Molecular characterization of the tumor microenvironment in breast cancer.

By M. Allinen, Rameen Beroukhim, Li Cai, C. Brennan, J. Lahti-Domenici, Haiyan Huang, D. Porter, Min Hu, L. Chin, A. Richardson and 3 more. Cancer Cell, 2004

1,266 citations recorded by the source corpus.

Subfields: Immunology, Immunology and Allergy, Oncology

View Paper: https://www.semanticscholar.org/paper/491740d97d81af147e6b19b396427eab5d144368

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Citations in the corpus

PDGF-C mediates the angiogenic and tumorigenic properties of fibroblasts associated with tumors refractory to anti-VEGF treatment. (2009, background): “TAFs have been reported to upregulate CXCL14 and SDF-1 (CXCL12), which may directly stimulate tumor cell proliferation (Allinen et al., 2004; Orimo et al., 2005).”
Fibroblast Heterogeneity and Immunosuppressive Environment in Human Breast Cancer. (2018, neutral): “, 2014), tumor-promoting activities of CAFs have been widely described (Olumi et al., 1999; Allinen et al., 2004; Orimo et al., 2005; Kalluri and Zeisberg, 2006; Erez et al., 2010; Toullec et al., 2010; Hammer et al., 2017).”
Modeling tissue morphogenesis and cancer in 3D. (2007, positive): “Gene expression is selectively altered in the tumor microenvironment (Allinen et al., 2004), and specific stromal factors can promote tumor growth and angiogenesis (Bissell and Labarge, 2005; Orimo et al., 2005).”
The tumour-induced systemic environment as a critical regulator of cancer progression and metastasis (2014, background): “Shown are tumour-derived factors that act to affect: (1) the initiating tumour from which they were derived; (2) distant tissues before metastatic dissemination; or (3) colonization and progression of disseminated micrometastases at distant anatomical sites.”
Cancer invasion and the microenvironment: plasticity and reciprocity. (2011, positive): “, 2008), as well as chronic growth factor stimulation and inflammation (Allinen et al., 2004; Polyak et al., 2009) (Figure 6B).”
Cysteine cathepsins: multifunctional enzymes in cancer (2006, background): “In ductal carcinoma in situ of the breast, there is increased expression of the cysteine cathepsins F, K and”
Fibroblast heterogeneity in the cancer wound (2014, background): “CXCL12 is highly overexpressed in CAFs (Allinen et al., 2004) and several in vitro and in vivo models have revealed a key role of CXCL12 and its receptor CXCR4 in tumor–stroma interactions.”
Gene expression profiling of the tumor microenvironment during breast cancer progression (2009, methodology): “Using the serial analysis of gene expression technique, Allinen and coworkers performed the first systematic profiling of the various stromal cell types isolated via cell-type-specific cell surface markers and magnetic beads [7].”
The tumour microenvironment as a target for chemoprevention (2007, background): “Genetic changes in stromal cells adjacent to breast cancer cells have been described in many publications, although these might not always be present (see Ref”
CXCL12/CXCR4/CXCR7 Chemokine Axis and Cancer Progression (2010, background): “As seen in other tumors, hypoxia is able to induce a significant increase in the expression levels of CXCR4 on NSCLC cells through the VHL-HIF-1α pathway, supporting the notion that HIF-1α-mediated upregulation of CXCR4 may be a common response of tumor cells to hypoxia [90, 91].”
Bone marrow-derived myofibroblasts contribute to the mesenchymal stem cell niche and promote tumor growth (2011, positive): “CAFs isolated from breast cancer tissue promote proliferation of cancer cell lines, increase angiogenesis to a greater extent, and have a distinct gene expression pattern compared to normal fibroblasts (Allinen et al., 2004).”
CXCR4 Regulates Growth of Both Primary and Metastatic Breast Cancer (2004, background): “High levels of CXCL12 are produced in sites commonly affected by breast cancer metastases, and expression of the cognate receptor CXCR4 is higher in premalignant breast epithelium and breast cancer cells compared with normal breast epithelium (3, 6, 7).”