Background Adenosquamous carcinoma (ASC)with concurrent gastric carcinoma with lymphoid stroma (GCLS) are extremely rare tumors. There are only limited cases reported in the literature. Epstein–Barr virus (EBV) infection was found in the concomitant GCLS, but none in the ASC. Here, we report the first case of gastric cancer with EBV infection detected in both ASC and GCLS. Case presentation A 59-year-old man complained of intermittent upper abdominal pain. The gastric endoscopy revealed a type IIc tumor located in the gastric body near the fundus of the stomach. Histological examination of the gastric tumor showed the coexistence of ASC and GCLS. Both components were positive for EBV-encoded RNA (EBER) in situ hybridization. Neoplastic nests of the former were positive for p63, p40 and CK5/6. The glandular components showed positive acid mucus in the Alcian-blue periodic-acid-schiff (AB-PAS) staining. There was significant difference in the expression of epidermal growth factor receptor (EGFR) between adenocarcinoma and squamous carcinoma, but not in other proteins such as human epidermal growth factor receptor 2 (HER2), p53 and mismatch repair proteins. The role of EGFR signaling pathway needs to be further explored in the differentiation of squamous carcinoma in the gastric ASC. Finally, a diagnosis of early EBV associated gastric ASC with concurrent GCLS (pT1bN1) was made. The patient took a single-drug S1 periodically for half a year after the surgery and has been disease free during 8 months of medical follow-up. Conclusions This is the first case of EBV associated gastric ASC with concurrent GCLS, and pathologists and clinicians should recognize and pay attention to this type of tumor.
Pancreatic cancer is a leading cause of cancer death due to its early metastasis and limited response to the current therapies. Metastasis is a complicated multistep process, which is determined by complex genetic alterations. Despite the identification of many metastasis-related genes, distinguishing the drivers from numerous passengers and establishing the causality in cancer pathophysiology remains challenging. Here, we established a high-throughput and piggyBac transposon-based genetic screening platform, which enables either reduced or increased expression of chromosomal genes near the incorporation site of the gene search vector cassette that contains a doxycycline-regulated promoter. Using this strategy, we identified YWHAZ as a key regulator of pancreatic cancer metastasis. We demonstrated that functional activation of Ywhaz by the gene search vector led to enhanced metastatic capability in mouse pancreatic cancer cells. The metastasis-promoting role of YWHAZ was further validated in human pancreatic cancer cells. Overexpression of YWHAZ resulted in more aggressive metastatic phenotypes in vitro and a shorter survival rate in vivo by modulating epithelial-to-mesenchymal transition. Hence, our study established a high-throughput screening method to investigate the functional relevance of novel genes and validated YWHAZ as a key regulator of pancreatic cancer metastasis.
What is known and objective Anti‐CD19 CAR‐T cell therapy is effective in B‐cell lymphoma. However, it is rarely used in lymphoma combined with other malignant tumours. Case description A relapsed/refractory follicular lymphoma (r/r FL) patient underwent anti‐CD19 CAR‐T cell therapy and achieved complete response to lymphoma. However, gastric adenocarcinoma (GAC) was diagnosed during the cellular therapy. After infusion of CAR‐T cells, he received curative treatment for GAC, and maitained complete response in both r/r FL and GAC after the treatment. What is new and conclusion Anti‐CD19 CAR‐T therapy is an effective treatment for r/r FL, also provided opportunity for the sequential therapy of GAC, and remained significant quality of life afterwards.
The short‐tandem‐repeats (STR) profiles of MGc80‐3 and HeLa partially overlap, raising suspicion of contamination in the MGc80‐3 cell line. However, there has not been any relevant study demonstrating whether MGc80‐3 was fully replaced by HeLa cells, just mixed with HeLa cells (co‐existing), or was a somatic hybrid with HeLa cells. In addition to STR profiling, various approaches, including single nucleotide polymorphisms genotyping, polymerase chain reaction, screening for human papillomaviruses type 18 (HPV‐18) fragment, chromosome karyotyping, pathological examination of xenografts, tissue‐specific‐90‐gene expression signature and high‐throughput RNA sequencing were used to determine the nature of MGc80‐3. Our study found that the abnormal STR profile, partially overlapping with that of HeLa cells (64.62% to 71.64%), could not verify MGc80‐3 as a HeLa cell line. However, the STR 13.3 repeat allele in the D13S317 locus that seemed to be unique to HeLa cells was detected in MGc80‐3. Almost all the MGc80‐3 cells exhibited HPV‐18 fragments in the genome as well as certain HeLa marker chromosomes, such as M7 and M12. The molecular assay of the 90‐gene expression signature still considered MGc80‐3 as a stomach cancer using an algorithmic analysis. The expression pattern of multiple genes in MGc80‐3 was quite different from that in HeLa cells, which showed that certain characteristics belonged to gastric cancer cell lines. High throughput RNA sequencing showed the distinct patterns of gene expression in MGc80‐3. In conclusion, MGc80‐3 cell line is a somatic hybrid with HeLa cells rather than a pure gastric cancer cell line.
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