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Background: Hepatic leukemia factor (HLF) is associated with cancer onset, growth, and progression; however, little is known regarding its biological role in pan-cancer. In order to further evaluate the diagnostic and prognostic value of HLF in pan-cancer and colorectal cancer (CRC), we performed comprehensive bioinformatics analyses of the molecular mechanism of HLF in pan-cancer, with subsequent verification in CRC. Methods: We downloaded data (gene expression, clinical data, follow-up duration, and immune-related data) related to 33 solid tumor types from UCSC Xena (University of California Santa Cruz cancer database, https://xena.ucsc.edu/). HLF expression was analyzed in pan-cancer, and its diagnostic efficacy, prognostic value, and correlation with pathological stage and cancer immunity were determined. We also analyzed gene alterations in HLF and biological processes involved in its regulation in pan-cancer. Using CRC data in The Cancer Genome Atlas (TCGA), we assessed correlations between HLF and CRC diagnosis, prognosis, and drug sensitivity and performed functional enrichment analyses. Moreover, we constructed an HLF-related ceRNA regulatory network. Finally, we externally validated HLF expression and diagnostic and prognostic value in CRC using Gene Expression Omnibus (GEO) database, as well as by performing in vitro experiments. Results: HLF expression was downregulated in most tumors, and HLF showed good predictive potential for pan-cancer diagnosis and prognosis. It was closely related to the clinicopathological stages of pan-cancer. Further, HLF was associated with tumor microenvironment and immune cell infiltration in many tumors. Analyses involving cBioPortal revealed changes in HLF amplifications and mutations in most tumors. HLF was also closely associated with microsatellite instability and tumor mutational burden in pan-cancer and involved in regulating various tumor-related pathways and biological processes. In CRC, HLF expression was similarly downregulated, with implications for CRC diagnosis and prognosis. Functional enrichment analysis indicated the association of HLF with many cancer-related pathways. Further, HLF was associated with drug (e.g., oxaliplatin) sensitivity in CRC. The ceRNA regulatory network showed multigene regulation of HLF in CRC. External validation involving GEO databases and quantitative real-time polymerase chain reaction (qRT-PCR) data substantiated these findings. Conclusions: HLF expression generally exhibited downregulation in pan-cancer, contributing to tumor occurrence and development by regulating various biological processes and affecting tumor immune characteristics. HLF was also closely related to CRC occurrence and development. We believe HLF can serve as a reliable diagnostic, prognostic, and immune biomarker for pan-cancer.

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BACKGROUND: FHIP1A-DT is a long non-coding RNA (lncRNA) obtained by divergent transcription whose mechanism in pan-cancer and colorectal cancer (CRC) is unclear. We elucidated the molecular mechanism of FHIP1A-DT through bioinformatics analysis and in vitro experiments. METHODS: Pan-cancer and CRC data were downloaded from the University of California, Santa Cruz (UCSC) Genome Browser and the Cancer Genome Atlas (TCGA). We analyzed FHIP1A-DT expression and its relationship with clinical stage, diagnosis, prognosis, and immunity characteristics in pan-cancer. We also analyzed FHIP1A-DT expression in CRC and explored the relationship between FHIP1A-DT and CRC diagnosis and prognosis. Then, we analyzed the correlation between FHIP1A-DT and drug sensitivity, immune cell infiltration, and the biological processes involved in FHIP1A-DT. The competing endogenous RNA (ceRNA) regulatory network associated with FHIP1A-DT was explored. External validation was conducted using external data sets GSE17538 and GSE39582 and in vitro experiments. RESULTS: FHIP1A-DT expression was different in pan-cancer and had excellent diagnostic and prognostic capability for pan-cancer. FHIP1A-DT was also related to the pan-cancer tumor mutation burden (TMB), microsatellite instability (MSI), and immune cell content. FHIP1A-DT was downregulated in CRC, where patients with CRC with low FHIP1A-DT expression had a worse prognosis. A nomogram combined with FHIP1A-DT expression demonstrated excellent predictive ability for prognosis. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses indicated that FHIP1A-DT was associated with epigenetic modification and regulated many cancer-related pathways. The ceRNA network demonstrated the potential gene regulation of FHIP1A-DT. FHIP1A-DT was related to many chemotherapeutic drug sensitivities and immune cell infiltration such as CD4 memory resting T cells, monocytes, plasma cells, neutrophils, and M2 macrophages. The FHIP1A-DT expression and prognostic analysis of GSE17538 and GSE39582, and qPCR yielded similar external verification results. CONCLUSION: FHIP1A-DT was a novel CRC-related lncRNA related to CRC diagnosis, prognosis, and treatment sensitivity. It could be used as a significant CRC biomarker in the future.

