The tumor microenvironment and its role in promoting tumor growth
Oncogene, 2008
2,221 citations recorded by the source corpus.
The tumor microenvironment is created by the tumor and dominated by tumor-induced interactions. Although various immune effector cells are recruited to the tumor site, their anti-tumor functions are downregulated, largely in response to tumor-derived signals. Infiltrates of inflammatory cells present in human tumors are chronic in nature and are enriched in regulatory T cells (Treg) as well as myeloid suppressor cells (MSC). Immune cells in the tumor microenvironment not only fail to exercise antitumor effector functions, but they are co-opted to promote tumor growth. Sustained activation of the NF-κB pathway in the tumor milieu represents one mechanism that appears to favor tumor survival and drive abortive activation of immune cells. The result is tumor escape from the host immune system. Tumor escape is accomplished through the activation of one or several molecular mechanisms that lead to inhibition of immune cell functions or to apoptosis of anti-tumor effector cells. The ability to block tumor escape depends on a better understanding of cellular and molecular pathways operating in the tumor microenvironment. Novel therapeutic strategies that emerge are designed to change the pro-tumor microenvironment to one favoring acute responses and potent anti-tumor activity.
Subfields: Cancer Research, Immunology
View Paper: https://www.semanticscholar.org/paper/82d011f32c9d3cc56ab2e233c0f92ed98ef5ac7a
Citations in the corpus
- Activation of the PD-1 pathway contributes to immune escape in EGFR-driven lung tumors (2013, background): “…factors may act in paracrine to stimulate and transform neighboring cells, while recruiting myeloid derived suppressor cells (MDSC) and Tregs, which are associated with a poor prognosis, in contrast to the tumor infiltrating cytotoxic lymphocytes, which are associated with a better prognosis (28).”
- ER Stress Sensor XBP1 Controls Anti-tumor Immunity by Disrupting Dendritic Cell Homeostasis (2015, background): “In most solid cancers, nonmalignant cells such as leukocytes, vascular cells, and fibroblasts are exposed to similarly harsh microenvironmental conditions while stimulating tumor development and progression (Whiteside, 2008).”
- Core-shell nanoscale coordination polymers combine chemotherapy and photodynamic therapy to potentiate checkpoint blockade cancer immunotherapy (2016, methodology): “When the primary tumours reached B100mm3, mice were randomly divided into seven groups (n1⁄4 6): (1) PBS with irradiation, NCP@pyrolipid (2) without or (3) with irradiation, NCP@pyrolipid plus anti-PD-L1 (4) without or (5) with irradiation, (6) porphysome with irradiation plus anti-PD-L1 and (7) oxa”
- Cancer-Associated Fibroblasts Are Activated in Incipient Neoplasia to Orchestrate Tumor-Promoting Inflammation in an NF-kappaB-Dependent Manner. (2010, background): “Although the involvement of innate and adaptive immune cells in cancer-promoting inflammation is well established (Condeelis and Pollard, 2006; de Visser et al., 2006; Whiteside, 2008), few studies have implicated fibroblasts in this process.”
- New functionalities in the TCGAbiolinks package for the study and integration of cancer data from GDC and GTEx (2019, methodology): “According to the standard defined by the TCGA consortium, 60% tumor purity is the recommended threshold for analyses [29].”
- Why don’t we get more cancer? A proposed role of the microenvironment in restraining cancer progression (2011, background): “Tumors are composed of multiple cell types capable of supporting the malignant cells through the complex network of interactions discussed abov”
- ROS Generation and Antioxidant Defense Systems in Normal and Malignant Cells (2019, background): “This forms a distinct tumor microenvironment that comprises cell-cell and cell-extracellular matrix interactions, as well as many soluble factors [253, 254].”
- CD44v6 is a marker of constitutive and reprogrammed cancer stem cells driving colon cancer metastasis. (2014, background): “The interaction between tumor and its microenvironment is critical for cancer progression, which is promoted by different cytokines produced by stroma or accessory cells present in proximity to the tumor lesion (Whiteside, 2008).”