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1.
J Oncol ; 2022: 7531452, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-35342424

RESUMO

Background and Aims: Conflicting results are often observed in the prognosis of patients with ruptured hepatocellular carcinoma (rHCC), and there are currently very few studies on the long-term postoperative outcomes of ruptured hepatocellular carcinoma patients. This study aimed to distinguish between the postoperative prognosis of rHCC patients with cirrhosis (rHCC-C) and those without cirrhosis (rHCC-NC) using some serum markers. Methods: We collected the data of 151 rHCC patients treated at our centers from January 2010 to March 2021. 62 had no cirrhosis, and 89 had cirrhosis. The prognosis of rHCC-C and rHCC-NC groups was compared using the Kaplan-Meier method. We used multivariate Cox regression to analyze prognostic factors in rHCC patients, and subgroup analysis was performed on the two groups of patients. Results: The long-term prognosis of rHCC-NC patients was better than that of rHCC-C patients. Tumor diameter, Barcelona clinic liver cancer (BCLC) stage, HBsAg, positive Hepatitis C virus (HCV) antibodies, elevated creatinine, and elevated T-bilirubin were prognostic factors for overall survival (OS) in rHCC-C patients. However, only alpha-fetoprotein (AFP) > 92 ng/mL was a prognostic factor for OS in rHCC-NC patients. In noncirrhotic patients, HBsAg positivity was only associated with OS. Similarly, the presence or absence of microvascular invasion (MVI) also had different results in the two groups. Conclusions: There are differences in serum alpha-fetoprotein (AFP) levels, the presence of microvascular invasion (MVI), and HBsAg positivity between rHCC-C and rHCC-NC patients, indicating that the analysis of these prognostic factors may help improve the management of rHCC patients and provide a direction for future treatment options.

2.
Ann Surg ; 2022 Jan 25.
Artigo em Inglês | MEDLINE | ID: mdl-35081573

RESUMO

OBJECTIVE: To compare the short- and long-term outcomes of robot-assisted (RALR), laparoscopic (LLR), or open liver resection (OLR) in the treatment of BCLC stage 0-A hepatocellular carcinoma (HCC). SUMMARY BACKGROUND DATA: Following the Balliol IDEAL classification, long-term oncological outcomes can be used to evaluate the value of minimally invasive techniques in the treatment of HCC, and to assess whether they should become a standard practice. METHODS: Data from prospective cohorts of patients with BCLC stage 0-A HCC who underwent curative liver resection using OLR, LLR, or RALR at Tongji Hospital were reviewed. The short-term and long-term oncological outcomes of these three different surgical approaches after adequate follow-up were compared using propensity score matching to reduce selection bias. RESULTS: Of 369 patients included in this study (71, RALR; 141, LLR; and 157, OLR), 56 patients in each of the three groups were chosen for further comparison, after PSM. In the minimally invasive group (RALR+LLR), both the operative time and duration of Pringle's maneuver were significantly longer than those in the OLR group; however, the length of hospital stay was significantly shorter. There were no significant differences in the other intraoperative parameters and the incidence of postoperative complications among the three groups. HCC recurrence in the minimally invasive group when compared with the OLR group was characterized by a significantly higher proportion of single lesion or early stage HCC. However, there were no significant differences in the 5-year disease-free survival (DFS) (63.8%, 54.4%, and 50.6%) or overall survival rates (80.8%, 78.6%, and 75.7%, respectively) among the three groups. Clinically significant portal hypertension (CSPH) was the only risk factor that negatively affected the 5-year DFS rate. Multivariate Cox regression analysis showed that CSPH, serum alpha-fetoprotein level (≥400 ng/ml), and Edmondson-Steiner grading (III+IV) were independent risk factors for poor long-term survival. CONCLUSION: Both robotic and laparoscopic hepatectomies were safe and effective for patients with BCLC stage 0-A HCC when compared with open hepatectomy.

3.
BMC Surg ; 22(1): 6, 2022 Jan 08.
Artigo em Inglês | MEDLINE | ID: mdl-34996410

RESUMO

BACKGROUND: Ingestion of fish bones leading to gastric perforation and inducing abscess formation in the caudate lobe of the liver is very rare. CASE PRESENTATION: A 67-year-old man presented to our hospital with a 2-day history of subxiphoid pain. There were no specific symptoms other than pain. Laboratory tests showed only an increase in the number and percentage of neutrophils. Contrast-enhanced Computerized tomography (CT) of the abdomen showed two linear dense opacities in the gastric cardia, one of which penetrated the stomach and was adjacent to the caudate lobe of the liver, with inflammatory changes in the caudate lobe. We finally diagnosed his condition as a caudate lobe abscess secondary to intestinal perforation caused by a fishbone based on the history and imaging findings. The patient underwent 3D laparoscopic partial caudate lobectomy, incision and drainage of the liver abscess, and fishbone removal. The procedure was successful and we removed the fishbone from the liver. The patient was discharged on the 9th postoperative day without other complications. CONCLUSIONS: Liver abscess caused by foreign bodies requires multidisciplinary treatment. Especially when located in the caudate lobe, we must detect and remove the cause of the abscess as early as possible. Foreign bodies that perforate the gastrointestinal tract can penetrate to the liver and cause abscess formation, as in this case. When exploring the etiology of liver abscesses, we should investigate the general condition, including the whole gastrointestinal tract.


