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Pancreatic cancer (PC) is a common gastrointestinal cancer with high invasiveness and high mortality. Curcumin is a natural polyphenol with anti-tumor activity against different cancers, including PC. Curcumin has been verified to mediate the expression of circular RNAs (circRNAs) to inhibit tumor development. This study aimed to explore the function and regulatory mechanism of curcumin on circ_0079440 in PC. PC cells were treated with different concentrations of curcumin (0, 5, 10 or 15 µM) for 24 h. Gene expression in PC cells and tissues was detected using RT-qPCR. Cell malignant phenotypes were determined by functional assays. The levels of EMT-related proteins were tested using western blot. RNA interaction was determined using RNA pulldown assay, luciferase reporter assay and RIP assay. The results showed that curcumin suppressed cell proliferative, migratory, and invasive capabilities, and weakened epithelial-mesenchymal transition (EMT) in a concentration-dependent way. Circ_0079440 was expressed at a high level in PC and its level was reduced via curcumin administration in PC cells. Rescue assays showed that circ_0079440 overexpression reversed the suppressive effects of curcumin on PC cell malignant phenotypes. Furthermore, in the xenograft mouse models, curcumin treatment inhibited tumor growth and metastasis, and circ_0079440 upregulation reversed the function of curcumin. Additionally, circ_0079440 was revealed to bind to miR-522-3p to upregulate eukaryotic initiation factor 4A1 (EIF4A1) expression in PC cells. EIF4A1 expression was also downregulated by curcumin, and EIF4A1 overexpression abolished the suppressive functions of curcumin. Moreover, EIF4A overexpression or miR-522-3p inhibition counteracted the anti-tumor effects of circ_0079440 depletion on PC development. To sum up, curcumin suppresses PC development by targeting the circ_0079440/miR-522-3p/EIF4A1 pathway, which might provide novel therapeutic targets for treatment of PC.
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The p53 protein, encoded by TP53, is a tumor suppressor that plays a critical role in regulating apoptosis, cell cycle regulation, and angiogenesis in tumor cells via controlling various downstream signals. Natural killer (NK) cell-mediated immune surveillance is a vital self-defense mechanism against cancer and other diseases, with NK cell activity regulated by various mechanisms. Among these, p53 plays a significant role in immune regulation by maintaining the homeostasis and functionality of NK cells. It enhances the transcriptional activity of NK cell-activating ligands and downregulates inhibitory ligands to boost NK cell activation and tumor-killing efficacy. Additionally, p53 influences NK cell cytotoxicity by promoting apoptosis, autophagy, and ferroptosis in different tumor cells. p53 is involved in the regulation of NK cell activity and effector functions through multiple pathways. p53 also plays a pivotal role in the tumor microenvironment (TME), regulating the activity of NK cells. NK cells are critical components of the TME and are capable of directly killing tumor cells. And p53 mutates in numerous cancers, with the most common alteration being a missense mutation. These mutations are commonly associated with poor survival rates in patients with cancer. This review details p53's role in NK cell tumor immunosurveillance, summarizing how p53 enhances NK cell recognition and tumor destruction. We also explore the potential applications of p53 in tumor immunotherapy, discussing strategies for modulating p53 to enhance NK cell function and improve the efficacy of tumor immunotherapy, along with the associated challenges. Understanding the interaction between p53 and NK cells within the TME is crucial for advancing NK cell-based immunotherapy and developing p53-related novel therapeutics.
