Human MED12 peptide

Purpose of review Uterine leiomyomas are the most common benign uterine smooth muscle tumors. On the basis of imaging, these masses are often presumed to be benign conventional leiomyomas and surgical excision is a common treatment choice. After myomectomy or hysterectomy for presumed leiomyomas, the surgical pathology report may reveal an unexpected diagnosis of another type of mesenchymal tumor. These can range from a variant of benign smooth muscle tumors to smooth muscle tumors of uncertain malignant potential to malignant sarcomas. This review describes these variant pathologies and reviews data on recurrence risk and postoperative management. Recent findings The majority of benign smooth muscle tumors will be classified as leiomyomas. Cellular, bizarre nuclei, mitotically active, epitheliod, myxoid, and dissecting are all terms that describe pathologic variants of benign leiomyomas. Smooth muscle tumors of uncertain malignant potential contain both benign and malignant features and should be referred to Gynecologic Oncology for follow-up. Leiomyosarcomas and low-grade endometrial stromal sarcomas may present preoperatively as benign tumors but are malignant with a high risk of recurrence and should be referred to Gynecologic Oncology. We advocate for the continued benefits of minimally invasive procedures in appropriately selected patients. Despite these measures, unexpected pathologic diagnoses can occur and should be managed appropriately.

MED12 is a transcriptional mediator complex subunit, which negatively regulates the transforming growth factor beta (TGF-beta) pathway. The TGF-beta pathway plays a major role in the induction of epithelial-mesenchymal transition 9EMT). MED12 loss induces activation of the TGF-beta pathway, resulting in EMT and drug resistance to epidermal growth factor receptor (EGFR)-targeted therapy. We aimed to investigate the clinical significance of MED12 loss detected by immunohistochemistry in patients with colorectal cancer (CRC). A total of 100 patients diagnosed with stage I-IV CRC were enrolled in this retrospective study. MED12 expression was evaluated immunohistochemically, and classified as either positive (>= 20%) or negative (<20%) with regard to the percentage of immunoreactive cells. The relationships between MED12 loss and clinicopathological characteristics and RAS mutation status were analyzed. Overall, 79 and 21 patients were classified as MED12 positive and MED12 negative, respectively. MED12 negativity was significantly associated with tumor budding (P = 0.034), N category (P = 0.010), and M category (P = 0.031). Among stage IV CRC patients, 18 of 31 patients had the RAS wild-type gene; 6 of these patients were MED12 negative, and were considered to have the potential for resistance to EGFR-targeted therapy despite the presence of the wild-type gene. In conclusion, MED12 loss is associated with tumor budding, nodal metastasis, and distant metastasis in patients with CRC, suggesting that MED12 loss induces activation of the TGF-beta pathway resulting in EMT. Future treatment strategies focusing on patients MED12 loss may improve the prognosis of patients with CRC.