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Transcatheter arterial chemoembolization (TACE) is a standard treatment for intermediate-stage hepatocellular carcinoma (HCC). However, TACE can cause deterioration of liver functions. We aimed to identify the factors that influence deterioration of liver function after TACE. We retrospectively analyzed 262 patients who underwent TACE as initial treatment for HCC with Child–Pugh grade A. We divided them into three groups stratified by the etiology of underlying liver disease. Patients were classified into hepatitis B virus (HBV) group, hepatitis C virus (HCV) group, and non-HBV / non-HCV (NBNC) group. Liver functions at one month after TACE and time to Child–Pugh grade B or C were compared between the three groups. The HBV, HCV and NBNC groups contained 23, 123 and 116 patients, respectively. The decline in albumin level after TACE was significantly higher in NBNC group than other groups (p = 0.02). NBNC group showed a shorter time to Child–Pugh grade deterioration compared with HBV group and HCV group (p < 0.001). Multivariate Cox regression analysis showed that NBNC group was a significant factor for Child–Pugh grade deterioration (Hazard ratio 3.74, 95% confidence interval 1.89–7.40, p < 0.001). These results revealed that liver functions worsened most remarkably in NBNC group after TACE.

Lenvatinib has become a first line treatment for unresectable hepatocellular carcinoma (HCC). However, continued administration is impossible in many patients due to treatment resistance and severe adverse events. This study aimed to identify predicting factors to select patients likely to benefit from lenvatinib treatment. We retrospectively analyzed 53 patients who were treated with lenvatinib for unresectable HCC. They were divided to two groups; low C-reactive protein (CRP) group with pretreatment serum CRP level < 1.0 mg/dL and high CRP group with serum CRP level ≥ 1.0 mg/dl. Overall survival (OS), total amount administered, and period of treatment were compared between the two groups. The high CRP group showed a significantly poorer OS than the low CRP group (0.0% vs 71.5%/ 1year, p < 0.01). Multivariate analyses revealed that high CRP was a significant negative factor for OS (HR: 7.69, 95% confidence interval: 2.43-24.3, p < 0.001), and this result was independent of Child-Pugh score and existing tumor factors. Relative dose intensity at 8 weeks was lower (p = 0.01) and time to treatment failure was shorter (P < 0.001) in the high CRP group. CRP level was associated with OS in HCC patients treated with lenvatinib. CRP could be a useful marker to identify patients most likely to benefit from lenvatinib treatment.

Liver function is a most important prognostic factor in patients with liver cirrhosis. Also, portal hypertension is a fatal complication of liver cirrhosis and variceal treatment is indispensable. However, changes of liver functions after endoscopic variceal treatments are unknown. The aim of this study was to evaluate prognosis and liver functions after endoscopic injection sclerotherapy (EIS) and endoscopic variceal ligation (EVL). A total of liver cirrhotic 103 patients who underwent prophylactic EIS and EVL were enrolled. Overall survival rate was higher in EIS group than EVL group (p = 0.03). Multivariate analysis showed that EIS was a negative factor for death (HR: 0.46, 95% confidence interval: 0.24–0.88, p = 0.02). Liver functions were assessed by blood test taken at before and 3 months after treatment. In EIS group, albumin and prothrombin time improved (p < 0.01), leading to improvement of Child–Pugh score, ALBI score and MELD score (p < 0.05). However, these did not improve in EVL group. EIS was a significant factor related to the elevated value of albumin after treatment in linear regression analysis (estimated regression coefficient: 0.17, 95% confidence interval: 0.05–0.29, p = 0.005). These results revealed that EIS could improve liver functions and prognosis.