Assuntos
Corpos Estranhos , Migração de Corpo Estranho , Laparoscopia , Abscesso Hepático , Idoso , Animais , Corpos Estranhos/complicações , Corpos Estranhos/diagnóstico por imagem , Corpos Estranhos/cirurgia , Migração de Corpo Estranho/complicações , Migração de Corpo Estranho/diagnóstico por imagem , Migração de Corpo Estranho/cirurgia , Humanos , Abscesso Hepático/diagnóstico por imagem , Abscesso Hepático/etiologia , Abscesso Hepático/cirurgia , Masculino
4.
Am J Chin Med ; 50(1): 313-332, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-34963428

RESUMO

18[Formula: see text]-glycyrrhetinic acid (GA) is the active ingredient of the traditional Chinese medicinal herb Glycyrrhizae radix et rhizoma. We previously demonstrated that GA inhibited tumor growth in hepatocellular carcinoma (HCC). However, the effect of GA on transforming growth factor-[Formula: see text] (TGF-[Formula: see text]-induced epithelial-mesenchymal transition (EMT) and metastasis were still unclear. In this study, in vitro transwell assays and immunofluorescence (IF) demonstrated that GA inhibited TGF-[Formula: see text]-induced migration, invasion and EMT of HCC cells. However, it had little effect on the inhibition of proliferation by TGF-[Formula: see text]. Moreover, we confirmed that GA suppressed the metastasis of HCC cells in vivousing an ectopic lung metastasis model. Furthermore, we found that GA inhibited TGF-[Formula: see text]-induced EMT mainly by reducing the phosphorylation of signal transducer and activator of transcription 3 (STAT3), which played an essential role in TGF-[Formula: see text]-induced EMT and cell mobility. Mechanistically, GA inhibited the phosphorylation of STAT3 by increasing the expression of Src homology 2 domain-containing protein tyrosine phosphatases 1 and 2 (SHP1 and SHP2). Therefore, we concluded that GA inhibited TGF-[Formula: see text]-induced EMT and metastasis via the SHP1&SHP2/STAT3/Snail pathway. Our data provide an attractive therapeutic target for future multimodal management of HCC.


Assuntos
Carcinoma Hepatocelular , Ácido Glicirretínico , Neoplasias Hepáticas , Carcinoma Hepatocelular/tratamento farmacológico , Carcinoma Hepatocelular/genética , Carcinoma Hepatocelular/metabolismo , Linhagem Celular Tumoral , Movimento Celular , Transição Epitelial-Mesenquimal , Ácido Glicirretínico/farmacologia , Humanos , Neoplasias Hepáticas/patologia , Invasividade Neoplásica , Fator de Transcrição STAT3/metabolismo , Fator de Crescimento Transformador beta1/genética , Fator de Crescimento Transformador beta1/metabolismo
5.
Clin Transl Med ; 11(11): e635, 2021 11.
Artigo em Inglês | MEDLINE | ID: mdl-34841685

RESUMO

BACKGROUND: Aberrant TAK1 (transforming growth factor ß-activated kinase 1) activity is known to be involved in a variety of malignancies, but the regulatory mechanisms of TAK1 remain poorly understood. GRAMD4 (glucosyltransferase Rab-like GTPase activator and myotubularin domain containing 4) is a newly discovered p53-independent proapoptotic protein with an unclear role in HCC (hepatocellular carcinoma). RESULTS: In this research, we found that GRAMD4 expression was lower in HCC samples, and its downregulation predicted worse prognosis for patients after surgical resection. Functionally, GRAMD4 inhibited HCC migration, invasion and metastasis. Mechanistically, GRAMD4 interacted with TAK1 to promote its protein degradation, thus, resulting in the inactivation of MAPK (Mitogen-activated protein kinase) and NF-κB pathways. Furthermore, GRAMD4 was proved to recruit ITCH (itchy E3 ubiquitin protein ligase) to promote the ubiquitination of TAK1. Moreover, high expression of TAK1 was correlated with low expression of GRAMD4 in HCC patients. CONCLUSIONS: GRAMD4 inhibits the migration and metastasis of HCC, mainly by recruiting ITCH to promote the degradation of TAK1, which leads to the inactivation of MAPK and NF-κB signalling pathways.