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Células Matadoras Naturais , Neoplasias , Microambiente Tumoral , Proteína Supressora de Tumor p53 , Humanos , Células Matadoras Naturais/imunologia , Células Matadoras Naturais/metabolismo , Proteína Supressora de Tumor p53/metabolismo , Proteína Supressora de Tumor p53/genética , Proteína Supressora de Tumor p53/imunologia , Neoplasias/imunologia , Microambiente Tumoral/imunologia , Animais , Imunoterapia/métodos , Citotoxicidade ImunológicaRESUMO
OBJECTIVE: Using the preoperative pan-immune-inflammation value (PIV) and the monocyte to high-density lipoprotein ratio (MHR) to reflect inflammation, immunity, and cholesterol metabolism, we aim to develop and visualize a novel nomogram model for predicting the survival outcomes in patients with colorectal cancer (CRC). METHODS: A total of 172 patients with CRC who underwent radical resection were retrospectively analyzed. Survival analysis was conducted after patients were grouped according to the optimal cut-off values of PIV and MHR. Univariate and multivariate analyses were performed using Cox proportional hazards regression to screen the independent prognostic factors. Based on these factors, a nomogram was constructed and validated. RESULTS: The PIV was significantly associated with tumor location (P < 0.001), tumor maximum diameter (P = 0.008), and T stage (P = 0.019). The MHR was closely related to gender (P = 0.016), tumor maximum diameter (P = 0.002), and T stage (P = 0.038). Multivariate analysis results showed that PIV (Hazard Ratio (HR) = 2.476, 95% Confidence Interval (CI) = 1.410-4.348, P = 0.002), MHR (HR = 3.803, 95%CI = 1.609-8.989, P = 0.002), CEA (HR = 1.977, 95%CI = 1.121-3.485, P = 0.019), and TNM stage (HR = 1.759, 95%CI = 1.010-3.063, P = 0.046) were independent prognostic indicators for overall survival (OS). A nomogram incorporating these variables was developed, demonstrating robust predictive accuracy for OS. The area under the curve (AUC) values of the predictive model for 1-, 2-, and 3- year are 0.791,0.768,0.811, respectively. The calibration curves for the probability of survival at 1-, 2-, and 3- year presented a high degree of credibility. Furthermore, Decision curve analysis (DCA) for the probability of survival at 1-, 2-, and 3- year demonstrate the significant clinical utility in predicting survival outcomes. CONCLUSION: Preoperative PIV and MHR are independent risk factors for CRC prognosis. The novel developed nomogram demonstrates a robust predictive ability, offering substantial utility in facilitating the clinical decision-making process.
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Neoplasias Colorretais , Lipoproteínas HDL , Monócitos , Nomogramas , Humanos , Masculino , Feminino , Neoplasias Colorretais/mortalidade , Neoplasias Colorretais/cirurgia , Neoplasias Colorretais/sangue , Neoplasias Colorretais/patologia , Neoplasias Colorretais/imunologia , Estudos Retrospectivos , Pessoa de Meia-Idade , Idoso , Lipoproteínas HDL/sangue , Prognóstico , Inflamação/sangue , Período Pré-Operatório , Estadiamento de Neoplasias , Adulto , Modelos de Riscos ProporcionaisRESUMO
Background: MYRF-related mild encephalopathy with reversible myelin vacuolization (MMERV) is an inherited neurological disorder characterized by dysfunction in the central nervous system and widespread reversible leukoencephalopathy. This paper presents a confirmed case of familial MMERV and summarizes pertinent features to offer guidance for future diagnosis and treatment of MMERV. Case Introduction: We have diagnosed a case of MMERV based on a history of seizures during early childhood and recurrent speech fluency issues in adulthood, reversible abnormal intensities in bilateral white matter in the centrum semiovale and corpus callosum, and the identification of myelin regulatory factor (MYRF) heterozygous variants. Conclusion: MYRF-related mild encephalopathy with reversible myelin vacuolization is a rare autosomal dominant genetic disease, with early clinical manifestations often being seizures. The definitive diagnosis of MMERV can be confirmed through genetic analysis. Minimizing infections can help reduce disease recurrence. However, future research should explore the impact of MYRF heterozygous variants in the wider MMERV population.
