Carcinoma-associated fibroblasts stimulate tumor progression of initiated human epithelium
By A. Cleton-Jansen, HM van Beerendonk, NT ter Haar, P. Eilers, HC van Houwelingen, B. Bonsing, V. Smit, G-JB van Ommen, C. Cornelisse. Breast Cancer Research, 2000
1,276 citations recorded by the source corpus.
TP53 mutation is a strong independent marker for survival in breast cancer with some heterogeneity in the clinical phenotype of various types of mutations. Based on 315 patients with breast carcinoma, we suggest a new model for the differentiation of TP53 mutations. Although TP53 mutation in general was associated with aggressive tumor/patient characteristics, missense mutations outside any conserved or structural domain did not affect the clinical outcome (risk of disseminated disease and death). In contrast, patients with missense mutations affecting amino acids directly involved in DNA or zinc binding displayed a very aggressive clinical phenotype. Null mutations (including missense mutations disrupting the tetramerization domain) and the remaining missense mutations displayed an intermediate aggressive clinical phenotype. When patients with primary early breast cancer were divided into three groups (wild-type together with missense mutations outside structural/conserved domains, null mutations and missense mutations with intermediate clinical phenotype, and very aggressive missense mutations), disease-specific survival rates were 89%, 58%, and 35% (5-year actuarial values, P < 0.0001), respectively. In a Cox proportional hazards analysis, separation of TP53 mutations according to these criteria eliminated the prognostic importance of all investigated classical factors except nodal status.
Subfields: Immunology and Allergy, Oncology, Radiology, Nuclear Medicine and Imaging
View Paper: https://www.semanticscholar.org/paper/14d83677e20c4f78e41a328dc5d53fbe9482be9f
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In Immunology and Allergy
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Citations in the corpus
- Exosome-Based Cell-Cell Communication in the Tumor Microenvironment (2018, background): “Fibroblasts are the most abundant cells in the majority of solid tissues, participating in responses to environmental cues and constituting a frequent target of tumor-derived signals (Olumi et al., 1999; Orimo et al., 2005; Hu et al., 2015).”
- 3D Cell Culture Systems: Advantages and Applications (2015, positive): “Malignancy was induced only when immortalized epithelial cells were grafted along with cancerous fibroblasts (Olumi et al., 1999).”
- Senescent cells, tumor suppression, and organismal aging: good citizens, bad neighbors. (2005, background): “These carcinomamassociated fibroblasts are components of the so-called areactive stroma, which facilitates the progression of epirthelial cancers (Olumi et al., 1999; Park et al., 2000; Tlsty cand Hein, 2001).”
- The Hallmarks of Cancer Review (2000, background): “Indeed, in some tumors, these cooperating cells may eventually depart from normalcy, coevolving with their malignant neighbors in order to sustain the growth of the latter (Kinzler and Vogelstein, 1998; Olumi et al., 1999).”