Assuntos
Carcinoma Hepatocelular/tratamento farmacológico , MAP Quinase Quinase Quinases/antagonistas & inibidores , Proteínas Mitocondriais/farmacologia , Metástase Neoplásica/tratamento farmacológico , Carcinoma Hepatocelular/fisiopatologia , Humanos , Neoplasias Hepáticas/tratamento farmacológico , Neoplasias Hepáticas/fisiopatologia , MAP Quinase Quinase Quinases/uso terapêutico , Proteínas Mitocondriais/uso terapêutico , Metástase Neoplásica/prevenção & controle , Proteínas Repressoras/farmacologia , Proteínas Repressoras/uso terapêutico , Transdução de Sinais/efeitos dos fármacos , Transdução de Sinais/fisiologia , Ubiquitina-Proteína Ligases/farmacologia , Ubiquitina-Proteína Ligases/uso terapêutico
6.
World J Gastrointest Surg ; 13(8): 796-805, 2021 Aug 27.
Artigo em Inglês | MEDLINE | ID: mdl-34512903

RESUMO

Hepatocellular carcinoma (HCC) is the most common type of liver cancer with a high mortality rate worldwide. The percentage of HCC patients with vascular invasion is high. However, tumor thrombus in the hepatic vein (HVTT) has a lower incidence than tumor thrombus in the portal vein (PVTT). Conventionally, HCC patients with HVTT are treated the same as HCC patients with PVTT and offered sorafenib or other systemic agents. However, according to recent studies, it is evident that HCC with HVTT shows different outcomes when classified into different subgroups. In this review, we discuss the recent progress and changes in treatment of HCC with HVTT.

7.
Adv Sci (Weinh) ; 8(15): e2100233, 2021 08.
Artigo em Inglês | MEDLINE | ID: mdl-34085419

RESUMO

Aberrant mechanical properties and immunosuppression are the two key factors that limit the antitumor efficacy of T cell immune checkpoint blockade inhibitors, e.g., programmed cell death-1 antibody (PD-1 Ab), against solid tumors in the clinic. This study leverages hyperbaric oxygen (HBO) for the first time to address these two issues and reports the PD-1-Ab-mediated immune responses against various stroma-rich solid malignancies. The results demonstrate that HBO promoted PD-1 Ab delivery and T cells infiltration into tumor parenchyma by depleting the extracellular matrix's main components, such as collagen and fibronectin. Furthermore, HBO disrupts hypoxia-mediated immunosuppression and helps PD-1 Ab trigger robust cytotoxic T lymphocytes and long-lasting immunological memory to inhibit tumor relapses. Such enhanced immune responses are effective in solid tumors from rodents and the cancer cells from hepatocellular carcinoma patients. The results illustrate that HBO bolsters antitumor efficacy of PD-1 Ab, and the HBO-PD-1 Ab combination is a promising stroma-rich solid tumors' treatment in the clinic.


Assuntos
Oxigenação Hiperbárica/métodos , Imunidade/imunologia , Neoplasias Hepáticas/imunologia , Neoplasias Hepáticas/terapia , Receptor de Morte Celular Programada 1/imunologia , Linfócitos T/imunologia , Animais , Linhagem Celular Tumoral , Modelos Animais de Doenças , Camundongos , Camundongos Endogâmicos BALB C
8.
Medicine (Baltimore) ; 100(20): e25785, 2021 May 21.
Artigo em Inglês | MEDLINE | ID: mdl-34011038

RESUMO

RATIONALE: Esophageal carcinoma is an aggressive cancer with extremely poor therapeutic outcomes due to its high metastatic potential and a significant risk of recurrence after radical resection. Liver is the most common metastatic target organ of esophageal carcinoma, followed by the lungs, bones, and brain. Few cases of solitary pancreatic and hepatic metastases of esophageal carcinoma have been reported. PATIENT CONCERNS: We report the case of a 67-year-old male presenting with pancreatic and hepatic lesions. In addition, a friable lesion with an irregular nodular surface in the distal esophagus was detected by esophagogastroduodenoscopy. DIAGNOSIS: Pathohistological examination confirmed esophageal squamous cell carcinoma. The pancreatic lesion was also biopsied via ultrasound-guided fine needle aspiration, which also revealed squamous cell carcinoma. The hepatic lesion was also identified as metastatic carcinoma by magnetic resonance imaging, most likely of the same origin. INTERVENTIONS: Due to comorbidities that precluded surgery, the patient was administered adjuvant therapy and a multidisciplinary decision was made for palliative care. OUTCOMES: The patient died 1 month later due to multiorgan failure caused by hemorrhage from a peptic ulcer. CONCLUSION: To our knowledge, this is only the sixth case of pancreatic metastasis of esophageal squamous cell carcinoma. This case report suggests to clinicians the importance of considering potential comorbidities in every patient with advanced cancer, such as gastric ulcer and cachexia.


