Investigation of the Lobular Carcinoma in Situ, Using Molecular Genetic Techniques, for the Involvement of Novel Genes
Annual summary rept. 20 May 2003-19 May 2004
MOUNT SINAI HOSPITAL TORONTO (ONTARIO)SAMUEL LUNENFIELD RESEARCH INST
Pagination or Media Count:
Atypical lobular hyperplasia ALH and lobular carcinoma in situ LCIS, i.e. lobular neoplasia LN, are lesions of significance in terms of implication to the patient in the development of invasive carcinoma. A correlation between the lobular histological type and the inactivation of E-cadherin, a cell adhesion protein, has been reported. As well, mutations in CDHl have been reported in invasive lobular carcinoma ILC and LCIS with adjacent ILC. Our study proposes to investigate LN lesions, lacking any adjacent invasive carcinoma, for alterations in and expression of known and novel genesproteins in order to characterize a profile for lobular neoplasia. We have obtained 22 LN cases 14 ALH and 14 LCIS lesions. LN cases have been found to be negative for E-cadherin 2626, beta-catenin 2526 and alpha-catenin 2123 protein expression. CDHl alterations have been found to characterize LCIS lesions 1414 but not ALH lesions 114. Moreover, LOH at the 16q locus was found to be an infrequent event 325. Studies are now in progress to evaluate p120-catenin protein expression, E-cadherin promoter methylation, and the involvement of novel genes at the stage of LN by CGH microarray. The completion of these analyses will provide insight into the molecular genetic profile for lobular neoplasia.
- Medicine and Medical Research