Background and aim: Non-melanoma skin CANCERs (NMSC) are one of the most prevalent malignancies of the human. Although the morality rate is not high for these CANCERs, they may cause high morbility for the patients. In addition to the skin type, factors such as sun exposure, head and neck radiotherapy, inappropriate use of sunscreen and cultural changes may increase the incidence of these CANCERs. The objective of this study was to determine NMSC in Isfahan.Materials and Methods: We used data of the CANCER resistery center for performing this study and the incidence of NMSC per 100,000 populations was determined. Results: Overall 1681 cases were registered. The incidence of NMSC was calculated to be 10.67/100,000population. The most common site for BCC and SCC was middle face. Conclusion: NMSC incidence in Isfahan is lower than west countries although this incidence is 10.67/100,000in a year. It means that 5-6 thousand cases of NMSC occur in Iran each year. We can prevent its morbidity and mortality by early correct diagnosis.

Epidemiological studies link ovulation and epithelial OVARIAN CANCER, which frequently develops from the OVARIAN surface epithelium (OSE). Ovulation can be likened to an inflammatory reaction initiated by the mid-cycle luteinizing hormone surge. Each ovulation involves proteolytic breakdown of the follicle wall and OVARIAN surface to allow shedding of the oocyte. Serial injury and repair of the OSE thereby creates the potential for inflammation-associated genetic damage leading to neoplasia. Since ovulation is normally so regular and frequent, natural mechanisms must exist to localize and limit OVARIAN inflammation and minimize emergent disease. Our research suggests a role for cytokine up-regulation of HSD11B1 gene expression in this process. HSD11B1 encodes the steroidogenic enzyme 11bhydroxysteroid dehydrogenase type 1 (11bHSD1) that metabolizes substrate cortisone to anti-inflammatory cortisol. We find 11bHSD1 mRNA and enzymatic activity strongly up-regulated by the ovulation-associated cytokine interleukin-1a (IL-1 a) in cultured human OSE cells. Moreover, cortisol enhances IL1a-induced up-regulation of 11bHSD1 mRNA, providing feed-forward amplification of local anti-inflammatory signaling in these cells. We therefore propose that cytokine activation of cortisol regeneration via 11bHSD1 can provide a mechanism for anti-inflammatory ‘protection’ of ovary during ovulation. In support of this concept, we find that IL1a up-regulates matrix metalloproteinase (MMP) 9 (gelatinase B) activities in OSE cells and this is suppressed by glucocorticoid receptor-mediated cortisol action in vitro. Suppression of MMP9 gene expression through locally regenerated glucocorticoids has implications both for normal ovulation and OVARIAN CANCER spread. Many OVARIAN CANCER cell lines are unable to respond normally to IL- a in terms of 11bHSD1 mRNA. Likewise, many primary epithelial OVARIAN CANCER cells show a deficient 11bHSD1 mRNA response to IL- 1a relative to normal OSE. If this translates into deficient glucocorticoid suppression of MMP9 in primary OVARIAN CANCER, this could be a mechanism of promoting metastatic tumour spread in vivo.

OVARIAN CANCER is the most lethal gynecological CANCER and about 70% of the patients are advanced stagein the time of diagnosis. Decision about management (surgical debulking versus neoadjuant chemotherapy) in OVARIAN CANCER patients is dependent on initial staging by abdominopelvic MDCT or MRI, so, Radiologist expertise on OVARIAN CANCER staging is very important. Involvement of mesenteric root, peritoneal implante larger than 2 cm, lymphadenopathy superior to renal hilum and implants near hepatic veins are criteria for nonresectability of OVARIAN CANCER and radiologist must be familiar and expert on the imaging protocol and findings on MDCT for OVARIAN CANCER staging.