Assuntos
Neoplasias Esofágicas/diagnóstico , Carcinoma de Células Escamosas do Esôfago/diagnóstico , Neoplasias Hepáticas/diagnóstico , Cuidados Paliativos/métodos , Neoplasias Pancreáticas/diagnóstico , Idoso , Quimioterapia Adjuvante , Aspiração por Agulha Fina Guiada por Ultrassom Endoscópico , Endoscopia do Sistema Digestório , Neoplasias Esofágicas/patologia , Neoplasias Esofágicas/terapia , Carcinoma de Células Escamosas do Esôfago/secundário , Carcinoma de Células Escamosas do Esôfago/terapia , Esôfago/diagnóstico por imagem , Esôfago/patologia , Evolução Fatal , Humanos , Fígado/diagnóstico por imagem , Fígado/patologia , Neoplasias Hepáticas/secundário , Neoplasias Hepáticas/terapia , Imageamento por Ressonância Magnética , Masculino , Pâncreas/diagnóstico por imagem , Pâncreas/patologia , Neoplasias Pancreáticas/secundário , Neoplasias Pancreáticas/terapia
9.
Theranostics ; 11(3): 1345-1363, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-33391538

RESUMO

During the past decades, drugs targeting transforming growth factor-ß (TGFß) signaling have received tremendous attention for late-stage cancer treatment since TGFß signaling has been recognized as a prime driver for tumor progression and metastasis. Nonetheless, in healthy and pre-malignant tissues, TGFß functions as a potent tumor suppressor. Furthermore, TGFß signaling plays a key role in normal development and homeostasis by regulating cell proliferation, differentiation, migration, apoptosis, and immune evasion, and by suppressing tumor-associated inflammation. Therefore, targeting TGFß signaling for cancer therapy is challenging. Recently, we and others showed that blocking TGFß signaling increased chemotherapy efficacy, particularly for nanomedicines. In this review, we briefly introduce the TGFß signaling pathway, and the multifaceted functions of TGFß signaling in cancer, including regulating the tumor microenvironment (TME) and the behavior of cancer cells. We also summarize TGFß targeting agents. Then, we highlight TGFß inhibition strategies to restore the extracellular matrix (ECM), regulate the tumor vasculature, reverse epithelial-mesenchymal transition (EMT), and impair the stemness of cancer stem-like cells (CSCs) to enhance cancer chemotherapy efficacy. Finally, the current challenges and future opportunities in targeting TGFß signaling for cancer therapy are discussed.


Assuntos
Antineoplásicos/farmacologia , Antineoplásicos/uso terapêutico , Neoplasias/tratamento farmacológico , Neoplasias/metabolismo , Transdução de Sinais/efeitos dos fármacos , Fator de Crescimento Transformador beta/metabolismo , Animais , Apoptose/efeitos dos fármacos , Movimento Celular/efeitos dos fármacos , Transição Epitelial-Mesenquimal/efeitos dos fármacos , Matriz Extracelular/efeitos dos fármacos , Humanos , Microambiente Tumoral/efeitos dos fármacos
10.
Carcinogenesis ; 42(4): 631-639, 2021 04 30.
Artigo em Inglês | MEDLINE | ID: mdl-33367515

RESUMO

The TGF-ß receptor kinase inhibitors (TRKI) have been reported to inhibit tumorigenicity in colon cancer. However, there is no direct evidence showing that these inhibitors function through inhibiting the TGF-ß- mediated tumor-promoting effects in vivo. We established a TGF-ß inducible reporter system by inserting a luciferase reporter gene to the vector downstream of TGF-ß-inducible promoter elements, and transfected it into colon cancer cell lines. TRKIs SB431542 and LY2109761 were used to treat TGF-ß inducible cells in vitro and in vivo. The luciferase activity was induced 5.24-fold by TGF-ß in CT26 inducible cells, while it was marginally changed in MC38 inducible cells lacking Smad4 expression. Temporary treatment of mice with SB431542 inhibited the TGF-ß pathway and TGF-ß induced bioluminescence activity in vivo. Long-term treatment with LY2109761 inhibited tumorigenicity and liver metastasis in vivo in concomitant with reduced luciferase activity in the tumor. In this study, we established a model to monitor the TGF-ß pathway in vivo and to compare the antitumor effects of TRKIs. Based on this novel experimental tool, we provided direct evidences that LY2109761 inhibits tumorigenicity and liver metastasis by blocking the pro-oncogenic functions of TGF-ß in vivo.


Assuntos
Carcinogênese/efeitos dos fármacos , Neoplasias do Colo/tratamento farmacológico , Receptores de Fatores de Crescimento Transformadores beta/genética , Fator de Crescimento Transformador beta/genética , Animais , Benzamidas/farmacologia , Linhagem Celular Tumoral , Proliferação de Células/efeitos dos fármacos , Neoplasias do Colo/genética , Neoplasias do Colo/patologia , Dioxóis/farmacologia , Modelos Animais de Doenças , Humanos , Camundongos , Inibidores de Proteínas Quinases/farmacologia , Pirazóis/farmacologia , Pirróis/farmacologia , Receptores de Fatores de Crescimento Transformadores beta/antagonistas & inibidores , Transdução de Sinais/efeitos dos fármacos
11.
World J Clin Cases ; 9(36): 11495-11503, 2021 Dec 26.
Artigo em Inglês | MEDLINE | ID: mdl-35071583