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Objectives: Elderly population with cognitive impairment has been accelerating in China. This study aimed to explore the relationship between each risk factor and each cognitive domain to provide evidence for risk prevention of controlling impaired cognitive function in elderly. Methods: This cross-sectional study analyzed the cognitive status of the elderly aged 65 and above in three communities in Shizhong District of Jinan City. Cognitive status was assessed by MMSE. The influencing factors of cognitive impairment were analyzed by chi square test, correlation analysis and regression analysis. Results: Among 1,171 participants, 643 were defined as cognitive impairment with an incidence of 54.9%. And we found that there were significant differences in the incidence of cognitive impairment among residents with different gender, age, education level, hypertension and LDL-C (P < 0.05). However, BMI, marital status, smoking, physical exercise, T2DM, TC, TG and HDL-C had no significant differences in the incidence of cognitive impairment. In addition, education level (b = 1.194, P <0.001), age (b = -0.040, P = 0.001), LDL-C (b = 0.169, P = 0.018) had statistical significance on the total score of MMSE according to binary logistic regression analysis. Conclusion: Gender, age, education level, hypertension and LDL-C had significant differences in the incidence of cognitive impairment. And these risk factors could provide a basis for the early screening and intervention of cognitive impairment in the elderly.
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Emerging evidence suggests that microRNAs (miRNAs) participate in hepatocellular carcinoma (HCC) progression. Nevertheless, the mechanism of miR-7-5p in HCC cells has not been researched. In the research, the underlying biological function of miR-7-5p and SPC24 in HCC was explored. qRT-PCR was performed to measure the miR-7-5p and SPC24 level in HCC tissues and cells. The effect of miR-7-5p on HCC progression was detected by performing CCK-8, BrdU, and transwell assay. The relationship between miR-7-5p and SPC24 was determined using luciferase and RNA pull-down assays. Our findings showed that miR-7-5p was downregulated in HCC whereas SPC24 was upregulated in HCC. It was also showed that miR-7-5p upregulation restricted malignant behaviors of HCC cells, but this inhibitory effect of miR-7-5p could be relieved by its target gene SPC24. In conclusion, this research suggested that by inhibiting SPC24, miR-7-5p could act as a tumor inhibitory factor in HCC.
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Carcinoma Hepatocelular/metabolismo , Carcinoma Hepatocelular/patologia , Neoplasias Hepáticas/metabolismo , Neoplasias Hepáticas/patologia , MicroRNAs/genética , Proteínas Associadas aos Microtúbulos/antagonistas & inibidores , Apoptose/fisiologia , Carcinoma Hepatocelular/genética , Linhagem Celular , Linhagem Celular Tumoral , Movimento Celular/fisiologia , Proliferação de Células/fisiologia , Biologia Computacional/métodos , Humanos , Neoplasias Hepáticas/genética , MicroRNAs/metabolismo , Proteínas Associadas aos Microtúbulos/biossíntese , Proteínas Associadas aos Microtúbulos/genética , Proteínas Associadas aos Microtúbulos/metabolismo , Transdução de SinaisRESUMO
Dysregulation of the Wnt/ß-catenin signaling pathway is critically involved in gastric cancer (GC) progression. However, current Wnt pathway inhibitors being studied in preclinical or clinical settings for other cancers such as colorectal and pancreatic cancers are either too cytotoxic or insufficiently efficacious for GC. Thus, we screened new potent targets from ß-catenin destruction complex associated with GC progression from clinical samples, and found that scaffolding protein RACK1 deficiency plays a significant role in GC progression, but not APC, AXIN, and GSK3ß. Then, we identified its upstream regulator UBE2T which promotes GC progression via hyperactivating the Wnt/ß-catenin signaling pathway through the ubiquitination and degradation of RACK1 at the lysine K172, K225, and K257 residues independent of an E3 ligase. Indeed, UBE2T protein level is negatively associated with prognosis in GC patients, suggesting that UBE2T is a promising target for GC therapy. Furthermore, we identified a novel UBE2T inhibitor, M435-1279, and suggested that M435-1279 acts inhibit the Wnt/ß-catenin signaling pathway hyperactivation through blocking UBE2T-mediated degradation of RACK1, resulting in suppression of GC progression with lower cytotoxicity in the meantime. Overall, we found that increased UBE2T levels promote GC progression via the ubiquitination of RACK1 and identified a novel potent inhibitor providing a balance between growth inhibition and cytotoxicity as well, which offer a new opportunity for the specific GC patients with aberrant Wnt/ß-catenin signaling.
