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World Journal of Gastroenterology Apr 2015To evaluate the utility of carbohydrate antigen 19-9 (CA19-9) for differential diagnosis of pancreatic carcinoma and chronic pancreatitis. (Meta-Analysis)
Meta-Analysis Review
AIM
To evaluate the utility of carbohydrate antigen 19-9 (CA19-9) for differential diagnosis of pancreatic carcinoma and chronic pancreatitis.
METHODS
We searched the literature for studies reporting the sensitivity, specificity, and other accuracy measures of serum CA19-9 levels for differentiating pancreatic carcinoma and chronic pancreatitis. Pooled analysis was performed using random-effects models, and receiver operating characteristic (ROC) curves were generated. Study quality was assessed using Standards for Reporting Diagnostic Accuracy and Quality Assessment for Studies of Diagnostic Accuracy tools.
RESULTS
A total of 34 studies involving 3125 patients with pancreatic carcinoma and 2061 patients with chronic pancreatitis were included. Pooled analysis of the ability of CA19-9 level to differentiate pancreatic carcinoma and chronic pancreatitis showed the following effect estimates: sensitivity, 0.81 (95%CI: 0.80-0.83); specificity, 0.81 (95%CI: 0.79-0.82); positive likelihood ratio, 4.08 (95%CI: 3.39-4.91); negative likelihood ratio, 0.24 (95%CI: 0.21-0.28); and diagnostic odds ratio, 19.31 (95%CI: 14.40-25.90). The area under the ROC curve was 0.88. No significant publication bias was detected.
CONCLUSION
Elevated CA19-9 by itself is insufficient for differentiating pancreatic carcinoma and chronic pancreatitis, however, it increases suspicion of pancreatic carcinoma and may complement other clinical findings to improve diagnostic accuracy.
Topics: Area Under Curve; Biomarkers, Tumor; CA-19-9 Antigen; Carcinoma; Diagnosis, Differential; Humans; Odds Ratio; Pancreatic Neoplasms; Pancreatitis, Chronic; Predictive Value of Tests; Prognosis; ROC Curve; Up-Regulation
PubMed: 25892884
DOI: 10.3748/wjg.v21.i14.4323 -
Journal of the National Medical... Jun 1980Carcinoma of pancreas is not uncommon in Africa where the prognosis seems to be worse than in cases seen in Europe and North America. The reason for this poor prognosis...
Carcinoma of pancreas is not uncommon in Africa where the prognosis seems to be worse than in cases seen in Europe and North America. The reason for this poor prognosis is because patients with this disease are seen in medical institutions at late stages.There seems to be a rise also in the incidence of this disease in our environment. This increased incidence may be real or apparent, and may be related to the rise in hospital consciousness in the population.As seen in Ibadan, the pattern of the disease is not much different from that reported from other parts of Africa.
Topics: Adolescent; Adult; Aged; Child; Female; Humans; Male; Middle Aged; Nigeria; Pancreatic Neoplasms
PubMed: 7392077
DOI: No ID Found -
World Journal of Gastroenterology Feb 2017Familial pancreatic cancer (FPC) is broadly defined as two first-degree-relatives with pancreatic cancer (PC) and accounts for 4%-10% of PC. Several genetic syndromes,... (Review)
Review
Familial pancreatic cancer (FPC) is broadly defined as two first-degree-relatives with pancreatic cancer (PC) and accounts for 4%-10% of PC. Several genetic syndromes, including Peutz-Jeghers syndrome, hereditary pancreatitis, hereditary breast-ovarian cancer syndrome (HBOC), Lynch syndrome, and familial adenomatous polyposis (FAP), also have increased risks of PC, but the narrowest definition of FPC excludes these known syndromes. When compared with other familial tumors, proven genetic alterations are limited to a small proportion (< 20%) and the familial aggregation is usually modest. However, an ethnic deviation (Ashkenazi Jewish > Caucasian) and a younger onset are common also in FPC. In European countries, "anticipation" is reported in FPC families, as with other hereditary syndromes; a trend toward younger age and worse prognosis is recognized in the late years. The resected pancreases of FPC kindred often show multiple pancreatic intraepithelial neoplasia (PanIN) foci, with various K- mutations, similar to colorectal polyposis seen in the FAP patients. As with HBOC patients, a patient who is a mutation carrier with unresectable pancreatic cancer (accounting for 0%-19% of FPC patients) demonstrated better outcome following platinum and Poly (ADP-ribose) polymerase inhibitor treatment. Western countries have established FPC registries since the 1990s and several surveillance projects for high-risk individuals are now ongoing to detect early PCs. Improvement in lifestyle habits, including non-smoking, is recommended for individuals at risk. In Japan, the FPC study group was initiated in 2013 and the Japanese FPC registry was established in 2014 by the Japan Pancreas Society.
