Sudden death of a young female patient: a case of arrhythmogenic right ventricular dysplasia

Arrhythmogenic right ventricular dysplasia ARVD is a disorder which is characterized by replacement of right ventricular myocardium by fat and fibrous tissue. Although it generally causes arrhythmias originating from the right ventricle, sudden deaths might be seen. A 30-year-old woman with no previous symptoms of a particular disorder was found dead in her house. The organs of her body were sent to the pathology department after the autopsy was carried out by the Department of Forensic Medicine of Adnan Menderes University, Aydin, Turkey. Grossly, the heart weight was within the normal limits. Nonetheless, it was detected that the right ventricle wall was thinned remarkably and had yellow color. In the microscopic examination, it was observed that myocardium was replaced mostly by fat and fibrous tissue. The other sections of heart were normal. This lesion was diagnosed as ARVD and suggested as the cause of death

Breast carcinogenesis. Transition from hyperplasia to invasive lesions

To examine the balance loss between proliferation and apoptosis that play a role in breast cancer development, and to explore the places of various genes and molecules within this process in this supposed multistep process. We obtained the specimens from 40 patients between 2002 and 2004 at the Department of Pathology, Medical Faculty, Adnan Menderes University, Aydin, Turkey. We categorized the lesions ductal hyperplasia [DH], atypical ductal hyperplasia [ADH], in situ ductal carcinoma [DCIS], and invasive ductal carcinoma [IDC]. We determined the tumor size, histological grade and lymph node status of invasive cases and we used nottingham prognostic index [NPI]. We applied ER, PR, c-erbB2, p53, Ki-67, bcl-2, dUTP nick end labeling [TUNEL], breast cancer gene-1, matrix metalloproteinases-1 and tissue inhibitor matrix metalloproteinases-1 stains to each lesion using the immunohistochemical method. We observed that ER and PR decreased in ADH when compared with DH [p=0.0001 and p=0.019]. However, we determined that in DCIS as c-erbB2 [p=0,005] and Ki-67 [p=0.004] increase, TUNEL [p=0.04] and bcl-2 [p=0.005] decrease, when compared with ADH. When compared with DCIS lesions, we observed the existence of a higher c-erbB2 [p=0,003] and a lower TUNEL [p=0,012] in invasive tumors. Furthermore, we found that there is a higher MMP-1 [p=0,04] in invasive lesions, when compared with non-invasive lesions. We detected higher PR [p=0,049], lower TUNEL and c-erbB2 [p=0,017] in low grade group of NPI, when compared with high grade group of NPI. As a result, it has been shown that together with increase in proliferation, decrease in apoptosis, too, contributes to the proliferation/apoptosis imbalance that occurs in breast carcinogenesis. Increase in proliferation and decrease in apoptosis are parallel with the progression of lesions. We also showed that the changes, beginning with loss of ER and PR in ADH step, can cause malign transformation, which is especially notable both in DCIS step due to Ki-67 and c-erbB2 increase, and also with bcl-2 and TUNEL decrease