RESUMO

BACKGROUND: Hepatocellular carcinoma (HCC) accompanied by a tumor thrombus is very common. However, the treatment strategy is controversial and varies by the location of the thrombus. CASE SUMMARY: We report herein a case of HCC with a tumor thrombus in the suprahepatic inferior vena cava (IVC), which was successfully treated by hepatectomy combined with thrombectomy following sorafenib chemotherapy. A 47-year-old woman with chronic hepatitis was diagnosed with HCC. Computed tomography and magnetic resonance imaging showed that the tumor lesion was located in the right half of the liver, and a tumor thrombus was detected in the suprahepatic IVC near the right atrium. After multi-departmental discussion and patient informed consent, right major hepatectomy and total removal of the tumor thrombus were successfully performed under cardiopulmonary bypass. There were no serious complications after surgery. Following sorafenib treatment, no recurrence has been detected so far (11 mo later). CONCLUSION: Surgical treatment followed by adjuvant sorafenib therapy might be an acceptable choice for HCC patients with tumor thrombosis in the IVC.

12.
Am J Cancer Res ; 10(2): 662-673, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32195034

RESUMO

Type-2 11ß-hydroxysteroid dehydrogenase (HSD11B2) is a key enzyme which converts cortisol to inactive cortisone and is involved in tumor progression and metastasis. Several studies have shown that the promotion of tumor progression and metastasis by HSD11B2 resulted from its physiological function of inactivating glucocorticoids (GC). However, the underlying molecular mechanisms by which HSD11B2 drives metastasis, in addition to inactivating GC, are still unclear. In our study, a series of in vivo and in vitro assays were performed to determine the function of HSD11B2 and the possible mechanisms underlying its role in CRC metastasis. mRNA transcriptome array analysis was used to identify the possible downstream targets of HSD11B2. We found that the ectopic expression of HSD11B2 significantly promoted the migration, invasion and metastasis of colorectal cancer (CRC) cells both in vitro and in vivo, while it did not affect their proliferation in either case. Mechanically, HSD11B2 appeared to enhance cell migration and invasion by upregulating the expression of fibroblast growth factor binding protein 1 (Fgfbp1), and subsequently increasing the phosphorylation of AKT. Furthermore, AKT activation partially mediated the increased expression of Fgfbp1 induced by HSD11B2. HSD11B2 expression was positively correlated with Fgfbp1 and p-AKT expression in clinical samples of CRC. Additionally, knockdown of either Fgfbp1 or AKT impaired the migration and invasion capability of CRC cells with HSD11B2 overexpression, suggesting that HSD11B2 promoted the migration, invasion and metastasis of CRC cells via the Fgfbp1-AKT pathway. Therefore, targeting HSD11B2 or Fgfbp1 may be a novel treatment strategy for inhibiting the metastasis of CRC.

13.
Medicine (Baltimore) ; 98(45): e17832, 2019 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-31702638

RESUMO

INTRODUCTION: The prognosis for recurrent intrahepatic cholangiocarcinoma with bone metastasis remains dismal and its treatment poses a challenge for oncologists. To date, only 2 cases were reported in which pembrolizumab, an agent against programmed cell death protein-1 (PD-1), combined with chemotherapy led to a complete response. The safety and efficacy of nivolumab-based immunotherapy combined with lenvatinibin intrahepatic cholangiocarcinoma is unknown. PATIENT CONCERNS: A 40-year-old female was identified as having a lesion of 7.0 cm in diameter in the right lobe of the liver. In addition, calculi in the main and left hepatic bile ducts as well as the gallbladder were found. DIAGNOSIS: Based on the results of imaging studies and tumor biomarker level, the patient was initially diagnosed as having intrahepatic cholangiocellular carcinoma and cholelithiasis, after which surgery was performed. The pathological examination confirmed that the tumor was cholangiocarcinoma. Adjuvant chemotherapy was administered after surgery. However, the patient developed recurrent lesions at the 5th month after surgery, and the cholangiocarcinoma expanded to the right thoracic vertebral pedicle (T7-8) at the 6th month. INTERVENTIONS: The patient underwent percutaneous microwave ablation after recurrence in the liver was identified. After that, the patient received nivolumab plus lenvatinib. OUTCOMES: The lesions in the liver decreased in size and disappeared after treatment with nivolumab plus lenvatinib. Additionally, the metastases in the right thoracic vertebral pedicle were stable after 9 months of therapy. LESSONS: Immunotherapy has revolutionized the treatment of non-small-cell lung cancer, melanoma, and advanced renal cell carcinoma. In this case, the patient achieved an excellent radiological and symptomatic response after receiving nivolumab plus lenvatinib combination therapy. Patients suffering from cholangiocarcinoma with dMMR status and a high tumor mutation burden (TMB) may have a consistent eutherapeutic effect with anti-PD-1-directed treatment.


