Background Thyroid cancer represents quite possibly the most regular endocrine malignancy in humans, ranging through the much more differenti ated carcinomas with papillary or follicular histotypes, for the unusual and clinically a lot more aggressive anaplastic carcinomas. Quite a few on the genetic occasions leading to the onco genic and metastatic probable of those distinct malignan cies have previously been identified. Papillary thyroid carcinomas frequently harbor activating rearrange ments of RET or NTRK1 genes, each coding for receptor tyrosine kinases that exert management more than a wide selection of transcription variables. Some PTC may well show, rather, mutually exclusive stage mutations in RAS or BRAF. resulting in the constitu tive activation with the RAS RAF MEK ERK signaling path way. Follicular thyroid carcinomas. however, are identified to harbor PAX8 PPAR gene fusions and in addition mutations in RAS.
Undifferentiated thyroid carcinomas might dis perform RET rearrangements or stage muta tions in RAS or BRAF. also as mutations in TP53. and that is in accordance with the hypothesis that most UTC originate from well differentiated lesions via the multi phase accumula tion of genetic aberrations. Deregulation with the phosphatidylinositol three kinase Akt pathway by way of amplification or activating mutations with the cata lytic subunit of PI3K. or selleck chemical BAY 11-7082 inactivating mutations of critical inhibitors such as PTEN. also plays a relevant role in UTC etiology. The molecular mechanisms behind a considerable pro portion of thyroid carcinomas continue to be nonetheless unclear, and substantial hard work has been placed in building in vitro and in vivo models of thyroid carcinogenesis. selleck Numerous cell lines derived from PTC, FTC, and UTC carcinomas are already established and therefore are widely made use of to assess novel oncogenic events or molecular markers with diag nostic, prognostic and or therapeutic likely.
The genetic articles of many of those cell lines, however, is poorly or only partially characterized, which makes it challenging to assess the pathogenetic part of unique gene rearrange ments within the absence of a common picture with the genomic background of each cell line. To contribute on the genetic characterization on the in vitro designs of non medullary thyroid carcinogenesis, we per formed chromosome banding examination and chromosomal comparative genomic hybridization on eight human thyroid carcinoma cell lines originating from pap illary carcinomas. follicular carcinoma or undifferentiated carcinomas. We additionally evaluation the karyotypic and CGH facts obtainable while in the litera ture for these three thyroid carcinoma histotypes, so that you can assess the main tumor representativeness of those cell lines.