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Background Small cell lung cancer (SCLC) is a highly aggressive lung malignancy which is characteristic of rapid tumor proliferation, metastasis as well as paraneoplastic neurological syndromes (PNS). Recent studies have shown that neuro-oncological ventral antigen-1 (NOVA1) plays a crucial role in the progression of various tumors. However, its effect on SCLC is still exclusive. This study was aimed to explore NOVA1 expression in tumor tissues of SCLC patients as well as its correlation with clinicopathological characteristics and cancer-specific overall survivals. Methods In this study, the patients pathologically diagnosed with new primary SCLC were enrolled. Firstly, we compared NOVA1 expression in SCLC tissues and adjacent normal tissues by immunohistochemistry. We further investigated the association of NOVA1 expression with clinicopathological markers (especially the categories of PNS) and survival time in SCLC patients. Results Our finding exhibited that NOVA1 was remarkably expressed in SCLC tumorous tissues compared with adjacent normal lung tissues (P

Background To investigate the expression of neuro-oncological ventral antigen-1 (Nova1) in small-cell lung cancer (SCLC) and its value in clinical pathological diagnosis of SCLCs. Methods Nova1 expression in the SCLC cell line H446, lung adenocarcinoma cell line A549, squamous cell carcinoma (SCC) cell line H226 and bronchial epithelial cell line BEAS-2B were examined by RT-PCR. It’s expression in paraffin specimens of 100 SCLC cases, 15 specimens of lung adenocarcinoma cases and 15 specimens of lung SCC cases, as well as adjacent normal tissue was determined by immunohistochemistry. The positive rate of Nova1 in SCLC tissue was compared with those of traditional neuroendocrine markers CD56, Syn and CgA. Results Nova1 expression in SCLC cell line H446 was significantly higher than that of bronchial epithelial cell line BEAS-2B and lung adenocarcinoma cell line A549 and SCC cell line H226. The positive rate of Nova1 in SCLC tissue was similar to that of CD56 but higher than those of Syn and CgA. Nova1 was neither expressed in the cancer tissue nor in the adjacent normal tissue of the 15 cases of SCC and the 15 cases of adenocarcinoma. In all six cases of combined SCLC, Nova1 was expressed in the SCLC component, whereas markers of SCC or adenocarcinoma were absent. Conclusions Nova1 can be used as a novel neuroendocrine marker for pathological diagnosis of SCLC in clinical practice with high sensitivity and specificity, in addition to its role as an independent prognostic marker of overall survival and tumour recurrence, as suggested by previous studies.

Pancreatic adenocarcinoma is one of the most lethal diseases with a 5-year survival rate of about 8%. ASXL2 is an epigenetic regulator associated with various tumors including colorectal cancer, breast cancer, and myeloid leukemia. However, the role of ASXL2 in pancreatic cancer remains unclear. This is the first research focusing on the prognostic value of ASXL2 in pancreatic cancer. In this research, we aimed to explore the correlation between ASXL2 and the prognosis, as well as other features in PAAD. We obtained gene expression profiles of PAAD and normal tissues from TCGA, GEO, and Xena databases. TIMER and CIBERSORT algorithms were employed to investigate the effect of ASXL2 on tumor microenvironment. GSEA along with GO and KEGG enrichment analyses were conducted to uncover the biological functions of ASXL2. The response to various chemotherapeutic drugs was estimated by algorithms in R package “pRRophetic”, while the sensitivity to immunotherapy was quantified by TIDE score. We found that ASXL2 was upregulated in the PAAD samples and elevated expression of ASXL2 was linked to poor overall survival. ASXL2 DNA methylation contributed to ASXL2 expression. Functional annotation indicated that ASXL2 was mainly involved in inflammatory response and epithelial mesenchymal transition. Patients with high ASXL2 expression were more likely to benefit from immune checkpoint blockade, gemcitabine, and mitomycin-C. Finally, external datasets and biospecimens were used and the results further validated the aberrant expression of ASXL2 in PAAD samples. In summary, our results highlight that ASXL2 is a potential prognostic and predictive biomarker in pancreatic cancer.

Background Aggressive systemic mastocytosis (ASM) is a very rare form of systemic mastocytosis (SM). The diagnosis of ASM requires the presence of SM criteria with C finding and does not meet the criteria for mast cell leukaemia. Herein, we report an ASM case that initially mimicked lymphoma based on clinical and radiographic analyses. Case presentation: A 87-year-old woman was admitted to our hospital due to the enlargement of cervical lymph nodes and weight loss. The lymph node biopsy is infiltrated by neoplastic mast cells with pale, faintly granular cytoplasm, and with reactive eosinophils in the lesions. The infiltrate is often parafollicular in distribution and the remnant of normal follicles can be seen. The neoplastic cell population was subsequently revealed to exhibit differentiation towards the mast cell lineage by expressing CD117 and CD25. Mutation analysis of c-KIT identified D816V mutation in exon 17. Conclusion ASM diagnosis can be challenging due to its rarity. This diagnosis can be confirmed or disregarded using immunohistochemical markers, such as CD117, CD2 and CD25, in combination with molecular analysis (KITD816V).

New radiosensitizers are urgently needed for radiation therapy patients with localized hepatocellular carcinoma (HCC) that is refractory to radical surgery. We previously found that genistein, a major soy isoflavone, exerts radioprotective effects on L-02 normal liver cells at low concentrations. Here, we report that 5 µM genistein shows less harm to L-02 cells than HCC cells and that it significantly enhances the radiosensitivity of HCC cells by enhancing DNA damage, chromosomal aberrations and cell cycle arrest at G2/M phase and by exacerbating apoptosis. Mechanistically, genistein aggravates X-ray-induced decreases in the levels of phospho-Bad (Ser136) but enhances the levels of phospho-Chk2 (Thr68), phospho-ATM (Ser1981) and γ-H2AX. Micro-array analysis indicated that downregulation of POU6F and CCNE2 expression and upregulation of FBXO32 and cyclin B1 expression might play vital roles in genistein-induced radiosensitivity. These findings suggest genistein as an interesting candidate for adjuvant radiotherapy for HCC and indicate that genistein causes less harm to normal cells than HCC cells by inducing G2/M arrest and apoptosis.

Supplemental Digital Content is available in the text, Nasal-type natural killer/T-cell (NK/T-cell) lymphoma is a more aggressive sub-group of non-Hodgkin lymphoma, which is more common in Asia. The phosphatase and tensin homolog (PTEN) was originally discovered as a candidate tumor suppressor mutated and lost in various cancers. However, its clinical value and role in NK/T-cell lymphoma remain to be further explored. In the present study, we analyzed PTEN protein expression in 60 cases of human NK/T-cell lymphoma tissues and 40 cases of control nasal mucosa tissues specimens by immunohistochemical analysis. As a result, positive rate of PTEN protein expression in NK/T-cell lymphoma tissues (33.3%) is significantly lower than that of control nasal mucosa tissues (85.0%) (P .05). Instead, PTEN protein was inversely corrected with Ki-67 expression, indicating a functional role in PTEN in human NK/T-cell lymphoma (P