Topics: Antineoplastic Agents; BRCA1 Protein; BRCA2 Protein; Carcinoma; Early Detection of Cancer; Europe; Genetic Predisposition to Disease; Humans; Incidence; Japan; Mutation; Pancreatectomy; Pancreatic Neoplasms; Risk Factors; United States
PubMed: 28246467
DOI: 10.3748/wjg.v23.i6.935 -
BMC Complementary and Alternative... Jun 2019Elemene is an effective anticancer component extracted from Zingiberaceae plants. This work was aimed to evaluate the anti-tumor effect and mechanism actions of elemene...
BACKGROUND
Elemene is an effective anticancer component extracted from Zingiberaceae plants. This work was aimed to evaluate the anti-tumor effect and mechanism actions of elemene on pancreatic carcinoma in vitro and in vivo.
METHODS
The anti-proliferation experiment was measured by Methylthiazolyldiphenyl-tetrazolium bromide (MTT) method in the time of 24, 48 and 72 h in three different dosages. The cell cycle was detected by flow cytometer after 12 h treatment. Forty-eight nude mice were subcutaneously xenograft with BxPC-3 pancreatic cancer cells and divided into four groups: Control group and high, medium, low dosage of elemene (20, 40 and 60 mg/kg) treatment groups. Immunoblot and immunohistochemical methods were applied to detect the protein expression of P53 and Bcl-2 in the tumor of pancreatic cancer xenografts. H & E staining was used to detect the histopathological changes in each group.
RESULTS
A significant inhibition effect was observed in the anti-proliferation of BxPC-3 and Panc-1 cells in vitro in the time course of 24, 48 and 72 h with a dose dependent manner. The cell cycle results showed that elemene could arrest pancreatic cancer cells in the S phase after 12 h treatment in BxPC-3 and Panc-1 cell line. The in vivo BxPC-3 xenografts study exhibited that elemene was significantly decreased the tumor size in the high dosage group, compared to control group. And there is no any significant change in body weight of all animals. H&E pathology section result showed that treatment with elemene significantly decreased the inflammation cells and reduced the histopathological changes with a dose-dependent manner. Meanwhile, treatment with elemene significantly up-regulates the protein expression of P53, while down-regulate the protein expression of Bcl-2 in the tumor tissues, respectively. Furthermore, the western blot result showed that treatment with elemene increased the expression of P53 and decreased the expression of Bcl-2, compared with the control group, which is similar to the results of immunohistochemical staining.
CONCLUSIONS
This study suggests that elemene has a potential anti pancreatic cancer effect, down-regulation the protein expression of Bcl-2 and up-regulation the protein expression of P53 in a dose dependent manner may be is the anti-tumor mechanism.