Assuntos
Neoplasias dos Ductos Biliares/tratamento farmacológico , Ductos Biliares Intra-Hepáticos/patologia , Neoplasias Ósseas/tratamento farmacológico , Neoplasias Ósseas/secundário , Colangiocarcinoma/tratamento farmacológico , Adulto , Anticorpos Monoclonais Humanizados/uso terapêutico , Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico , Neoplasias dos Ductos Biliares/cirurgia , Ductos Biliares Intra-Hepáticos/cirurgia , Colangiocarcinoma/cirurgia , Feminino , Humanos , Recidiva Local de Neoplasia , Compostos de Fenilureia/uso terapêutico , Quinolinas/uso terapêutico , Ablação por Radiofrequência , Análise de Sobrevida , Resultado do Tratamento
14.
Eur J Surg Oncol ; 45(10): 1887-1894, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31405632

RESUMO

BACKGROUND: Partial hepatectomy has been used to treat patients with resectable hepatocellular carcinoma (HCC) which spontaneously ruptured. It is still controversial as to whether emergency partial hepatectomy (EmPH) should be carried out at the time of rupture, or the patients should initially be managed by operative or non-operative treatment to stop the bleeding, followed by staged early or delayed partial hepatectomy when the patient's condition becomes stable. METHODS: Consecutive 10-year patients with ruptured HCC managed at our center were included in this study. Patients who underwent partial hepatectomy were further subdivided into the EmPH group, the staged early partial hepatectomy (SEPH) group, and the staged delayed partial hepatectomy (SDPH) group. Univariate and multivariate analyses of factors affecting overall survival(OS) were conducted before and after propensity score matching analyses amongst the included patients. OS, postoperative mortality, recurrence free survival (RFS), and peritoneal metastatic rates were compared. The risk factors of peritoneal metastases were determined using the COX regression analysis. RESULTS: The 130 patients who underwent partial hepatectomy were subdivided into the EmPH group (surgery at the time of rupture, n = 30), the SEPH group (surgery ≤ 8 days of rupture, n = 67), and the SDPH group (surgery > 8 days of rupture, n = 33). The remaining 86 patients underwent non-surgical treatment. Partial hepatectomy was an independent predictor of better OS (HR 2.792, P < 0.001). For resectable HCC, the 30-day mortality, OS, and RFS were similar between the EmPH group, and the staged partial hepatectomy (SPH) group which included the patients who underwent SEPH and SDPH. The SEPH group had significantly better OS and RFS. Multivariate COX regression analysis demonstrated that SDPH was strongly associated with postoperative peritoneal dissemination (OR 28.775, P = 0.003). CONCLUSION: Partial hepatectomy provided significantly better survival than non-surgical treatment for patients who presented with ruptured HCC. Early partial hepatectomy within 8 days of rupture which included EmPH (carefully selected) and SEPH, resulted in significantly less patients with peritoneal dissemination and better long-term survival outcomes (especially RFS) than SDPH.


Assuntos
Carcinoma Hepatocelular/cirurgia , Emergências , Hepatectomia/métodos , Neoplasias Hepáticas/cirurgia , Estadiamento de Neoplasias , Pontuação de Propensão , Carcinoma Hepatocelular/diagnóstico , Carcinoma Hepatocelular/mortalidade , China/epidemiologia , Feminino , Seguimentos , Humanos , Neoplasias Hepáticas/diagnóstico , Neoplasias Hepáticas/mortalidade , Masculino , Pessoa de Meia-Idade , Estudos Retrospectivos , Fatores de Risco , Ruptura Espontânea , Taxa de Sobrevida/tendências , Fatores de Tempo , Resultado do Tratamento
15.
Front Oncol ; 9: 587, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31338327

RESUMO

Small nucleolar RNAs (SnoRNAs) are a class of non-coding RNAs divided into two classes: C/D box snoRNAs and H/ACA box snoRNAs. The canonical function of C/D box and H/ACA box snoRNAs are 2'-O-ribose methylation and pseudouridylation of ribosomal RNAs (rRNAs), respectively. Emerging evidence has demonstrated that snoRNAs are involved in various physiological and pathological cellular processes. Mutations and aberrant expression of snoRNAs have been reported in cell transformation, tumorigenesis, and metastasis, indicating that snoRNAs may serve as biomarkers and/or therapeutic targets of cancer. Hence, further study of the functions and underlying mechanism of snoRNAs is valuable. In this review, we summarize the biogenesis and functions of snoRNAs, as well as the association of snoRNAs in different types of cancers and their potential roles in cancer diagnosis and therapy.

