RESUMEN
OBJECTIVES: This study aimed to evaluate the accuracy and interobserver reliability of diagnosing and subtyping gastric intestinal metaplasia (IM) among general pathologists and pathology residents at a university hospital in Thailand, focusing on the challenges in the histopathologic evaluation of gastric IM for less experienced practitioners. METHODS: The study analyzed 44 non-neoplastic gastric biopsies, using a consensus diagnosis of gastrointestinal pathologists as the reference standard. Participants included 6 general pathologists and 9 pathology residents who assessed gastric IM and categorized its subtype (complete, incomplete, or mixed) on digital slides. After initial evaluations and receiving feedback, participants reviewed specific images of gastric IM, as agreed by experts. Following a one-month washout period, a reevaluation of the slides was conducted. RESULTS: Diagnostic accuracy, interobserver reliability, and time taken for diagnosis improved following training, with general pathologists showing higher accuracies than residents (median accuracy of gastric IM detection: 100 % vs. 97.7 %). Increased years of experience were associated with more IM detection accuracy (p-value<0.05). However, the overall median accuracy for diagnosing incomplete IM remained lower than for complete IM (86.4 % vs. 97.7 %). After training, diagnostic errors occurred in 6 out of 44 specimens (13.6 %), reported by over 40 % of participants. Errors involved omitting 5 slides with incomplete IM and 1 with complete IM, all showing a subtle presence of IM. CONCLUSIONS: The study highlights the diagnostic challenges in identifying incomplete gastric IM, showing notable discrepancies in accuracy and interobserver agreement. It underscores the need for better diagnostic protocols and training to enhance detection and management outcomes.
Asunto(s)
Metaplasia , Variaciones Dependientes del Observador , Patólogos , Humanos , Metaplasia/patología , Biopsia/métodos , Reproducibilidad de los Resultados , Internado y Residencia , Estómago/patología , Tailandia , Patología Clínica/métodos , Patología Clínica/educación , Femenino , Errores Diagnósticos/estadística & datos numéricos , Errores Diagnósticos/prevención & control , Neoplasias Gástricas/patología , Neoplasias Gástricas/diagnóstico , MasculinoRESUMEN
Background: Pogonatherum paniceum (P. paniceum) (Lam.) Hack. plays an important role in detoxification. However, its anticancer activity has not yet been elucidated. The aim of our study was to examine the suppressive proliferation, anti-migration and mutagenic/antimutagenic properties of P. paniceum. Moreover, we set out to determine the cellular mechanism underlying its antiproliferation. Methods: To investigate P. paniceum's anticancer ability, HCT116 and HT29 cell lines were treated with a water extract containing P. paniceum, and then the cell viability was examined using the trypan blue exclusion method which were compared to HEK293 (non-cancerous cells). The anticancer effects were investigated by MTS (3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium) and colony formation assay. Apoptosis induction, cell cycle distribution, and migration abilities were assessed by cell death detection enzyme-linked immunoassay (ELISA), flow cytometry, and wound healing assay. Finally, the mutagenicity and antimutagenicity were evaluated using the micronucleus assay. Results: Treatment with P. paniceum caused a loss of cell viability in HCT116 and HT29 cells (not found in HEK293), which had an IC50 (half-maximal inhibitory concentration) of 1,156.2 and 1,207.0 µg/mL, respectively. We found that P. paniceum significantly inhibited the proliferative function of HCT116 and HT29 cells. To find the mechanism that exerts a suppressive proliferation effect on P. paniceum, we determined the DNA fragmentation and cell cycle distribution. We also found that P. paniceum treatment increased apoptosis and arrested of the cell cycle at G0/G1 remarkably when compared with the control group. Moreover, P. paniceum could decrease the migration of HCT116 and HT29 cancer cells. Finally, the treatment of P. paniceum did not induce micronucleus formation but did decrease the micronucleus frequency against mutagen-mitomycin C. Conclusions: P. paniceum did not possess any toxicity (cytotoxic and mutagenic) but has the potential for anticancer activity against human colorectal cells by increasing apoptosis, which leads to the suppression of cell proliferation. P. paniceum also inhibits cell migration and exerts antimutagenicity, thereby suggesting that P. paniceum might be useful for colorectal cancer treatment.