Topics: Animals; Antineoplastic Agents, Phytogenic; Apoptosis; Cell Cycle; Cell Line, Tumor; Cell Proliferation; Drugs, Chinese Herbal; Female; Humans; Mice; Mice, Inbred BALB C; Mice, Nude; Pancreatic Neoplasms; Sesquiterpenes; Tumor Suppressor Protein p53; Xenograft Model Antitumor Assays; Zingiberaceae
PubMed: 31215421
DOI: 10.1186/s12906-019-2544-2 -
Cell Communication and Signaling : CCS May 2017This article focusses on the role of TGF-β and its signaling crosstalk with the RHO family GTPases RAC1 and RAC1b in the progression of breast and pancreatic carcinoma.... (Review)
Review
This article focusses on the role of TGF-β and its signaling crosstalk with the RHO family GTPases RAC1 and RAC1b in the progression of breast and pancreatic carcinoma. The aggressive nature of these tumor types is mainly due to metastatic dissemination. Metastasis is facilitated by desmoplasia, a peculiar tumor microenvironment and the ability of the tumor cells to undergo epithelial-mesenchymal transition (EMT) and to adopt a motile and invasive phenotype. These processes are controlled entirely or in part by TGF-β and the small RHO GTPase RAC1 with both proteins acting as tumor promoters in late-stage cancers. Data from our and other studies point to signaling crosstalk between TGF-β and RAC1 and the related isoform, RAC1b, in pancreatic and mammary carcinoma cells. Based on the exciting observation that RAC1b functions as an endogenous inhibitor of RAC1, we propose a model on how the relative abundance or activity of RAC1 and RAC1b in the tumor cells may determine their responses to TGF-β and, ultimately, the metastatic capacity of the tumor.
Topics: Animals; Breast Neoplasms; Humans; Pancreatic Neoplasms; Signal Transduction; Transforming Growth Factor beta; rac1 GTP-Binding Protein
PubMed: 28499439
DOI: 10.1186/s12964-017-0175-0 -
Computational and Mathematical Methods... 2022Studies have demonstrated that zinc finger protein 488 (ZNF488) is highly expressed in pancreatic carcinoma (PC), but its effect on PC and its molecular mechanism...
OBJECTIVE
Studies have demonstrated that zinc finger protein 488 (ZNF488) is highly expressed in pancreatic carcinoma (PC), but its effect on PC and its molecular mechanism remains unclear.
METHODS
Real-time fluorescent quantitative PCR (RT-qPCR) was employed to detect the ZNF488 expression in PC patients' cancer tissues and cell lines. After interfering with or overexpressing ZNF488 in PANC-1 and AsPC-1 cells, respectively, the CCK-8, cell cloning, Transwell, and scratch assays were performed to detect cell proliferation, cell viability, invasion ability, and migration ability. In addition, Western blot was applied to assess the protein expression of Akt, p-Akt, mTOR, and p-mTOR in the Akt-mTOR pathway.
RESULTS
The ZNF488 expression was evidently raised in PC tissues and cell lines, and the starBase V3.0 database indicated that the higher the ZNF488 expression, the lower the survival rate of PC patients. Furthermore, we discovered that overexpressing ZNF488 can markedly promote the proliferation, invasion, and migration of PC cells. At the same time, highly expressed ZNF488 distinctly increased the p-Akt and p-mTOR expressions and the p-Akt/Akt and p-mTOR/mTOR ratios. However, after knocking down the ZNF488 expression, it had the opposite results. In addition, the Akt agonist SC79 can alleviate the effect of ZNF488 knockdown on Akt/mTOR pathway-related proteins, while Akt inhibitor AZD5363 had the opposite effect.
CONCLUSION
ZNF488 could promote the proliferation, invasion, and migration of PC cells, and its mechanism may be related to the activation of the Akt/mTOR pathway. This study demonstrated that ZNF488 could be used as a molecular target for diagnosing and treating PC.
Topics: Biomarkers, Tumor; Cell Line, Tumor; Cell Movement; Cell Proliferation; Computational Biology; Gene Expression Regulation, Neoplastic; Humans; Kruppel-Like Transcription Factors; Neoplasm Invasiveness; Pancreatic Neoplasms; Proto-Oncogene Proteins c-akt; Signal Transduction; TOR Serine-Threonine Kinases; Zinc Fingers
PubMed: 35111235
DOI: 10.1155/2022/4622877 -
EBioMedicine Feb 2019Pancreatic carcinoma (PC) is one of the most aggressive cancers affecting human health. It is essential to identify candidate biomarkers for the diagnosis and prognosis...