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Digestive system cancer and COVID-19 significantly affect the digestive system, but the mechanism of interaction between COVID-19 and the digestive system cancers has not been fully elucidated. We downloaded the gene expression of COVID-19 and seven digestive system cancers (oral, esophageal, gastric, colorectal, hepatocellular, bile duct, pancreatic) from GEO and identified hub differentially expressed genes. Multiple verifications, diagnostic efficacy, prognostic analysis, functional enrichment and related transcription factors of hub genes were explored. We identified 23 common DEGs for subsequent analysis. CytoHubba identified nine hub genes (CCNA2, CCNB1, CDKN3, ECT2, KIF14, KIF20A, KIF4A, NEK2, TTK). TCGA and GEO data validated the expression and excellent diagnostic and prognostic ability of hub genes. Functional analysis revealed that the processes of cell division and the cell cycle were essential in COVID-19 and digestive system cancers. Furthermore, six related transcription factors (E2F1, E2F3, E2F4, MYC, TP53, YBX1) were involved in hub gene regulation. Via in vitro experiments, CCNA2, CCNB1, and MYC expression was verified in 25 colorectal cancer tissue pairs. Our study revealed the key biomarks and common pathogenesis of digestive system cancers and COVID-19. These may provide new ideas for further mechanistic research.

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BACKGROUND: Colon cancer (CC) is a common tumor that causes significant harm to human health. Bacteria play a vital role in cancer biology, particularly the biology of CC. Genes related to bacterial response were seldom used to construct prognosis models. We constructed a bacterial response-related risk model based on three Molecular Signatures Database gene sets to explore new markers for predicting CC prognosis. METHODS: The Cancer Genome Atlas (TCGA) colon adenocarcinoma samples were used as the training set, and Gene Expression Omnibus (GEO) databases were used as the test set. Differentially expressed bacterial response-related genes were identified for prognostic gene selection. Univariate Cox regression analysis, least absolute shrinkage and selection operator-penalized Cox regression analysis, and multivariate Cox regression analysis were performed to construct a prognostic risk model. The individual diagnostic effects of genes in the prognostic model were also evaluated. Moreover, differentially expressed long noncoding RNAs (lncRNAs) were identified. Finally, the expression of these genes was validated using quantitative polymerase chain reaction (qPCR) in cell lines and tissues. RESULTS: A prognostic signature was constructed based on seven bacterial response genes: LGALS4, RORC, DDIT3, NSUN5, RBCK1, RGL2, and SERPINE1. Patients were assigned a risk score based on the prognostic model, and patients in the TCGA cohort with a high risk score had a poorer prognosis than those with a low risk score; a similar finding was observed in the GEO cohort. These seven prognostic model genes were also independent diagnostic factors. Finally, qPCR validated the differential expression of the seven model genes and two coexpressed lncRNAs (C6orf223 and SLC12A9-AS1) in 27 pairs of CC and normal tissues. Differential expression of LGALS4 and NSUN5 was also verified in cell lines (FHC, COLO320DM, SW480). CONCLUSIONS: We created a seven-gene bacterial response-related gene signature that can accurately predict the outcomes of patients with CC. This model can provide valuable insights for personalized treatment.

