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Tumor proliferation other receptors

Sulindac is a racemic sulfoxide. Its deoxygenated metabolite (i.e., a sulfide) induces apoptosis, probably through inhibition of PPAR (Peroxisome Proliferator-Activated Receptor) It is probably the reason why suhndac seems to protect against colorectal cancers. Indeed, sulindac inhibits colorectal tumor cell growth. One other metabolite of sulindac, the sulfone exulind, is an inductor of apoptosis, and is currently in Phase III clinical trials for treatment of tumors (Figure 8.3). [Pg.317]

The t(2 3)(ql3 p25) translocation, found in a subset of thyroid follicular carcinomas, results in fusion of the DNA binding domains of the thyroid transcription factor PAX-8 to domains A-F of the peroxisome proliferation-activated receptor (PPAR) y 1 (Hg. 10.13). Studies using PCR and immunohistochemistry demonstrated that most follicular carcinomas positive for PPAR Y were widely invasive while tumors lacking the rearrangement were PPAR y negative. Papillary carcinomas and Hurthle cell tumors were negative. Other studies, however, have reported positivity both in follicular carcinomas and adenomas. [Pg.302]


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See also in sourсe #XX -- [ Pg.21 ]




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