Background: Ovarian leiomyoma is a rare benign tumor that accounts for 0.5 to 1% of all benign ovarian tumors. It probably arises from smooth muscle cells in the ovarian hilar blood vessels but there are other possible origins including cells in the ovarian ligament, smooth muscle cells or multipotential cells in the ovarian stroma, undifferentiated germ cells, or cortical smooth muscle metaplasia. Additionally, smooth muscle metaplasia of endometriotic stroma, smooth muscle present in mature cystic teratomas, and smooth muscle in the walls of mucinous cystic tumor may explain their occurrence in the ovary in some cases.
Breast cancer is the most frequently diagnosed cancer and the leading cause of cancer-related deaths among female population worldwide. Metastases are the common cause of morbidity and mortality in breast cancer, and can remain latent for several years after surgical removal of the primary tumour.Thus, the identification and functional characterisation of molecular factors that promote oncogenic signalling in mammary tumour development and progression could provide new entry points for designing targeted therapeutic strategies for metastatic breast cancer. In the present study, we investigated the expression of proteins involved in cell signalling (GHR and NEDD9) and cell-cell adhesion (plakoglobin) in epithelial and stromal compartments of primary ductal invasive breast carcinomas and their axillary lymph node metastases versus non-metastatic tumours. Obtained data revealed remarkable increase in the expression levels of GHR and NEDD9 proteins in both, epithelial and stromal components of axillary lymph node metastases in comparison with non-metastatic tumours suggesting that the expression of these two proteins may provide biomarkers for tumour aggressiveness.
The present study was designated to analyze correlation between the presence and extent of peritumoral retraction clefting and various clinicopathologic features in esophageal squamous cell carcinoma (ESCC), and to possibly establish the significance of this phenomenon in ESCC. Fifty-four consecutive patients with advanced ESCC were included in the study. The presence of peritumoral retraction clefting was classified on the basis of the proportion of tumor nests exhibiting this phenomenon. Tumors with clefts that affected up to 25% of tumor nests were classified as group I; with clefts that affected >25% to 50% of tumor nests as group II; with clefts that affected >50% to 75% of tumor nests as group III; and tumors with clefts that affected more than 75% of tumor nests were classified as group IV. Statistical analysis showed a correlation between presence and extent of peritumoral clefting and lymph node metastasis. T3 tumors and tumors with lymph node metastasis had significantly more pronounced peritumoral clefting compared with T2 tumors and tumors without lymph node metastasis. The presence of peritumoral clefting was not associated with the number of affected lymph nodes. There was no correlation between the presence and extent of peritumoral clefting with patient age and sex, and tumor location, diameter and grade. The association of peritumoral retraction clefting in ESCC with local invasiveness and lymph node metastasis indicated that peritumoral clefting could be a simple and useful morphological feature of tumor aggressiveness and may contribute to the pathological and clinical assessment of patients with ESCC.
Retraction clefting is known to appear in various types of tumors, but it has only recently been recognized as a specific histological phenomenon. Previously, it was considered merely a laboratory procedure artifact, but lately, there have been some assumptions that peritumoral retractions actually represent lymphatic spaces. In our study, we analyzed neoplastic glands in 52 specimens of prostatic adenocarcinoma. Immunohistochemical analysis was performed using D2-40 antibody, to highlight lymphatic endothelium and thereby differentiate actual lymph vessels or lymphovascular invasion from periacinar retractions. Our results showed that the number of lymph vessels was significantly lower in tumorous tissue compared to adjacent normal prostatic tissue. On the other hand, the number of lymph vessels in tumorous tissue was significantly higher than the number of lymph vessels mimicking periacinar retractions. Overall, the number of lymph vessels mimicking periacinar clefts was particularly low. These results are in accordance with our previous studies, which had shown that periacinar clefting appears due to lack of basal cells and stromal changes around tumorous acini. Also, these results support our hypothesis that retractions do not represent lymph vessels but should be considered a distinct entity, which is proven to be helpful both as diagnostic and predictive factor.
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