Insulinoma-associated protein 1 (INSM1) is an important biomarker of Achaete-scute homolog-like 1-driven pathways. For diagnosis of pancreatic neuroendocrine tumors (PanNET), chromogranin A (CGA), synaptophysin (SYP), and neural cell adhesion molecule (NCAM) were also considered as potential biomarkers. However, it is often difficult to diagnose it immunohistochemically. Hence, we examined the expression pattern of INSM1 in pancreatic solid tumors. We detected INSM1, CGA, SYP, and NCAM immunohistochemically, in 27 cases of NET [pure type: 25 cases, mixed adenoneuroendocrine carcinoma (MANEC): 2 cases]. We included 5 cases of solid-pseudopapillary neoplasm (SPN), 7 cases of acinar cell carcinoma (ACC), and 15 cases of pancreatic ductal adenocarcinoma (PDAC) as the control group. Nuclear expression of INSM1 was found in all PanNET pure type cases. However, expression of INSM1 was negative in PDAC, ACC, and SPN in all cases, whereas faint expression was seen in the cytoplasm from SPN. MANEC comprises of two components: neuroendocrine carcinoma and adenocarcinoma components. The NET component was positive for INSM1 expression, whereas the PDAC component does not express INSM1, which aids in distinguishing these components. Our results suggest that INSM1 is a useful immunohistochemical marker for diagnosing pancreatic neuroendocrine tumor.
Purpose The prospective pilot study was designed to evaluate the preventive effects of amino-acid-rich elemental diet (ED), Elental ® , on chemotherapy-induced oral mucositis in patients with colorectal cancer. The factors influencing its efficacy are also investigated. Methods A total of 22 eligible patients with colorectal cancer experiencing grade 1–3 oral mucositis during treatment with fluorouracil-based chemotherapy entered the current study. Their average age was 67 years. There were 10 male and 12 female. The PS was 0 in the majority of patients. Patients received two courses of the same chemotherapy regimen and Elental ® concurrently after recovery to grade 0 or 1 oral mucositis. Results FOLFOX6 + bevacizumab in 8 patients, FOLFIRI + bevacizumab in 8 patients, FOLFIRI + panitumumab in 1 patient, FOLFIRI in 1 patient, XELOX + bevacizumab in 2 patients, and S-1 + cetuximab in 2 patients were used as first-line (16 cases) or as second-line (6 cases) chemotherapy. Dose reduction of 5-fluorouracil (5-FU) or oral fluoropyrimidine was performed in the 2 patients achieving grade 3 oral mucositis and in the 3 patients achieving grade 2 oral mucositis. The maximum grade of oral mucositis decreased in 18 of the 22 patients during the first treatment course with Elental ® ( p = 0.0002) and in 20 of the 22 patients in the second course ( p < 0.0001). Multivariate analyses found that the dose reduction in 5-FU or oral fluoropyrimidine, ED intake, and the prior administration of ED were each a significant factor for the preventive efficacy on oral mucositis. Conclusion The amino-acid-rich elemental diet Elental ® may be useful as a countermeasure for 5-FU-based chemotherapy-induced oral mucositis in patients with colorectal cancer.