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Proteínas de Neoplasias/genética , Receptores de Quinase C Ativada/genética , Neoplasias Gástricas/tratamento farmacológico , Enzimas de Conjugação de Ubiquitina/genética , beta Catenina/genética , Animais , Complexo de Sinalização da Axina/genética , Linhagem Celular Tumoral , Proliferação de Células/efeitos dos fármacos , Feminino , Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos , Humanos , Masculino , Camundongos , Proteínas de Neoplasias/antagonistas & inibidores , Receptores de Quinase C Ativada/antagonistas & inibidores , Neoplasias Gástricas/genética , Neoplasias Gástricas/patologia , Enzimas de Conjugação de Ubiquitina/antagonistas & inibidores , Ubiquitinação/efeitos dos fármacos , Via de Sinalização Wnt/genética , Ensaios Antitumorais Modelo de XenoenxertoRESUMO
BACKGROUND: Pancreatic fistula is a common complication after pancreaticoduodenectomy, which could be caused by: soft pancreatic tissue, pancreatic duct diameter < 3 mm and body mass index ≥25 kg/m2. Here we report a case of pancreatic fistula due to obstruction of the jejunal loop due to compression of the jejunal loop by the superior mesenteric vessels. CASE PRESENTATION: A 68-year-old man was admitted to our ward due to intermittent epigastric distension and pain. After various examinations and treatments, he was diagnosed with middle bile duct cancer. Pancreaticoduodenectomy was performed, and pancreaticojejunostomy and hepaticojejunostomy were completed by lifting the jejunal loop from behind the superior mesenteric vessels to the upper region of the colon. On postoperative day 9, the patient developed acute diffuse peritonitis, and on postoperative day 10, the patient underwent a second exploratory laparotomy, during which it was confirmed that the pancreatic fistula was caused by obstruction of the jejunal loop due to compression of the jejunal loop by the superior mesenteric vessels, then the patient recovered and was discharged alive after retrograde drainage in the jejunum. CONCLUSIONS: The superior mesenteric vessels after pancreaticoduodenal surgery can compress the jejunal loop and cause obstruction leading to serious complications, and it is recommended that general surgeons should avoid lifting the jejunal loop from the posterior aspect of the superior mesenteric vessels to complete the anastomosis.
