The corresponding pairs of cis antisense transcripts are mRNAs that are at least partially comple mentary to each other. Cis read more antisense mRNAs that are naturally transcribed from a SAGP are known as naturally occurring sense antisense RNAs. Studies have shown that changes in the transcription of SAGPs could be implicated in pathological processes such as some cancers and neurological diseases. For example, it was shown experimentally in leukemia cells that genes BAL1 and BBA, which form a Inhibitors,Modulators,Libraries SAGP, are bi directionally transcribed and concordantly expressed due to INF gamma induction and that their products can directly interact at the protein level. Previously we reported that 12 high confidence SAGPs pairs are concordantly regulated in human breast cancer tissues.

Among these, two pairs are constitutively co regulated in breast tumors of different genetic grades, while the co expression of the CR590216 EAP30 SAGP is observed specifically in G3 genetic grade. In mammalian genomes, SAGPs can be organized in more complex sense antisense gene architectures in which at least one Inhibitors,Modulators,Libraries gene shares loci with Inhibitors,Modulators,Libraries two or more antisense partners. Many dozens of CSAGAs can be found in the human genome, therefore, it is an intriguing speculation that not only SAGPs, but also CSAGAs, as integrated modules, may play important roles in human diseases, including cancer. In this regard, the study of the co regulatory profiles of genes in the same CSAGA and, possibly, between different CSAGAs or other transcriptional modules would shed new light on the complex nature of the entire transcriptome.

There are Inhibitors,Modulators,Libraries many oncogenes on chromosome 17, although the localization of these genes is not uniform. For example, according to Cancer Genetics, the oncogenes TAF2N, NF1 and THRA are located on 17q11. 1 q12. ERBB2, a well known oncogene, is located Inhibitors,Modulators,Libraries on 17q12. The gene BIRC5 on 17q25. 3, which encodes the apoptosis inhibitor survivin, co amplifies with ERBB2 and correlates with high histological grade and a poor prognosis in breast cancer when overexpressed. Many other genes located close to ERBB2 on 17q12 could be over expressed or and amplified and are known or suspected to play a role in carcinogenesis, specifically, breast carcinogenesis. Previous studies have demon strated that the negative effect on the prognosis of breast cancer attributed to ERBB2 amplification could, in fact, be due to co amplification of the region adjacent to ERBB2.

The ERBB2 gene and its neighbour genes could be amplified and over example expressed in 25% of invasive breast carcinomas. In general, ERBB2 amplification and over expression confers an unfavour able prognosis, although its significance is less than that of the traditional prognostic factors of stage and grade. It also seems that the prognosis and response to therapy varies considerably within the spectrum of ERBB2 amplified breast carcinomas, indicating that they are biologically heterogeneous.