SummaryobjectIve. This study intends to verify the expression levels and correlation of aromatase, matrix metalloproteinase 2 (MMP-2), matrix metalloproteinase 9 (MMP-9) and CD44 in ductal carcinoma in situ (DCIS) and infiltrating ductal carcinoma (IDC) when both are found in the same breast. Methods. One hundred and ten cases were evaluated by tissue microarray (TMA) and immunohistochemically screened with anti-aromatase polyclonal antibodies, anti-MMP-2 monoclonal antibodies, anti-MMP-9 policlonal antibodies and anti-CD44 monoclonal antibodies. results. Aromatase was expressed in IDC and DCIS in 63 (57.3%) and 60 (67%) of the cases respectively; MMP-2 was similarly expressed in IDC and DCIS in 15 (13.60%) cases; MMP-9 was positively expressed in IDC and DCIS in 83 (75.50%) and 82 (74.50%) cases, respectively; CD44 was positively expressed in IDC and DCIS in 49 (44.50%) and 48 (42.60%) of the cases, respectively; all of them were highly correlated (p<0,001). The correlation analysis found positive, statistically significant correlation, in IDC between aromatase and MMP-2 (p<0.001) and between aromatase and MMP-9 (p=0.034). Positive correlation between aromatase and MMP-2 (p<0.001) and between MMP-9 and CD44 (p=0.030) were found in DCIS. conclusIon. These results allow us to conclude that aromatase through local estrogen synthesis in breast tissue plays an important role in breast carcinogenesis, mainly influencing MMP-2 and MMP-9 which are important participants in tumor cell invasion and dependence of their connection to CD44 for action.Key words: Aromatase. Matrix metalloproteinase 2. Matrix metalloproteinase 9. Antigens CD44. Carcinoma ductal breast.

Our study showed that the agreement among observers using traditional diagnostic criteria of cervical intraepithelial lesions can improve with the use of immunohistochemistry.

Background Carney's complex (CNC) is a rare genetic multiple neoplasia syndrome, with involvement in several systems, among them, acromegaly is a possible condition, according to the literature, seen in about 10% of cases. PPRKAR1A is the most known gene evolved. The genetic origin of 59% of patients with CNC has not yet been elucidated. ClinicalCases A 17-year-old malewithtall stature, withstigmaofgigantism, GH 9.89 ng/ml and IGF-1 1.5 times higher reference value, MRI with pituitary adenoma of 0.7cm. After resection transfenoidal endoscopic (TSE) thepathology of the tumor revealed a pure GH pituitary adenoma. Echocardiogram showed cardiac myxomas. For that reason, a Carney complex was established. In the search for other alterations present in the syndrome, a nodule was found in the right testicle, which after nodulectomy shown a Leydig Cell Tumor. After these findings, we invited all family members to perform screening to identify possible involvement of the CNC. Two brothers, including a twin, and their mother also had stigma of acromegaly, all with pituitary adenoma and laboratorial diagnostic. The two menunderwentTSE surgery reassuring GH secretion by the tumor. The elderly brother had aggressive microcalcilfications in bilateral testicles. After bilateral orchiectomy was diagnosed witha large cell calcifying sertoli cell tumor. The twin brother also had cardiac mixomas and macrocalcifications in testicle but without signs of malignancy. The mother had athyroid ultrasound showing a multinodular goiter and breast lesions also with no signs of malignancy. She also had a pituitary microadenoma,butrefused the surgery and is currently using thesomatostatinanalog. CNC is a multiple neoplasia syndromeusually characteriszed by lentiginosis, multiple neoplasias and signs of endocrine overactivity, particularly Primary Pigmented Nodular Adrenal Disease (PPNAD) and myxomas. It is a rare condition and its prevalence remains unknown. A patogenic allelic variant (PAV) of PRKAR1A is found in 37% of patients with sporadic CNC and more than 70% of patients with familial CNC. To this date, at least 130 different mutations have been described in more than 400 families around the world, distributed across the ten coding exons (PRKAR1A has 11 exons, but exon 1 is non-coding and rarely mutated) and in the adjacent intronic sequences. In 2014, a germline triplication of the exon of PRKACB gene has been identified in pacient who did not harbour a PRKAR1A mutation. In our case, a search of PAV was realized by exome NGS and CG-Array but we found no evidence of variant that can explain the occurence of CNC. Conclusion We describe the follow-up of a family with CNC without PAV identified so far. Presentation: No date and time listed