Backgrounds Poorly differentiated clusters (PDCs), defined as solid cancer nests comprising ≥ 5 cancer cells lacking tubular formation, may reflect the phenotype of epithelial-mesenchymal transition. The diagnostic utility in pathological practice and clinical significance in pancreatic ductal carcinoma (PDAC) has not been fully explored. This study aimed to investigate the presence of PDCs in PDAC and evaluate their clinical implications. Methods We examined the presence of PDCs in 102 cases with PDAC. Tumor clusters with ≥ 5 clusters were classified as high PDCs and < 5 were classified as low PDCs. The association of pathological parameters and survival was assessed for high and low PDCs. Subgroup analyses were also performed for 37 cases following neoadjuvant chemotherapy (NAT). Results High PDCs were significantly associated with larger tumors, advanced pT category (≥ T3), lymphatic and vascular invasion, positive surgical margins, high tumor budding (TB), elevated CA19-9 levels, and increased recurrence risk ( P  = 0.014, 0.021, 0.011, 0.013, 0.026, < 0.001, 0.016, 0.027, respectively). Moreover, this was associated with worse overall survival and disease-free survival of PDAC, especially in cases following NAT ( P  < 0.001). Additionally, high PDCs in cases following NAT was an independent prognostic factor for shorter overall (Hazard ratio (HR): 9.131, P  = 0.012) and disease-free survival (HR: 3.896, P  = 0.018) in multivariable Cox regression analysis, exceeding TB in prognostic impact. Conclusion PDCs in the actual pathological diagnosis are more useful as a prognostic marker for PDAC than TB. Due to the limited sample size and broad confidence intervals, the findings of this study should be interpreted with caution and require validation in larger, independent cohorts.

A 73‐year‐old man visited our hospital due to hyperintestinal peristalsis and diarrhea. He had been undergoing regular annual checkups for dust lung disease. Contrast‐enhanced computed tomography scan showed edematous thickening of the rectal wall with contrast effect. A colonoscopy revealed a submucosal tumor‐like protrusion in the Rb lesion of the rectum without neoplastic epithelial changes. Forceps biopsies of the overlying mucosa were non‐diagnostic; however, endoscopic ultrasound‐guided fine needle biopsy revealed that the specimen was poorly differentiated non‐small cell invasive carcinoma. Then, we performed a chest computed tomography and a newly detected mass lesion in the upper lobe of the right lung. Based on immunohistochemical analysis and image findings, the patient was diagnosed with rectal metastasis from lung cancer. Subsequently, sputum cytology confirmed the diagnosis of lung adenocarcinoma. Rectal submucosal tumor‐like protrusions are occasionally encountered. When a non‐exposed rectal tumor is identified, it is important to differentiate metastatic diseases, consider endoscopic ultrasound‐guided fine needle biopsy, and make a definitive diagnosis through detailed immunohistochemical evaluation and systemic imaging surveillance.

We examined the epidemiological trends, including the distribution of sex, age, and disease etiology, in HCC incident cases, over 24 years. Data of 20,547 HCC patients (1996–2019) were analyzed in this prospective study. We divided the study period into four 6-yearly quarters. HCC etiology was categorized as hepatitis B virus (HBV) infection, HBV + hepatitis C virus (HCV) infection, HCV infection, and both negative (non-BC). The incident cases of HCC per quarter of the study period were 4311 (21.0%), 5505 (26.8%), 5776 (28.1%), and 4955 (24.1%), sequentially. Overall, 14,020 (68.2%) patients were male. The number of HCC cases in patients < 60 years, 60–69 years, 70–79 years, and ≥ 80 years were 3711 (18.1%), 6652 (32.4%), 7448 (36.2%), and 2736 (13.3%), respectively. The average age of newly-diagnosed patients increased in each quarter. HCC was associated with HBV, HBV + HCV, and HCV infections and non-BC in 2997 (14.6%), 187 (0.9%), and 12,019 (58.5%), and 5344 (26.0%) cases, respectively. The number of HCV-associated cases decreased in each quarter, while that of non-BC-associated cases increased. HCC incident cases tend to increase in the elderly and in non-BC patients; in contrast, HCC incident cases due to HCV tend to decrease.

