Introduction: Breast cancer remains the prominent cause of mortality in women. Several biomarkers are used to evaluation the response and targeting to therapy. Tumor suppressor candidate 1 (TUSC1) gene was newly identified as a probable tumor suppressor in human cancers. Nevertheless, the expression and potential function of TUSC1 in breast cancer stay undecided. Therefore, this study aimed the evaluation of TUSC1 gene expression in breast tumor samples.Methods: In this case-control study, 40 formalin-fixed paraffin embedded (FFPE) tumoral of breast cancer and 40 healthy tissues were enrolled. Followed were informed consent and completing clinical information for all samples. Total RNA was extracted and complementary DNA (cDNA) was synthesized. The relative gene expression was determined using quantitative real-time RT PCR (qRT-PCR) and evaluated by 2-DDct method.Results: The expression of TUSC1 gene was lower in tumor tissue compared to the healthy tissue adjacent and it was statistically significant (P=0.0003). Also, in metastatic state gene expression significantly decreased (P=0.027).Conclusion: Our study revealed that the expression of TUSC1 is lower in breast cancer. Subsequently, using considering all the data about the expression of TUSC1 gene from some cancers (e.g. Lung, Hepatocellular and gastric), it could be suggested that the TUSC1 gene might act as a tumor suppressor in breast cancer and influenced in metastasis. Therefore, supplementary studies should be done to elucidate the exact mechanism of action of the gene in tumor-genesis.

Colorectal cancer (CRC) is mostly due to a series of genetic alterations that are being greatly under the influence of the environmental factors. These changes, mutational or epigenetic modifications at transcriptional forefront and/or post-transcriptional effects via miRNAs, include inactivation and the conversion of proto-oncogene to oncogenes, and/or inactivation of tumor suppressor genes (TSG). Here, a thorough review was carried out on the role of TSGs with the focus on the APC as the master regulator, mutated genes and mal-/dysfunctional pathways that lead to one type of hereditary form of the CRC; namely familial adenomatous polyposis (FAP). This review provides a venue towards defining candidate genes that can be used as new PCR-based markers for early diagnosis of FAP. In addition to diagnosis, defining the modes of genetic alterations will open door towards genome editing to either suppress the disease or reduce its progression during the course of action.