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Obstrução Intestinal/etiologia , Artéria Mesentérica Superior , Oclusão Vascular Mesentérica/etiologia , Fístula Pancreática , Neoplasias Pancreáticas , Pancreaticoduodenectomia , Idoso , Anastomose Cirúrgica/efeitos adversos , Humanos , Obstrução Intestinal/cirurgia , Doenças do Jejuno/etiologia , Doenças do Jejuno/cirurgia , Masculino , Fístula Pancreática/etiologia , Fístula Pancreática/cirurgia , Neoplasias Pancreáticas/cirurgia , Pancreaticoduodenectomia/efeitos adversos , Pancreaticojejunostomia/efeitos adversosRESUMO
BACKGROUND: Gastric cancer (GC) is one of the most globally prevalent cancers in the world. The pathogenesis of GC has not been fully elucidated, and there still lacks effective targeted therapeutics. The influence of altered kinesin superfamily protein 22 (KIF22) expression in GC progression is still unclearly. The aim of this study was to investigate the KIF22 effects on GC and related mechanisms. METHODS: Gastric carcinoma tissues and matching non-cancerous tissues were collected from patients with GC who have accepted a radical gastrectomy in Lanzhou University Second Hospital from May 2013 to December 2014. The expression of KIF22 was examined in GC of 67 patients and 20 para-carcinoma tissues by immunochemical staining. The relationship between the expression of KIF22 and clinicopathologic characteristics was next investigated in the remaining 52 patients except for 15 patients who did not complete follow-up for 5 years. Cell viability was performed via 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) test and colony formation assay in the MGC-803 and BGC-823 GC cells. Cell scratch and trans-well invasion assay was performed to assess migration ability in the MGC-803 and BGC-823 GC cells. Gene set enrichment analysis (GSEA) pathway enrichment analysis was performed to explore the potential functions. Cell cycle was detected by flow cytometry. In addition, the two GC cell lines were used to elucidate the underlying mechanism of KIF22 in GC in vitro via assessing the effects on mitogen-activated protein kinase and extracellular regulated protein kinases (MAPK/ERK) signal transduction pathway-related expressions by Western blotting assays. The differences were compared by t tests, one-way analysis of variance, and Chi-squared tests. RESULTS: The study showed that KIF22 was up-regulated in GC, and KIF22 high expression was significantly related to differentiation degree (χâ=â12.842, Pâ=â0.002) and poorly overall survivals. GSEA pathway enrichment analysis showed that KIF22 was correlated with the cell cycle. Silence of KIF22 decreased the ability of the proliferation and migration in gastric cells, induced G1/S phase cell cycle arrest via regulating the MAPK-ERK pathways. CONCLUSIONS: KIF22 protein level was negatively correlated with prognosis. KIF22 knockdown might inhibit proliferation and metastasis of GC cells via the MAPK-ERK signaling pathway.
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Movimento Celular/fisiologia , Proliferação de Células/fisiologia , Proteínas de Ligação a DNA/metabolismo , MAP Quinases Reguladas por Sinal Extracelular/metabolismo , Cinesinas/metabolismo , Neoplasias Gástricas/metabolismo , Western Blotting , Ciclo Celular/genética , Ciclo Celular/fisiologia , Linhagem Celular Tumoral , Movimento Celular/genética , Proliferação de Células/genética , Proteínas de Ligação a DNA/genética , MAP Quinases Reguladas por Sinal Extracelular/genética , Feminino , Citometria de Fluxo , Regulação Neoplásica da Expressão Gênica/genética , Regulação Neoplásica da Expressão Gênica/fisiologia , Humanos , Imuno-Histoquímica , Imunoprecipitação , Cinesinas/genética , Sistema de Sinalização das MAP Quinases/genética , Sistema de Sinalização das MAP Quinases/fisiologia , Masculino , RNA Interferente Pequeno/genética , RNA Interferente Pequeno/metabolismo , Neoplasias Gástricas/genéticaRESUMO
Primary synovial sarcoma of the duodenal bulb is a rare mesenchymal tumor with special morphological features. It usually originates from the major joints or tendon sheaths of the extremities and mostly seen in young population, but rarely found in gastrointestinal tract. In this manuscript, we reported the first case of synovial sarcoma arising between the intestinal wall of the duodenal bulb with a concomitant SYT/SSX type of the t(X;18) translocation. A 49-year-old male presented to our hospital with a 2-month history of upper abdominal pain along with a 4-day amply jaundice. Tumor marker testing showed only a slight increase of carbohydrate antigen 19-9 (CA19-9). A computed tomography scan of his abdomen showed that indeterminate tissue occupied the duodenal bulb wall, compressed the surrounding tissues, and measured roughly 5.0 cm × 7.7 cm × 8.7 cm. Since the sarcoma grows between the intestinal wall, which cannot be detected by endoscopy, an initial diagnosis of duodenal wall stromal tumor was made at that time. Postoperative Immunohistochemistry results showed that the tumor was positive for the expression of transducin-like enhancer of split 1, B-cell lymphoma 2, and Vimentin. These pathological findings were indicative of the diagnosis of synovial sarcoma, but still did not provide sufficient diagnostic evidence. Finally we confirmed the diagnosis by using fluorescence in situ hybridization (FISH) with detection of the t(X;18) (SYT-SSX) translocation. No such lesions were found on preoperative examination, so a diagnosis of primary duodenal synovial sarcoma was made. After literature review, we found four reports of duodenal synovial sarcomas, all of which could be detected endoscopically, but there were no results of long-term follow-up. This case is the first reported case of synovial sarcoma arising between the intestinal walls of the duodenal bulb treated twice with ifosfamide and followed up for 13 months without recurrence.
