Naslov
Molecular signaling in breast cancer

Autori
Levanat, Sonja ; Musani, Vesna ; Levačić Cvok, Mirela ; Čretnik, Maja

Vrsta, podvrsta i kategorija rada
Sažeci sa skupova, sažetak, znanstveni

Izvornik
Book of abstracts : XIV S.I.S. World congress on breast diseases / Drinković, Ivan - Zagreb : Medimond International Proceedings, 2006, 7-12

Skup
XIV S.I.S. World congress on breast diseases

Mjesto i datum
Zagreb, Hrvatska, 18.05.2006. - 21.05.2006

Vrsta sudjelovanja
Pozvano predavanje

Vrsta recenzije
Međunarodna recenzija

Ključne riječi
breast cancer ; tumors ; signaling

Sažetak
Breast cancer tumorigenesis is a multistep process in which the normal breast epithelium evolves via hyperplasia and carcinoma in situ into an invasive cancer , which eventually can disseminate via lymph and blood vascular system to form metastases. Each of these steps is thought to correlate with one or more distinct mutations in major regulatory genes. These genes play a role in maintaining balance between proliferation, apoptosis and differentiation, while other genes regulate expression of steroid receptors, cell adhesion molecules and angiogenic factors, and of various other proteins important for invasion and establishment of metastases. Hereditary breast cancer is characterized by an inherited susceptibility to breast cancer on basis of an identified germline mutation in one allele of a high penetrance susceptibility genes (such as BRCA 1 and 2, p53), which are acting as tumor suppressors. Sporadic breast cancers result from serial accumulation of acquired and uncorrected mutations, with mutational activation of oncogenes ( Myc, CCND1, HER-2/neu), often coupled with non- or mutational inactivation of tumor suppressor genes (p53). In both in hereditary and in sporadic cancer, early event can take place in a variety of specific genes, leading through different pathways, probably to different tumour types, which have a different clinical outcome. However, non-mutational functional suppression could result from various epigenetic mechanisms, i.e. impaired DNA methylation. Knowledge of different tumor development pathways, each starting from distinct and specific early event leading to specific clinically relevant subtype of tumours, would be of value for the clinics.

Izvorni jezik
Engleski

Znanstvena područja
Temeljne medicinske znanosti

POVEZANOST RADA