16.
Asian J Surg ; 42(9): 874-882, 2019 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-30704966

RESUMO

BACKGROUND/OBJECTIVE: Previous studies have proposed several objective means for liver function assessment in hepatocellular carcinoma (HCC) patients; however, their efficiency in predicting survival of HCC rupture is unknown. Our study aims to confirm which is a better liver function model for ruptured HCC. METHODS: A total of 230 patients with HCC ruptures at our center were included. Kaplan-Meier and Cox regression analyses were performed to compare long-term survival and short-term mortality. The 90-day mortality was compared with the area under the receiver characteristic curve. Logistic regression was used to determine the risk factors for 90-day deaths, and the discriminant ability of the model was measured. RESULTS: There were significant differences in predicting OS of the Child-Pugh (CP) score in all patients, the non-surgical subgroup, and the surgical subgroup (all P < 0.0001). But no statistical significance was shown of the ALBI score in the surgical (P = 0.8985) or non-surgical subgroup (P = 0.0634). The CP score yielded a better performance among all patients (AUC = 0.746 vs. 0.712), the surgical subgroup (AUC = 0.558 vs. 0.530), and the non-surgical subgroup (AUC = 0.715 vs. 0.634) compared to ALBI score in predicting ninety-day mortality. A similar result can be found in the subgroup of surgical and non-surgical treatment group. Moreover, the logistic model that included CP or MELD had a better discriminatory ability than ALBI in predicting ninety-day mortality. CONCLUSION: The CP or MELD rather than ALBI score should be used as a liver function classification criterion for HCC rupture. CLINICAL TRIAL NUMBER: NCT03534843 (retrospectively).


Assuntos
Carcinoma Hepatocelular/fisiopatologia , Testes de Função Hepática , Neoplasias Hepáticas/fisiopatologia , Adulto , Feminino , Humanos , Neoplasias Hepáticas/mortalidade , Modelos Logísticos , Masculino , Pessoa de Meia-Idade , Curva ROC , Ruptura Espontânea , Taxa de Sobrevida , Fatores de Tempo
17.
J Gastrointest Surg ; 23(9): 1788-1800, 2019 09.
Artigo em Inglês | MEDLINE | ID: mdl-30328072

RESUMO

BACKGROUND: Spontaneous tumor rupture is a rare and life-threatening complication of hepatocellular carcinoma (HCC). The best treatment strategy remains unclear. METHODS: The clinical data of 137 patients with spontaneously ruptured HCC from 2010 to 2015 were reviewed retrospectively. We investigated the outcome and prognostic factors of various treatment strategies. RESULTS: Of the 137 patients, 53, 45, 3, and 36 patients underwent transcatheter arterial chemoembolization (TACE) alone, liver resection (LR) (LR alone or TACE + LR), surgical hemostasis, and conservative therapy. The patients undergoing LR had longest overall survival (OS). In the TACE alone group, independent factors affecting 30-day mortality were MELD score ≥ 12, AFP ≥ 1000 ng/ml, and largest tumor size ≥ 10 cm. AFP ≥ 1000 ng/ml, largest tumor size ≥ 10 cm, and no tumor capsule were significantly associated with poorer OS. In the LR group, largest tumor size ≥ 10 cm and no tumor capsule were the only independent prognostic factors for poorer OS and recurrence-free survival (RFS). Hypovolemic shock was an independent prognostic factor for poorer OS. The differences in OS between the TACE + LR group and LR alone group were not significant (P = 0.955). However, the RFS is significantly better in the LR alone group than those in the TACE + LR group (P = 0.031). CONCLUSION: For resectable tumor, LR is the treatment of choice for patients with spontaneous ruptured HCC and preserved liver function. The delay in LR due to preoperative TACE may account for its worse RFS compared with LR alone. In patients with an unresectable tumor, TACE therapy alone improved survival over conservative therapy.


Assuntos
Carcinoma Hepatocelular/terapia , Quimioembolização Terapêutica/métodos , Hepatectomia/métodos , Neoplasias Hepáticas/terapia , Adulto , Carcinoma Hepatocelular/diagnóstico , Carcinoma Hepatocelular/mortalidade , China/epidemiologia , Feminino , Humanos , Neoplasias Hepáticas/diagnóstico , Neoplasias Hepáticas/mortalidade , Masculino , Pessoa de Meia-Idade , Prognóstico , Estudos Retrospectivos , Ruptura Espontânea , Taxa de Sobrevida/tendências
18.
Dig Liver Dis ; 51(5): 703-711, 2019 05.
Artigo em Inglês | MEDLINE | ID: mdl-30316787

RESUMO

BACKGROUND: Increasing evidence indicates that aberrant micro (mi)RNA-448 expression plays a critical role in the progression of several human cancers. However, the function of miRNA-448 in hepatocellular carcinoma (HCC) has not been fully investigated. METHODS: miRNA-448 expression levels in HCC tissues, adjacent non-cancerous tissues (ANTs), and HCC cell lines were examined by quantitative real-time polymerase chain reaction (qRT-PCR). HCC cells were treated with a miRNA-448 mimic or inhibitor, followed by cell viability measurements with the CCK-8 assay. Venn diagram analysis predicted, and dual luciferase reporter assays verified, the target gene of miRNA-448. Expression of the target gene was detected by qRT-PCR and immunohistochemistry. Growth of miRNA-448- or target gene-expressing HCC xenograft tumors in nude mice was measured. RESULTS: miRNA-448 was expressed at a lower level in HCC tissues than ANTs, and correlated with a larger tumor size, incomplete tumor encapsulation, and advanced Barcelona Clinic Liver Cancer stage. miRNA-448 inhibited HCC cell growth. The downstream target of miRNA-448 was BCL-2, which was highly expressed in HCC tissues and its mRNA level was negatively correlated with miRNA-448 expression. In vivo, BCL-2 attenuated the tumor inhibiting effect of miRNA-448. CONCLUSION: miRNA-448 functions as a tumor suppressor by targeting BCL-2 in HCC.


