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If you have a question about this talk, please contact Mala Jayasundera.
Experimental and clinical evidence points to the fact that inflammation, particularly chronic inflammation, affects all phases of carcinogenesis. Inflammation favours the initial genetic mutation or epigenetic mechanisms that drive cell transformation and cancer initiation: It acts as a tumour promoter by establishing a tissue microenvironment that allows the tumour to progress and metastasize and by establishing immunosuppressive mechanisms that prevent an effective immune response against the tumour.
The tumour microenvironment has a fundamental impact on growth and spread of malignant disease and contributes at least partially. Resistance to cytotoxic and targeted therapies can no longer be viewed as simply the failure of malignant cell kill. Inflammatory mediators and cells contribute to cancer-related inflammation. This systemic inflammation is in a functional relationship with energy metabolism and genetic instability predisposes individuals to cancer and regulates the neoplastic disease in all its aspects, including the individual response of the organism to the disease and overall morbidity and mortality.
Our research concentrates in particular on the role of myeloid cells within the tumour microenvironment. The evidence that myeloid cells provide tropic support to tumours and the genetic (and pharmacological) experiments that show that inhibition of this support leads to suppressed malignancy strongly argue that these cells or their unique signalling pathways are therapeutic targets.
Knowledge of the cancer-related inflammatory and immune pathways should make it possible to identify molecular targets and to plan rational preventive and therapeutic approaches.
This talk is part of the Cambridge Oncology Seminar Series series.
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Other listsBehavioural and Clincial Neuroscience Seminars Professor Sir Brian Heap Computer Laboratory talks
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