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Small intestinal hemangioma is a rare condition that can be divided histologically into capillary, cavernous or mixed types, among which the cavernous type is the most common. Here we report a case of small intestinal cavernous hemangioma with chronic hemorrhage in 44-year-old man. The patient complained of weakness and dizziness for 2 years that aggravated 1 month before admission accompanied by intermittent melena. Laboratory tests suggest severe anemia, and computed tomography, gastroscopy and colonoscopy all revealed signs of anemia. Capsule endoscopy detected small intestinal erosions, bleeding lesions and prominent neoplasms. An exploratory laparotomy was performed, in which the segment of the jejunum with lesions was resected. Pathological examination of the resected jejunum identified the neoplasm as cavernous hemangioma of the small intestine, which was the cause of severe anemia.
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Circular RNAs (circRNAs) are class of endogenous RNAs that have a role in the regulation of gene expression. The present study aimed to investigate the diagnostic value and role of circRNA in the pathogenesis of leukoaraiosis (LA). The present study performed Arraystar Human circRNA Array analysis of 6 samples from LA cases and 6 samples from control cases. Differentially expressed (DE) circRNAs between two samples were identified through foldchange (>1.5fold) screening. Afterwards, based on DE circRNAs, the gene ontology (GO) analysis of upregulated DE genes identified from DE circRNAs demonstrated that DE genes were primarily associated with cellular metabolic processes, membranebound organelles and binding. However, none were enriched in the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway. Downregulated DE genes were enriched in cellular localization, cytoplasm and kinase binding. For the KEGG pathways, the downregulated DE genes were primarily associated with the insulin signaling pathway. The results of the present study indicated that the DE genes from differently expressed circRNAs may have an important role in the pathogenesis of LA and may be a novel targfet for further research.
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Leucoaraiose/genética , RNA/genética , Transcriptoma , Idoso , Regulação para Baixo , Feminino , Perfilação da Expressão Gênica , Ontologia Genética , Humanos , Masculino , Pessoa de Meia-Idade , RNA Circular , Regulação para CimaRESUMO
Ubiquitin-conjugating enzymes (E2 enzymes) such as UBE2T target proteins for degradation via the proteasome. Here, we examined the effects of UBE2T on the progression of gastric cancer. UBE2T was highly expressed in gastric tumors and gastric cancer cells. siRNA-mediated suppression of UBE2T inhibited gastric cancer cell proliferation and colony formation by promoting cell cycle arrest at G2/M phase and increasing apoptosis. Suppression of UBE2T also attenuated the invasive and metastatic abilities of gastric cancer cells by altering expression of epithelial-mesenchymal transition (EMT)-related factors. A xenograft model in which nude mice were injected with UBE2T knockdown human gastric cancer cells confirmed that suppression of UBE2T also decreased tumor formation and growth in vivo. Expression levels of CCND1, Phospho-GSK3B, WNT family members, and MYC were all affected by UBE2T knockdown. These results suggest that UBE2T plays a critical role in gastric cancer, and that it may serve as a useful prognostic biomarker and therapeutic target in gastric cancer patients.