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BACKGROUND: Brunner's gland adenoma is a rare benign tumor arising from Brunner's glands. It is mostly small in size, and patients with this tumor are asymptomatic. CASE PRESENTATION: We report the case of a 63-year-old woman with upper gastrointestinal obstruction for almost 10 years, who was pathologically diagnosed with large Brunner's gland adenoma of the duodenum. Postoperatively, no sign of recurrence has been noted until now. CONCLUSION: This study may help clinicians to understand and provide a more accurate diagnosis of Brunner's gland adenoma.

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Itraconazole (ITZ) is an anti-fungal drug that has been used in clinical practice for nearly 35 years. Recently, numerous experiments have shown that ITZ possesses anti-cancer properties. The Hedgehog (Hh) pathway plays a pivotal role in fundamental processes, including embryogenesis, structure, morphology and proliferation in various species. This pathway is typically silent in adult cells, and inappropriate activity is linked to various tumor types. The most important mechanism of ITZ in the treatment of cancer is inhibition of the Hh pathway through the inhibition of smoothened receptors (SMO), glioma-associated oncogene homologs (GLI), and their downstream targets. In this review, we discuss the mechanisms of ITZ in the treatment of cancer through inhibition of the Hh pathway, which includes anti-inflammation, prevention of tumor growth, induction of cell cycle arrest, induction of apoptosis and autophagy, prevention of angiogenesis, and drug resistance. We also discuss the clinical use of ITZ in many types of cancers. We hope this review will provide more information to support future studies on ITZ in the treatment of various cancers.

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Hepatocellular carcinoma (HCC) is one of the most common cancers and has a high mortality rate in less developed countries, especially in China. Galangin (GA), one of the most important and naturally active flavonoids, extracted primarily from the root of Alpinia officinarum Hance, has been demonstrated to be effective in the treatment of HCC. It is a substance with defensive actions and a broad range of biological properties, including inhibitory effects on bacteria, fungi, viruses, the control of hypertension and diabetes, and chemoprevention of several cancers. Experiments have shown that GA prevents HCC through multiple anti-cancer mechanisms, anti-genotoxic activity against environmental and dietary carcinogens; anti-proliferative effects through reversal of the Warburg effect in HCC; arrest of the cell cycle in the G0/G1 phase; induction of apoptosis via stimulation of reactive oxygen species (ROS), endoplasmic reticulum (ER) stress, and the mitochondrial-dependent apoptosis pathway; induction of autophagy; and inhibition of angiogenesis, metastasis, and multidrug resistance (MDR). In addition, synergistic effects with other chemotherapy drugs have been demonstrated. Therefore, this review is focused on the anti-HCC mechanisms of GA.

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RATIONALE: Pleomorphic liposarcoma (PLS), is a rare subtype of liposarcoma, and is considered to be of the highest malignancy grade. PATIENT CONCERNS: We aimed to analyze the clinical features, diagnosis, treatment, and recurrence of the 6 cases of PLS. DIAGNOSES: Six cases with confirmed pathological PLS presented at out hospital from January 2003 to January 2017. The postoperative pathology of 5 cases confirmed PLS, and the other was confirmed as PLS with well-differentiated liposarcoma. INTERVENTIONS: All 6 patients underwent complete tumor resection at the time of the first definite diagnosis, and one of them had underwent 3 cycles of chemotherapy treatment. OUTCOMES: There were 4 cases with local recurrence and surgery was repeated after the first radical excision. One case was not recurrent after 27 months post-operation, and the other was lost. The shortest recurrence time of all of these cases was 4 months, and the longest was 29 months after the first radical surgery. LESSONS: PLS is a rare and high-grade malignancy with high recurrence, poor prognosis, and its treatment is still highly controversial. More studies are required to determine the appropriate treatment and therapeutic strategies to improve the survival rate of patients with PLS, as the disease is associated with frequent relapse.

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