Erscheinungsdatum: 27.11.2013, Medium: Taschenbuch, Einband: Kartoniert / Broschiert, Titel: Tumor-Associated Fibroblasts and their Matrix, Auflage: 2011, Redaktion: Fusenig, Norbert E. // Mueller, Margareta M., Verlag: Springer Netherlands // Springer Netherland, Sprache: Englisch, Schlagworte: Onkologie, Rubrik: Allgemeinmedizin // Diagnostik, Therapie, Seiten: 472, Informationen: Paperback, Gewicht: 699 gr, Verkäufer: averdo
Please note that the content of this book primarily consists of articles available from Wikipedia or other free sources online. The autophagic tumor stroma model of cancer proposes that epithelial cancer cells use oxidative stress as a weapon to extract recycled nutrients from adjacent stromal fibroblasts (i.e., connective tissue cells). The theory posits that oxidative stress in cancer associated fibroblasts forces these cells to eat themselves, by a process called autophagy or self-cannibalism . The resulting recycled nutrients, derived from catabolism in the tumor stroma, are then used to power the anabolic growth of cancer cells. Thus, cancer is a disease of energy imbalance , resulting from the vectorial and unilateral transfer of energy-rich nutrients from the tumor stroma to cancer cells. (This explains the phenomenon of cancer-associated cachexia (systemic wasting), in which patients with advanced cancer cannot maintain their normal body weight).
Oncogenes and tumor suppressor genes had been traditionally studied in the context of cell proliferation, differentiation, senescence, and survival, four relatively cell-autonomous processes. Consequently, in the late '80s-early '90s, neoplastic growth was described largely as an imbalance between net cell accumulation and loss, brought about through mutations in cancer genes. In the last ten years, a more holistic understanding of cancer has slowly emerged, stressing the importance of interactions between neoplastic and various stromal components: extracellular matrix, basement membranes, fibroblasts, endothelial cells of blood and lymphatic vessels, tumor-infiltrating lymphocytes, etc. The commonly held view is that changes in tumor microenvironment are "soft-wired", i.e., epigenetic in nature and often reversible. Yet, there exists a large body of evidence suggesting that well-known mutations in cancer genes profoundly affect tumor milieu. In fact, these non-cell-autonomous changes might be one of the primary reasons such mutations are preserved in late-stage tumors.