Browsing by Author "Berisavac, Milica (14622317400)"

Background. Malignant melanomas of the female reproductive system are rare. These are biologically highly aggressive tumors with poor prognosis. Preoperative establishment of the diagnosis is practically impossible. Therapeutic approach and treatment of patients with metastatic ovarian melanoma are highly dependent on precise histological analysis. Case report. A woman aged 48 was admitted to the clinic for occasional pains in the lower abdomen and suspected myomatous changes of the uterus. The patient underwent surgery for melanoma on her right arm five years ago. Classic hysterectomy with bilateral adnexectomy with infracolic omentectomy and selective iliac lymphadenectomy were performed. Macroscopic examination revealed an oval tumefaction on the left ovary sized 12.5 × 10 × 3.5 cm of solid structure. Tumor tissue was yellowish-brown colored, of solid structure and mostly localized subcortically with central edema. Microscopic examination showed positive reaction for HMB-45, anti-Melan-A and S-100 protein, but negative immunoreactivity for estrogen and progesterone receptors. Malignant disease caused death after a 4-year follow-up period following gynecological operation. Conclusion. The previous diagnosis of skin melanoma is also indicative of metastatic ovarian tumor, while immunohistochemical analyses confirmed the histopathological diagnosis.

Purpose: Since several studies have proposed that epithelial ovarian cancer should not be considered as a single disease entity and that it results from an accumulation of genetic changes, we aimed to assess the polymorphic expression of major cytosolic glutathione S-transferases (GSTM1, T1, A1 and P1) with respect to ovarian cancer susceptibility and aggressiveness. Methods: This case-control study was conducted on 93 newly diagnosed epithelial ovarian cancer patients and 178 healthy matched controls. The multiplex polymerase chain reaction (PCR) was used to detect homozygous deletions ofGSTMl and GSTT1 genes. Analysis of the single nucleotide polymorphism (SNP) GSTA1 C69T was performed using PCR-restrictionfragment length polymorphism (RFLP), while for SNP GSTP1 Ile105Val real-time PCR was used. Results: No significant association to ovarian cancer risk was found for individual GSTM1, GSTA1 and GSTP1 genotypes (p>0.05). However, the carriers of GSTT1-active genotype were at 2-fold higher risk of ovarian cancer development (95%C1: 1.00-4.01, p=0.049), which was even more elevated in the subgroup of patients with positive family history of cancer. Moreover, the frequency of all three GST genotypes that might be associated to ovarian cancer risk (GSTT1-active, GSTA1-active and GSTPl-referent) was significantly higher in patients than in the control group (p=0.042). Even more, patients who were carriers of combination of these three genotypes represented over 64% of the total number of patients within any of the International Federation of Gynecology and Obstetrics (FIGO) stages of ovarian cancer. Conclusions: This study provides supportive evidence that GSTs might affect both susceptibility and progression of ovarian cancer.

Purpose: Since several studies have proposed that epithelial ovarian cancer should not be considered as a single disease entity and that it results from an accumulation of genetic changes, we aimed to assess the polymorphic expression of major cytosolic glutathione S-transferases (GSTM1, T1, A1 and P1) with respect to ovarian cancer susceptibility and aggressiveness. Methods: This case-control study was conducted on 93 newly diagnosed epithelial ovarian cancer patients and 178 healthy matched controls. The multiplex polymerase chain reaction (PCR) was used to detect homozygous deletions ofGSTMl and GSTT1 genes. Analysis of the single nucleotide polymorphism (SNP) GSTA1 C69T was performed using PCR-restrictionfragment length polymorphism (RFLP), while for SNP GSTP1 Ile105Val real-time PCR was used. Results: No significant association to ovarian cancer risk was found for individual GSTM1, GSTA1 and GSTP1 genotypes (p>0.05). However, the carriers of GSTT1-active genotype were at 2-fold higher risk of ovarian cancer development (95%C1: 1.00-4.01, p=0.049), which was even more elevated in the subgroup of patients with positive family history of cancer. Moreover, the frequency of all three GST genotypes that might be associated to ovarian cancer risk (GSTT1-active, GSTA1-active and GSTPl-referent) was significantly higher in patients than in the control group (p=0.042). Even more, patients who were carriers of combination of these three genotypes represented over 64% of the total number of patients within any of the International Federation of Gynecology and Obstetrics (FIGO) stages of ovarian cancer. Conclusions: This study provides supportive evidence that GSTs might affect both susceptibility and progression of ovarian cancer.