Background/Aim: We investigated the antiproliferative effect of quercetin on liver cancer cell lines. Materials and Methods: Thirteen liver cancer cell lines were cultured followed by treatment with varying concentrations of quercetin (0-100 μM) or quercetin and 5-FU, and the cell viability was analysed by the MTT assay. Flow cytometry was also used to examine cell cycle progression after treatment with quercetin. Results: The addition of quercetin resulted in a dose-and time-dependent suppression of cell proliferation. In some cell lines, treatment with quercetin and 5-FU caused an additional or synergistic effect. Most cell lines displayed cell cycle arrest at different phases of the cell cycle. Conclusion: Quercetin inhibits the proliferation of liver cancer cells via induction of apoptosis and cell cycle arrest.Hepatocellular carcinoma (HCC) is the most frequent primary cancer, and an important medical problem (1). Many HCC patients have a history of chronic hepatitis or liver cirrhosis caused by Hepatitis B virus (HBV) or Hepatitis C virus (HCV) infection (2-4). Treatments for poor liver function associated with hepatitis are limited and outcomes are poor. Even with the most successful treatments, the 5year recurrence rate of HCC is very high (1). Treating and preventing recurrence is critical for improving survival rates.Quercetin is a type of flavonoid contained in many plants, and possesses antioxidant, anti-inflammatory, and immuno-logical capabilities (5). Quercetin can suppress cell proliferation and induce apoptosis in human cancers, including breast, lung, oral, and prostate; however, there is no report on its effect on liver cancer (6-9). In the current study, we examined the antitumor effects of quercetin on 13 HCC cell lines in vitro. Materials and MethodsCell lines and cell culture. This study utilized 11 HCC cell lines (KIM-1, KYN-1, KYN-2, KYN-3, HAK-1A, HAK-1B, HAK-2, HAK-3, HAK-4, HAK-5, and HAK-6), and 2 human combined hepatocellular and cholangiocarcinoma (CHC) cell lines (KMCH-1 and KMCH-2). The cell lines were originally established in the Department of Pathology, Kurume University Faculty of Medicine, and each of them retains the morphological and functional features of the original tumor as previously described (10-18). Each cell line was grown in Dulbecco's modified Eagle medium (Nissui Seiyaku, Co., Japan) supplemented with 2.5% heat-inactivated (56˚C, 30 min) fetal bovine serum (Bioserum, Victoria, Australia), 100 U/ml penicillin, 100 μg/ml streptomycin (GIBCO BRL/Life Technologies, Inc., Gaithersburg, MD, USA) and 12 mmol/l sodium bicarbonate, in a 5% CO 2 humidified atmosphere at 37˚C. Effects of quercetin on the proliferation of hepatocellular carcinoma and combined hepatocellular and cholangiocarcinoma cell lines in vitro.The effects of quercetin with and without 5-FU on proliferation were examined using 3-(4,5-dimethylthiazol-2yl-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay kit (Chemicon, Temecula, CA, USA) as previously described (10). Quercetin was obtained from Sigma Chem...
BackgroundInsulinoma‐associated protein 1 (INSM1) has been reported to be a useful marker for diagnosing pancreatic neuroendocrine tumours (PNETs). However, INSM1 expression in endoscopic ultrasound‐guided fine needle aspiration cytology has not been examined. We evaluated INSM1 expression in the cytology of cases diagnosed with PNETs.MethodsWe immunocytochemically stained INSM1 and Ki‐67 in 14 PNET cases, and according to the 2017 World Health Organisation criteria, seven PNET Grade 1 cases, four Grade 2 cases and three Grade 3/neuroendocrine carcinoma cases were identified. As a control for INSM1 and Ki‐67 expression, we used cytological specimens from 15 cases of pancreatic ductal adenocarcinoma.ResultsIn PNET cases, INSM1‐expressing tumour cells were identified in all cytological specimens of PNET. The median INSM1 expression rate in Grade 1 cases was 49.8% (mean ± standard deviation: 55.1 ± 12.5%, min: 39.3%, max: 74.1%), and in Grade 2 and Grade 3/neuroendocrine carcinoma cases was 81.1% (mean ± standard deviation: 77.6 ± 18.6%, min: 50.3%, max: 100%). However, there was no correlation between INSM1 and Ki‐67 expression (r = −0.15). The median expression rate in PNET cases was 64.3%, which was significantly higher than that in pancreatic ductal adenocarcinoma cases (P < 0.0001).ConclusionINSM1 immunocytochemistry of cytological specimens obtained from endoscopic ultrasound‐guided fine needle aspiration cytology can accurately diagnose PNETs; therefore, INSM1 could be an important diagnostic tool in assessing therapeutic strategies, including molecular‐targeted therapy.
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