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1.
Head Neck ; 46(3): 571-580, 2024 Mar.
Article in English | MEDLINE | ID: mdl-38124665

ABSTRACT

BACKGROUND: Laryngeal and hypopharyngeal cancers often require surgical treatment, which can lead to the development of pharyngocutaneous fistula (PCF). Our research aimed to assess the predictive value of skeletal muscle mass (SMM) and systemic inflammation indices for PCF and construct a clinically effective nomogram. METHODS: A nested case-control study of 244 patients matched from 1171 patients with laryngeal or hypopharyngeal cancer was conducted. SMM was measured at the third cervical level based on CT scans. A PCF nomogram was developed based on the univariate and multivariate analyses. RESULTS: Glucose, white blood cell count, platelet-to-lymphocyte ratio, and skeletal muscle index were independent risk factors for PCF. The area under the curve for the PCF nomogram was 0.841 (95% CI 0.786-0.897). The calibration and decision curves indicated that the nomogram was well-calibrated with good clinical utility. CONCLUSIONS: The nomogram we constructed may help clinicians predict PCF risk early in the postoperative period, pending external validation.


Subject(s)
Cutaneous Fistula , Hypopharyngeal Neoplasms , Laryngeal Neoplasms , Pharyngeal Diseases , Humans , Nomograms , Case-Control Studies , Retrospective Studies , Laryngeal Neoplasms/complications , Laryngectomy/adverse effects , Cutaneous Fistula/etiology , Cutaneous Fistula/surgery , Pharyngeal Diseases/etiology , Inflammation , Muscle, Skeletal , Hypopharyngeal Neoplasms/surgery
2.
Sci Rep ; 7(1): 16558, 2017 11 24.
Article in English | MEDLINE | ID: mdl-29176726

ABSTRACT

A correction to this article has been published and is linked from the HTML version of this paper. The error has been fixed in the paper.

3.
Sci Rep ; 7(1): 8273, 2017 08 15.
Article in English | MEDLINE | ID: mdl-28811622

ABSTRACT

Some recent studies have suggested that the use of dipeptidyl peptidase-4 inhibitors (DPP4i) is associated with cancer development. However, some other studies suggest no such association. The aim of the present study was to evaluate the effect of DPP4i on the risk of developing cancers. The electronic databases PubMed, Medline, EMBASE, Web of Science and Cochrane Library and the clinical trial registry were searched for published and unpublished randomized clinical trials on humans. Eligible studies were RCTs conducted in patients with type 2 diabetes mellitus, comparing DPP4i with a placebo or other active drugs. A total of 72 trials with 35,768 and 33,319 patients enrolled for DPP4i and the comparison drugs, respectively. Overall, no significant associations were detected between the use of DPP4i and cancer development, in comparison with the use of other active drugs or placebo. The results were consistent across pre-defined subgroups stratified by type of DPP4i, type of cancer, drug for comparison, trial duration, or baseline characteristics. The results of this meta-analysis suggest that patients with type 2 diabetes treated with DPP4i do not have a higher risk of developing cancers than patients treated with a placebo or other drugs.

4.
Cell Biochem Funct ; 32(3): 258-67, 2014 Apr.
Article in English | MEDLINE | ID: mdl-24122964

ABSTRACT

Pancreatic cancer (PC) has a high rate of mortality and a poorly understood mechanism of progression. Investigation of the molecular mechanism of PC and exploration of the specific markers for early diagnosis and specific targets of therapy are key points to prevent and treat PC effectively and to improve their prognosis. In our study, expression profiles experiment of para-carcinoma, carcinoma and relapse human PC was performed using Agilent human whole genomic oligonucleotide microarrays with 45 000 probes. Differentially expressed genes related with PC were screened and analysed further by Gene Ontology term analysis and Kyoto encyclopaedia of genes and genomes pathway analysis. Our results showed that there were 3853 differentially expressed genes associated with pancreatic carcinogenesis and relapse. In addition, our study found that PC was related to the Jak-STAT signalling pathway, PPAR signalling pathway and Calcium signalling pathway, indicating their potential roles in pancreatic carcinogenesis and progress.


Subject(s)
Pancreatic Neoplasms/metabolism , Paraneoplastic Syndromes/metabolism , Carcinogenesis/genetics , Carcinogenesis/metabolism , Gene Expression Profiling , Gene Ontology , Humans , Neoplasm Recurrence, Local/genetics , Neoplasm Recurrence, Local/metabolism , Neoplasm Recurrence, Local/prevention & control , Oligonucleotide Array Sequence Analysis , Pancreatic Neoplasms/genetics , Paraneoplastic Syndromes/genetics , Signal Transduction , Pancreatic Neoplasms
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