Background Long-chain fatty acyl CoA synthetase 4 (ACSL4) is crucial for lipid metabolism, primarily catalyzing the formation of 12–20 carbon chain fatty acids. ACSL4 is upregulated in various cancers and linked to aggressive behavior and poor survival. A bioinformatics study showing ACSL4 upregulation in pancreatic cancer. However, utility for actual pathological diagnosis and clinical significance in pancreatic ductal adenocarcinoma (PDAC) and intraductal papillary mucinous neoplasm (IPMN) are unexplored. This study aimed to investigate ACSL4 expression in PDAC and IPMN, and evaluate its clinical implications. Methods We examined ACSL4 expression using immunohistochemistry in 165 patients with PDAC and IPMN. Differences in ACSL4 expression between malignant and benign lesions were evaluated using the Pearson χ2 test. The association between ACSL4 expression, pathological parameters, and survival was assessed through Kaplan-Meier and Cox regression analyses in 96 patients with invasive cancer. Results Compared to normal pancreatic ducts, low-grade pancreatic intraepithelial neoplasm, and intraductal papillary mucinous adenoma (IPMA) (3.3%, 3.4%, and 2.7%, respectively), ACSL4 expression was significantly higher in invasive PDAC, noninvasive intraductal papillary mucinous carcinoma (IPMC), and invasive IPMC (77%, 86.7%, and 93.9%, respectively). In invasive cancers, low ACSL4 expression was associated with a higher frequency of lymphovascular invasion and recurrence and shorter disease-free survival ( P  = 0.006). Additionally, low ACSL4 expression was an independent prognostic factor for shorter disease-free survival in multivariable Cox regression analysis (HR = 2.409, 95% CI: 1.121–5.180, P  = 0.024). Conclusion ACSL4 expression helps differentiate cancerous from precancerous lesions in pancreatic cancer, but low expression is linked to a higher frequency of lymphovascular invasion and shorter disease-free survival in invasive cases. Due to the limited sample size and broad confidence intervals, the findings of this study should be interpreted with caution and require validation in larger, independent cohorts.

Patients with unresectable pancreatic ductal adenocarcinoma (UR-PDAC) are vulnerable to rapid nutritional deterioration. The clinical relevance of short-term nutritional change during the diagnostic-to-treatment interval (DTI) remains unclear. In this study, we evaluated whether a dynamic change in the Geriatric Nutritional Risk Index (ΔGNRI) during the DTI is associated with treatment tolerability, treatment continuity, and survival. This single-center retrospective study included 120 patients with histologically confirmed UR-PDAC who initiated first-line palliative chemotherapy between January 2016 and April 2024. ΔGNRI was defined as the GNRI immediately before chemotherapy minus the GNRI at the initial visit. ΔGNRI was primarily analyzed as a continuous variable, and an exploratory cut-off value of -6.8 was determined by receiver operating characteristic analysis. One-to-one propensity score matching was performed as a sensitivity analysis. Clinically significant adverse events (AEs) were defined as grade ≥3 AEs or AEs requiring treatment modification, hospitalization, or treatment discontinuation. Patients in the GNRI-decreased group had more frequent clinically significant non-hematologic AEs, including gastrointestinal AEs, higher hospitalization rates due to AEs, and more frequent early treatment discontinuation. ΔGNRI remained independently associated with early treatment discontinuation and failure to transition to second-line therapy in multivariable analyses. Patients in the GNRI-decreased group also had significantly shorter times to treatment failure and overall survival. These findings were consistent in propensity score-matched analyses. Dynamic nutritional decline during the DTI was associated with impaired treatment resilience and poor survival outcomes in UR-PDAC. ΔGNRI may help identify patients with emerging nutritional vulnerability before chemotherapy.

Zinc is an essential trace element and plays critical roles in cellular integrity and biological functions. Excess copper induced both oxidative stress and endoplasmic reticulum (ER) stress in liver-derived cultured cells. Excess copper also induced impairment of autophagic flux at the step of autophagosome–lysosome fusion, as well as Mallory–Denk body (MDB)-like inclusion body formation. Zinc ameliorated excess copper-induced impairment of autophagic flux and MDB-like inclusion body formation via the maintenance of ER homeostasis. Furthermore, zinc also ameliorated free fatty acid-induced impairment of autophagic flux. These results indicate that zinc may be able to protect hepatocytes from various ER stress-related conditions.