BACKGROUND
Pancreatic carcinoma (PC) is one of the most aggressive cancers affecting human health. It is essential to identify candidate biomarkers for the diagnosis and prognosis of PC. The present study aimed to investigate the diagnosis and prognosis biomarkers of PC.
METHODS
Differentially expressed genes (DEGs) were identified from the mRNA expression profiles of GSE62452, GSE28735 and GSE16515. Functional analysis and the protein-protein interaction network analysis was performed to explore the biological function of the identified DEGs. Diagnosis markers for PC were identified using ROC curve analysis. Prognosis markers were identified via survival analysis of TCGA data. The protein expression pattern of the identified genes was verified in clinical tissue samples. A retrospective clinical study was performed to evaluate the correlation between the expression of candidate proteins and survival time of patients. Moreover, comprehensive analysis of the combination of multiple genes/proteins for the prognosis prediction of PC was performed using both TCGA data and clinical data. In vitro studies were undertaken to elaborate the potential roles of these biomarkers in clonability and invasion of PC cells.
FINDINGS
In total, 389 DEGs were identified. These genes were mainly associated with pancreatic secretion, protein digestion and absorption, cytochrome P450 drug metabolism, and energy metabolism pathway. The top 10 genes were filtered out following Fisher's exact test. ROC curve analysis demonstrated that TMPRSS4, SERPINB5, SLC6A14, SCEL, and TNS4 could be used as biomarkers for the diagnosis of PC. Survival analysis of TCGA data and clinical data suggested that TMC7, TMPRSS4, SCEL, SLC2A1, CENPF, SERPINB5 and SLC6A14 can be potential biomarkers for the prognosis of PC. Comprehensive analysis show that a combination of identified genes/proteins can predict the prognosis of PC. Mechanistically, the identified genes attributes to clonability and invasiveness of PC cells.
INTERPRETATION
We synthesized several sets of public data and preliminarily clarified pathways and functions of PC. Candidate molecular markers were identified for diagnosis and prognosis prediction of PC including a novel gene, TMC7. Moreover, we found that the combination of TMC7, TMPRSS4, SCEL, SLC2A1, CENPF, SERPINB5 and SLC6A14 can serve as a promising indicator of the prognosis of PC patients. The candidate proteins may attribute to clonability and invasiveness of PC cells. This research provides a novel insight into molecular mechanisms as well as diagnostic and prognostic markers of PC. FUND: National Natural Science Foundation of China [No. 81602646 &81802339], Natural Science Foundation of Guangdong Province [No. 2016A030310254] and China Postdoctoral Science Foundation [No. 2016M600648].
Topics: Biomarkers, Tumor; Computational Biology; Gene Expression Profiling; Gene Ontology; Humans; Kaplan-Meier Estimate; Pancreatic Neoplasms; Prognosis; Proportional Hazards Models; Protein Interaction Mapping; Protein Interaction Maps; ROC Curve; Transcriptome
PubMed: 30639415
DOI: 10.1016/j.ebiom.2019.01.003 -
Gut and Liver Nov 2017Pancreatic cancer (PC) is the third most common cause of cancer-related death in the United States and the 12th most common worldwide. Mortality is high, largely due to... (Review)
Review
Pancreatic cancer (PC) is the third most common cause of cancer-related death in the United States and the 12th most common worldwide. Mortality is high, largely due to late stage of presentation and suboptimal treatment regimens. Approximately 10% of PC cases have a familial basis. The major genetic defect has yet to be identified but may be inherited by an autosomal dominant pattern with reduced penetrance. Several known hereditary syndromes or genes are associated with an increased risk of developing PC and account for approximately 2% of PCs. These syndromes include the hereditary breast-ovarian cancer syndrome, Peutz-Jeghers syndrome, familial atypical multiple mole melanoma, Lynch syndrome, familial polyposis, ataxia-telangiectasia, and hereditary pancreatitis. Appropriate screening using methods such as biomarkers or imaging, with endoscopic ultrasound and magnetic resonance imaging, may assist in the early detection of neoplastic lesions in the high-risk population. If these lesions are detected and treated before the development of invasive carcinoma, PC disease morbidity and mortality may be improved. This review will focus on familial PC and other hereditary syndromes implicated in the increased risk of PC; it will also highlight current screening methods and the future of new screening modalities.
