Cancer has been always considered as one of the main human health challenges worldwide. One of the main causes of cancer-related mortality is late diagnosis in the advanced stages of the disease, which reduces the therapeutic efficiency. Therefore, novel non-invasive diagnostic methods are required for the early detection of TUMORs and improving the quality of life and survival in cancer patients. MicroRNAs (miRNAs) have pivotal roles in various cellular processes such as cell proliferation, motility, and neoplastic transformation. Since circulating miRNAs have high stability in body fluids, they can be suggested as efficient noninvasive TUMOR MARKERs. MiR-96 belongs to the miR-183-96-182 cluster that regulates cell migration and TUMOR progression as an oncogene or TUMOR suppressor by targeting various genes in solid TUMORs. In the present review, we have summarized all of the studies that assessed the role of miR-96 during TUMOR progression. This review clarifies the molecular mechanisms and target genes recruited by miR-96 to regulate TUMOR progression and metastasis. It was observed that miR-96 mainly affects TUMORigenesis by targeting the structural proteins and FOXO transcription factors.

Background: Inhibin is a dimeric glycoprotein that has a depressive effect on the anterior hypophys secretion. The level of this TUMOR MARKER is undetectable in menopause women. In patients with gynecological cancer, especially granulosa and epidermal-type (mucinous), ovarian cancers considerable increase in the serum level of inhibin has been reported. The increased level of inhibin has been reported in patients with recurrent ovarian cancer.Methods: We measured total serum inhibin and CA125 TUMOR MARKER level in 38 postmenopausal women with pathologically confirmed ovarian cancer before and after surgery out of 51 suspected women. Our control group were postmenopausal women that attended to our clinic for routine gynecologic check up. Both TUMOR MARKERs were measured in these patients too.Results: Among 38 women with ovarian cancer, 13 (34.2%) had elevated serum levels of total inhibin. Among the 16 women with serous adenocarcinoma, 3 patients (18.8%) had elevated serum levels of inhibin. All the three women with granulosa cell TUMOR had elevated serum levels of inhibin (100%) and 3 of 4 (75%) women with mucinous ovarian cancer had the same result. three out of 38 women in control group had elevated serum levels of inhibin. Among all 38 patients, 6 (15.7%) showed TUMOR recurrence, that all were concomitant with rising of both serum CA125 and Inhibin levels (p=0/001).Conclusions: Serum inhibin level is a usefull TUMOR MARKER in granulosa cell and in mucinous TUMOR of ovary. In this study combined inhibin and CA125 assay showed better results in early detection of ovarian cancer in comparison to either CA125 or inhibin alone.

This research has been done in 100 patient with diagnosis of pelvic mass, since winter 1376 to spring 1378, in Amir and Emdad hospital were confined to bed and operation. This study is cross sectional.After the confined to bed, the biography and evaluation of TUMOR-makers "include CA125- aFp-BHCG-LDH, these tests have been done by Elyza except LDH by simple biochemistry", the surgical operation was done on the patient. After finding the answer of pathology, the –comparison among diagnosis before surgical operation with final diagnosis to calculate the sensitiveness of sonography and TUMORMARKERs.The results of research show that in 100 patient considered. The origin of 67 masses were of ovary and 21 of uterine, That 17 masses were leiomyoma, and 12 masses were except of ovary and uterine. 74% masses were in Reprudactive age. More of 90% masses were benign. We had only 6% malignancy that they were seen more in prepubertal ages (100% malignancy) and menopause ages (25% malignancy). In this study the sensitiveness of sonography at diagnosis of benign masses: was above 90% and about the malignancies masses however there were few patients, may be the accuracy of calculation was little. (50%).We conclude that sonography as a cheap and accessible facility with high sensitiveness, specifically in Benign masses is useful at diagnosis before operation of pelvic mass. Also to asses the TUMOR MARKERs at diagnosis of distinct of masses is useful. In this study, we control the ratio of TUMOR MARKERs, at each malignancies, the ratio was high with regard to the kind of mass. Meanwhile, It was very high at comparison with natural quantities and benign causes (In two pt's with serouscystadeno carcinoma, CA125 was above   200 u/ml and in pt's with Endodermal sinus TUMOR, afp was 268 ng/ml, since TUMOR MARKER increase in benign causes. So the measure of TUMOR MARKERs, alone is not enough for distinction of benign mass from malignancy in study befor operation.Therefore to take the biography and accurate physical examination by doing sonography and TUMOR MARKERs, altogether, they are advantage at intime recovery of surgical Indication.