Assuntos
Carcinoma Hepatocelular/patologia , Proliferação de Células , Neoplasias Hepáticas/patologia , MicroRNAs/genética , Proteínas Proto-Oncogênicas c-bcl-2/metabolismo , Animais , Carcinoma Hepatocelular/genética , Carcinoma Hepatocelular/metabolismo , Linhagem Celular Tumoral , Sobrevivência Celular , Feminino , Regulação Neoplásica da Expressão Gênica , Humanos , Neoplasias Hepáticas/genética , Neoplasias Hepáticas/metabolismo , Masculino , Camundongos , Camundongos Nus , Pessoa de Meia-Idade , Transplante de Neoplasias , Proteínas Proto-Oncogênicas c-bcl-2/genética
19.
J Gastrointest Surg ; 23(9): 1778-1787, 2019 09.
Artigo em Inglês | MEDLINE | ID: mdl-30406576

RESUMO

BACKGROUND: The objective of this study was to evaluate the learning curve effect on the safety and feasibility of robot-assisted liver resection (RALR). METHODS: In 140 consecutive cases, all data about demographic, surgical procedure, postoperative course were collected prospectively and analyzed. Risk-adjusted cumulative sum model was used for determining the learning curve based on the need for conversion. RESULTS: Among all 140 patients, no patients suffered from any organ dysfunction postoperatively and the operative mortality was 0%. The CUSUM analysis showed that at the 30th consecutive patient, the open conversion rate reached to the average value, and it further improved thereafter. In the last 70 patients, only 3 patients (4.3%) required conversion and 7 patients (10%) needed blood transfusion. Only 1 patient (1.3%) out of 79 patients with HCC had a positive resection margin. Univariate analyses showed the following risk factors associated with significantly higher risks of conversion (P < 0.05): tumor number > 1, lesions in segments 1/4a/7/8, right posterior sectionectomy, and lesions which were beyond the indications of the Louisville statement. Multivariate logistic analysis revealed that both tumor number > 1 (OR: 2.10, P < 0.05) and right posterior sectionectomy (OR: 11.19, P < 0.01) were risk factors of conversion. CONCLUSIONS: The robotic approach for hepatectomy is safe and feasible. A learning curve effect was demonstrated in this study after the 30th consecutive patient. The long-term oncological outcomes of robotic hepatectomy still need further investigation.


Assuntos
Carcinoma Hepatocelular/cirurgia , Hepatectomia/educação , Laparoscopia/educação , Curva de Aprendizado , Neoplasias Hepáticas/cirurgia , Robótica/educação , Adolescente , Adulto , Idoso , Criança , Pré-Escolar , Estudos de Viabilidade , Feminino , Hepatectomia/métodos , Humanos , Laparoscopia/métodos , Masculino , Pessoa de Meia-Idade , Duração da Cirurgia , Período Pós-Operatório , Adulto Jovem
20.
Cancer Lett ; 443: 47-55, 2019 02 28.
Artigo em Inglês | MEDLINE | ID: mdl-30503551

RESUMO

Although hepatitis B virus (HBV)-related cirrhosis and hepatocellular carcinoma (HCC) cause a sever health problem worldwide, the underlying mechanisms are still elusive. This study aimed to investigate the responses of different cell types isolated from HBV transgenic mice. A cross-sectional set of hepatocytes and oval cells were obtained from HBV transgenic and control mice. Flow cytometry, immunohistochemistry and microarray were applied to investigate the cell biology of the hepatocytes and oval cells. Our results showed that HBV induced the proliferation of both cell oval cells and hepatocytes, and induced cell death of HBV hepatocytes while had minimal effects on oval cells. Further molecular and pathways analysis identified some genes and signaling pathways may be responsible for the different responses between oval cells and hepatocytes. In addition, analyses of selectively ten genes by IHC staining in human samples were consistent with microarray data. In summary, HBV transgenic mice is a useful model for studying the biological behaviors of oval cells affected by HBV and HBV-cirrhosis. Also, our results help better understand the mechanisms of HBV induced cirrhosis, and provide novel progenitor markers or prognostic/therapeutic markers.


Assuntos
Perfilação da Expressão Gênica/métodos , Vírus da Hepatite B/patogenicidade , Hepatite B/genética , Hepatócitos/citologia , Cirrose Hepática/genética , Animais , Apoptose , Proliferação de Células , Estudos Transversais , Modelos Animais de Doenças , Redes Reguladoras de Genes , Hepatite B/metabolismo , Hepatócitos/metabolismo , Hepatócitos/virologia , Humanos , Cirrose Hepática/metabolismo , Cirrose Hepática/virologia , Camundongos , Camundongos Transgênicos , Análise de Sequência com Séries de Oligonucleotídeos
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