Clinicopathologic features of invasive breast carcinoma with dermatopathic lymphadenitis: a retrospective analysis.

PURPOSE: To understand and explore the clinical manifestations, pathologic features, immunohistochemical analysis, treatment, and prognosis of dermatopathic lymphadenitis (DPL) and review the literature. METHODS: Lymph node specimens were collected from 10 patients with DPL at Zhongnan Hospital of Wuhan University from 2016 to 2019. We identified 3 patients with invasive breast carcinoma with DPL. We examined 41 axillary lymph nodes from the 3 patients, and only 3 lymph nodes showed DPL. Samples were analyzed by paraffin embedding and sectioning and hematoxylin-eosin and immunohistochemical staining. RESULTS: The lymph node cortex and medulla were generally maintained, and lymphoid follicles were atrophic. Irregularly shaped and distributed patches in the subcapsular lymphatic sinusoid and paracortical areas palely stained were observed. Melanin was deposited in the cytoplasm and intercellular spaces. Large cytoplasm-rich cells were also found in the tissue. The boundaries between the cells were unclear, and cytoplasm was bright. Immunohistochemistry of all DPL cases showed CD1a (+) and S-100 (+); some cases were Langerin positive.

B7-H4 facilitates proliferation and metastasis of colorectal carcinoma cell through PI3K/Akt/mTOR signaling pathway.

B7-H4 is over-expressed in various tumors and may affect many aspects of cancer biology. Our previous studies have reported that the over-expressed B7-H4 in serum or tumor tissue of colorectal carcinoma (CRC) patients was closely related to CRC progression. However, B7-H4 in cell biological characteristics of CRC is not well studied. Here, we investigate the effect of the B7-H4 on cell proliferation, migration and its expression regulated by PI3K/Akt/mTOR signaling pathway in CRC. Firstly, pSilencer 4.1-B7-H4-shRNA vector was constructed and stable transfection was performed on HT-29 cells. Secondly, cell proliferation, cell cycle, cell apoptosis and cell migration were evaluated after B7-H4 silencing, and the expression of Bcl-2, caspase-3, MMP-2 and MMP-9 was also measured. Finally, the regulation of B7-H4 by PI3K/Akt/mTOR signaling pathway was measured followed by treatment with or without PI3K/Akt and mTOR inhibitor. The results showed that the viability of HT-29 cells was significantly decreased after B7-H4 silencing (P < 0.05). B7-H4 silencing significantly increased the apoptosis rate and caspase-3 protein expression while decreased Bcl-2 protein expression (P all < 0.05). B7-H4 silencing also significantly reduced the migration of HT-29 cells (P < 0.01) and the secretion of MMP-2 or MMP-9 (P all < 0.05). Following treatment with PI3K/Akt and mTOR inhibitor in HT-29 cells, the expression of B7-H4 was significantly downregulated compared with untreated group (P all < 0.05). Our results strongly suggest that B7-H4 may be involved in cell proliferation and migration by PI3K/Akt/mTOR signaling pathway. Therefore, blocking B7-H4 signaling might be a novel treatment strategy for CRC.

Downregulation of FOXP3 inhibits cell proliferation and enhances chemosensitivity to cisplatin in human lung adenocarcinoma.

Our study aimed to investigate the biological role of FOXP3 expression in human lung adenocarcinoma (LAD) tissues and evaluate its involvement in cell proliferation and chemosensitivity to cisplatin in LAD cells. Paraffin-embedded tissues from 50 LAD patients were collected to detect FOXP3 and Ki-67 expression using immunohistochemistry (IHC). Downregulation of FOXP3 in A549 cells was performed using siRNA transfection. Real-time PCR or western blot assay was performed to analyze FOXP3 expression in A549 cells. Cell proliferation and cisplatin cytotoxicity test were assessed by CCK-8 assay. The expression of FOXP3 was significantly associated with lymph node metastasis and TNM stage of LAD patients. The FOXP3 expression was positively correlated with Ki-67 labelling index(LI)in LAD tissues. The downregulated expression of FOXP3 by siRNA transfection significantly inhibited cell proliferation and enhanced chemosensitivity to cisplatin in A549 cells. The expression of FOXP3 was significantly upregulated following cisplatin treatment in A549 cells. Our study indicates that FOXP3 may potentially be a novel molecular target in combating drug resistance in the chemotherapy of LAD.