Background: breast cancer is the most common malignant cancer result in death in women. With respect to lower age of breast cancer in Iranian patients than other countries, we investigated the TUMOR MARKERs in breast cancer and age distribution of these MARKERs. Material and Methods: our cross sectional study was done among patient whom had positive pathology report for breast cancer and had immunohistochemistry profile.245 patient were enrolled. Patient’s age, TUMOR MARKERs and their pathology were analyzed.Results: average age of our patient was 49.47±12.50 .age range was between 20 and 86.The most common breast cancer before and after 50 years old was invasive ductal carcinoma. The most prevalent TUMOR MARKER before 50 years old was invasive ductal carcinoma .progesterone and estrogen MARKER the most presence of TUMOR MARKER was in age of 40 to 50. (P=0.033, P=0.031).Conclusion: being younger patient is an alarm signal and need more attention. It is more critical when we know that more than 50 percent of patient were in age of 50 and less .new point of view of this study was different distribution of TUMOR MARKER that differ from foreign study.

Objective: MicroRNAs (miRNAs) are small noncoding RNAs that negatively regulate expression of target mRNAs. The biological processes modulated by miRNAs include cell differentiation, proliferation and apoptosis. It is approved that abnormal expression of miRNAs could cause various diseases, including cancer. P53 is a master negative regulator of Nanog expression which is a key to maintenance of pluripotency in stem cells, thus loss of p53 promotes stemness and selfrenewal. miR-491 is known to negatively regulate TP53 therefore its aberrant expression could negatively affect TP53 regulatory pathway. Considering the potential role of miR-491to miss-regulate p53 and based on cancer stem cell (CSCs) hypothesis, deregulation of miR-491 might ignite the TUMORigenic process in adult stem cell and transform them into cancer stem cell state. The aim of our study is to find a potential link between the expression of miR-491 and TUMOR formation as a result of CSCs activation in lung tissue.Materials and Methods: In this study, RNA was extracted from lung TUMOR and non-TUMOR tissues. Real-time reverse transcription polymerase chain reaction (RT-PCR) assays were performed with specific stem-loop primer and EVA green master mix. The ability of primer to amplify specific microRNA was evaluated.Results: According to our data, stem-loop primer could amplify miR-491-5p specifically. RT-PCR results showed that expression level of miR-491-5p could be evaluated in lung TUMOR and non-TUMOR tissue. In addition, expression level of miR-491-5p might be significantly different in lung TUMOR and non-TUMOR tissue.Conclusion: Our data suggested a potential role of miR- 491-5p in TUMORgenecity. According our data and previous data we can say that miR-491 might have a role in stemness of stem cell and cancer stem cell.

Background: The 17beta-hydroxysteroid dehydrogenase type 1 (HSD17B) family has been implicated in the prognosis and treatment prediction of various malignancies; however, its association with bladder cancer (BLCA) remains unclear. This study aimed to evaluate the potential of HSD17B1, as a prognostic bioMARKER, for the survival of patients with BLCA and to determine its effectiveness as a supplemental bioMARKER for BLCA. Methods: A series of bioinformatics techniques were applied to investigate the expression of HSD17B1 in different types of cancer and its potential association with the prognosis of BLCA patients using diverse databases. The UALCAN, Human Protein Atlas, cBioPortal, Metascape, GEPIA, MethSurv, and TIMER were employed to analyze expression differences, mutation status, enrichment analysis, overall survival, methylation, and immune-infiltrating cells. The real-time reverse transcription-PCR (qRT-PCR) was implemented to detect the messenger ribonucleic acid (mRNA) expression levels of HSD17B1 in vitro. Results: Elevated mRNA and protein levels of HSD17B1, surpassing normal levels, were observed in BLCA samples. In addition, the BLCA patients with higher mRNA expression level of HSD17B1 significantly reduced the overall survival. Also, several immune infiltrating cells, including mast cell resting CIBERSORT-ABS, have been identified as TUMOR-associated bioMARKER genes, with the potential to significantly influence the immunological environment. Finally, qRT-PCR analysis revealed a significant upregulation of HSD17B1 mRNA expression level in the cancer cells compared to the human 293T cells, which was consistent with the bioinformatics data. Conclusion: There is a strong correlation between the elevated HSD17B1 expression and positive prognosis in patients with BLCA. Therefore, HSD17B1 can be used as a prognostic bioMARKER in these patients.