, 2005).”
Clodronate-liposome-mediated depletion of tumour-associated macrophages: a new and highly effective antiangiogenic therapy approach (2006, background): “Whereas functionally mature myeloid dendritic cells induce potent tumour-associated antigenspecific immunity in vivo, immature myeloid cells (IMCs) either suppress regulatory T cells (Treg) or lead to T-cell unresponsiveness (Zou, 2005).”
Virus-specific T cells engineered to coexpress tumor-specific receptors: persistence and antitumor activity in individuals with neuroblastoma (2008, background): “However, many tumors generate their own immunosuppressive environmen”
Therapeutic targeting of the tumor microenvironment. (2005, neutral): “This significantly dampens the antigen presenting function of DCs, which then contributes to immune tolerance (recently reviewed in Zou, 2005).”
The COX-2/PGE2 pathway: key roles in the hallmarks of cancer and adaptation to the tumour microenvironment. (2009, background): “However, in cancer patients, these anti-tumour immune responses are generally ineffective and increasing evidence suggests that tumours evolve several strategies to escape tumour-specific immunity [116,117].”
Tumor antigen-specific CD8 T cells infiltrating the tumor express high levels of PD-1 and are functionally impaired. (2009, neutral): “of patients 28 (100) Sex Male 16 (57) Female 12 (43) Age 11-20 1 (4) 31-40 5 (18) 41-50 7 (25) 51-60 12 (43) 61-70 3 (11) ECOG 0 17 (61) 1 5 (18) Not available 6 (21) Prior Rx Surgery 22 (79) Chemotherapy 8 (29) Radiotherapy 6 (21) Immunotherapy 17 (61) Any 2 or more 18 (64) Any 3 or more 11 (39) No”
Principles of Cancer Therapy: Oncogene and Non-oncogene Addiction (2009, positive): “However, in the vast majority of cases tumors are able to prevent rejection by effectively suppressing an immune response in the tumor microenvironment (Muller and Scherle, 2006; Zou, 2005).”
Paradoxical roles of the immune system during cancer development (2006, background): “Given that the immune system is designed to eradicate 'damaged' cells or tissues, why does inflammation potentiate cancer development rather than protect against it? One plausible explanation for why tumour cells escape immune-surveillance mechanisms is that neoplastic microenvironments favour polar”
PD-L1 (B7-H1) and PD-1 Pathway Blockade for Cancer Therapy: Mechanisms, Response Biomarkers and Combinations (2016, background): “Mechanistically, PD pathway blockade before ACT may prepare the specific “soil,” the less suppressive tumor microenvironment (1), for the transferred T cells to home and function.”
Inhibitory B7-family molecules in the tumour microenvironment (2008, background): “An imbalance in immune regulation profoundly affects tumour-specific T-cell immunity in the cancer microenvironment and can reshape tumour progression, metastasis and immunotherapy in patients with cance”