Nasosinus Adenocarcinomas—A Molecular Point of View

Abstract

Little is known about the genetic changes in adenocarcinoma (ACN). Because of its histopathological resemblance, most studies so far have focused on a limited number of genes and proteins often selected for their frequent involvement in colorectal adenocarcinoma. Indeed, mutations in K-ras and p53 occur also in ACN, although with lower frequencies. K-ras mutations varied in frequency bteween 0% and 15%. One study reported 50%, about the same as in colorectal adenocarcinoma. Also, H-ras mutations have been detected. Mutations in p53 ranged between 18% and 57%, and 50% of LOH was seen at 17p13, the chromosomal locus of p53. Further attempts to find genetic alterations as described in colorectal carcinoma concerned APC, b-catenin, and various mismatch repair genes and gave negative results. These results indicate that ACN and colorectal carcinoma have different genetic pathways of development and progression. Other investigations focused on genes involved in head and neck squamous carcinoma were reported as the promotor methylation of p14(ARF) and p16(INK4a) as well as LOH at the 9p21 locus. Gene amplification of CCND1, PIK3CA, and ERBB1 and ERBB2 was observed in low frequencies. Finally, c-erbB2 was also found overexpressed in 32% of 28 cases.