Topics: Carcinoma; Early Detection of Cancer; Female; Forecasting; Genetic Predisposition to Disease; Humans; Male; Neoplastic Syndromes, Hereditary; Pancreatic Neoplasms; Risk Assessment; Risk Factors
PubMed: 28609837
DOI: 10.5009/gnl16414 -
American Society of Clinical Oncology... Jan 2019Beyond breast and ovarian cancers, mutations in the and genes increase risks for pancreatic and prostate cancers and contribute to the prevalence of these cancers.... (Review)
Review
Beyond breast and ovarian cancers, mutations in the and genes increase risks for pancreatic and prostate cancers and contribute to the prevalence of these cancers. Mutations in a number of other genes have also been shown to increase the risk for these cancers as well. Genetic testing is playing an increasingly important role in the treatment of patients with pancreatic and prostate cancer and is now recommended for all patients with pancreatic or metastatic prostate cancer, as well as patients with high Gleason grade prostate cancer and a remarkable family history. Identification of an inherited mutation can direct evaluation of the patient for other cancer risks as well as identification and management of disease in at-risk relatives. Growing evidence suggests improved responses to PARP inhibitors and other therapies in patients with mutations in the and other DNA repair genes. Although more work must be done to clarify the prevalence and penetrance of mutations in genes other than and in patients with pancreatic and prostate cancer, in most cases, testing is now being done with a panel of multiple genes. Because of the complexities in panel testing and the increased likelihood of finding variants of uncertain significance, pre- and post-test genetic counseling are essential.
Topics: Biomarkers, Tumor; Carcinoma; Female; Genes, BRCA1; Genes, BRCA2; Genetic Predisposition to Disease; Genetic Testing; Humans; Male; Mass Screening; Mutation; Pancreatic Neoplasms; Prognosis; Prostatic Neoplasms
PubMed: 31099688
DOI: 10.1200/EDBK_238977 -
Annals of Surgery Feb 1995The author seeks to provide an update on the current management of pancreatic carcinoma, including diagnosis and staging, surgical resection and adjuvant therapy for... (Review)
Review
OBJECTIVE
The author seeks to provide an update on the current management of pancreatic carcinoma, including diagnosis and staging, surgical resection and adjuvant therapy for curative intent, and palliation.
SUMMARY BACKGROUND DATA
During the 1960s and 1970s, the operative mortality and long-term survival after pancreaticoduodenectomy for pancreatic carcinoma was so poor that some authors advocated abandoning the procedure. Several recent series have reported a marked improvement in perioperative results with 5-year survival in excess of 20%. Significant advances also have been made in areas of preoperative evaluation and palliation for advanced disease.
CONCLUSION
Although carcinoma of the pancreas remains a disease with a poor prognosis, advances in the last decade have led to improvements in the overall management of this disease. Resection for curative intent currently should be accomplished with minimal perioperative mortality. Surgical palliation also may provide the optimal management of selected patients.
Topics: Adenocarcinoma; Combined Modality Therapy; Diagnostic Imaging; Humans; Neoplasm Staging; Palliative Care; Pancreatic Neoplasms; Pancreaticoduodenectomy; Prognosis; Treatment Outcome
PubMed: 7531966
DOI: 10.1097/00000658-199502000-00003