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Técnicas de Silenciamento de Genes , Neoplasias Gástricas/patologia , Enzimas de Conjugação de Ubiquitina/genética , Enzimas de Conjugação de Ubiquitina/metabolismo , Animais , Ciclo Celular , Linhagem Celular Tumoral , Proliferação de Células , Sobrevivência Celular , Progressão da Doença , Transição Epitelial-Mesenquimal , Regulação Neoplásica da Expressão Gênica , Redes Reguladoras de Genes , Humanos , Camundongos , Camundongos Nus , Transplante de Neoplasias , Neoplasias Gástricas/genética , Neoplasias Gástricas/metabolismo , Regulação para CimaRESUMO
Bisdemethoxycurcumin (BDMC) is a demethoxy derivative of curcumin. In this study, a human gastric adenocarcinoma xenograft model was generated in vivo using nude mice and BDMC was observed to suppress the growth and activity of tumors, in addition to improving the physical and mental capacity of the mice. An increased number of apoptotic cells, decreased ratio of B-cell lymphoma 2 (Bcl-2)/Bcl-2-associated X protein and increased caspase-3 expression was also observed following treatment with BDMC, indicating that BDMC may promote apoptosis in tumors via mitochondrial modulation. The growth of SGC 7901 gastric cancer cells was inhibited and arrested at G1 phase. Specific indicators of mitochondrial dysfunction, a reduction in adenosine triphosphate generation, the inner mitochondrial membrane potential, augmentation of reactive oxygen species production and cytochrome c were also detected in the mitochondria following treatment with BDMC. These results indicate that BDMC attenuates gastric adenocarcinoma growth by inducing mitochondrial dysfunction.
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OBJECTIVE: To examine the incidence of hepatitis B virus (HBV) S gene mutation in recipients with recurrent HBV infection after liver transplantation (LT) and to evaluate the clinical significance of these mutants. METHODS: Two-hundred-and-ninety-nine patients who received LT for HBV-related liver diseases in single centre were enrolled in the study and followed up. Serum HBV DNA was amplified by fluorescence quantitative polymerase chain reaction, and HBV-S gene mutation was detected by Sanger's enzymatic method. RESULTS: Twelve of the 299 patients developed recurrent HBV after LT, and 2 of these 12 carried a mutant of the HBV-S gene (incidence rate of 16.67%). One of the patients had T126I and G145A mutations, and the other had a M 133L mutation. Cox regression modelling identified the risk factors of HBV recurrence after LT as HBV-YMDD mutants (P =0.01), HBV-S mutants (P =0.03) and compliance decrease (P =0.03). CONCLUSION: HBV-S mutants may contribute to recurrence of HBV after LT, and the mechanism should be addressed in future studies.
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Vírus da Hepatite B/genética , Hepatite B/virologia , Transplante de Fígado , Proteínas do Envelope Viral/genética , Adulto , DNA Viral/genética , Feminino , Variação Genética , Humanos , Masculino , Pessoa de Meia-Idade , Mutação , Período Pós-Operatório , RecidivaRESUMO
Glycolytic pyruvate kinase isoenzyme type M2 (M2-PK) plays a key role in tumor metabolism and energy production. Vascular endothelial growth factor (VEGF) is critical in regulating angiogenesis which is an essential process required for tumor growth and metastasis. These two genes may function in accordance with tumor development. The purpose of this study was to investigate the relationship between the expression of M2-PK and VEGF, and their association with clinicopathological features in patients with advanced gastric cancer. Expression of M2-PK and VEGF were examined in 142 cases of paraffin-embedded tissue blocks from patients with advanced gastric cancer. M2-PK expression was found to strongly correlate with that of VEGF (r = 0.718). In addition, expression of M2-PK and VEGF correlates with tumor size (p = 0.0001, and p = 0.0017, respectively), depth of invasion (p = 0.0024, and p = 0.0261, respectively), and lymph node metastasis (p = 0.036, and p = 0.028, respectively). The high expression levels of M2-PK and VEGF may indicate poor prognosis in patients with advanced gastric cancer.