The miRNAs diversity between pancreatic body/tail and head cancers
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE83496 | GEO | 2016/06/18
SECONDARY ACCESSION(S): PRJNA326134
REPOSITORIES: GEO
Similar Datasets
Project description:BackgroundTo our knowledge, there are no studies to systematically compare the detailed clinical significance between curatively resected pancreatic head (ph) and body-tail (pbt) ductal adenocarcinoma based on the new 8th edition of AJCC staging system (8th AJCC stage) that was just applied in clinical practice in 2018.MethodsThree hundred fifty-one patients with curatively resected pancreatic adenocarcinoma (PC) from three center hospitals were entered into this multicenter cohort study.ResultsIncreasing tumor size (P?<?0.001), T stage (T1?+?T2 vs T3?+?T4, P?=?0.003), frequent postoperative liver metastasis (PLM) (P?=?0.002) and 8th AJCC stage (IA to VI, P?<?0.001; I?+?II vs III?+?IV, P?=?0.002) were closely associated with the progression of pbt cancers compared with that in ph cancer patients. Moreover, tumor size?3?cm (P?=?0.012), 8th AJCC stage (III?+?IV) (P?=?0.025) and PLM (P?=?0.010) were identified as independent risk factors in pbt cancers in logistic analysis. Patients with pbt cancers had a significantly worse overall survival compared with ph cancer patients (P?=?0.003). Moreover, pbt was an independent unfavorable factor in multivariate analysis (P?=?0.011). In addition to lymph nodes metastasis, 8th AJCC stage, vascular invasion and PLM, increasing tumor size and advanced T stage were also closely associated with the poor prognosis in 131 cases of pbt cancer patients compared with Ph cancer patients.ConclusionPbt, as an independent unfavorable factor for the prognosis of PC patients, are much more aggressive than that in ph cancers according to 8th AJCC staging system. 8th AJCC staging system are more comprehensive and sensitive to reflect the malignant biology of pbt cancers.
| S-EPMC6805668 | biostudies-literature
Project description:BackgroundPancreatic head cancer and pancreatic body/tail cancer are considered to have different clinical presentations and to have altered outcomes.MethodsNinety cases of pancreatic adenocarcinoma (PDAC) from our institution were used as a discovery set and 166 cases of PDAC from the TCGA cohort were used as a validation set. According to the anatomical location, the cases of PDAC were divided into the pancreatic head cancer group and the pancreatic body/tail cancer group. Firstly, the different biological functions of the two groups were assessed by ssGSEA. Meanwhile, ESTIMATE and CIBERSORT were conducted to estimate immune infiltration. Then, a novel anatomical site-related risk score (SRS) model was constructed by LASSO and Cox regression. Survival and time-dependent ROC analysis was used to prove the predictive ability of our model in two cohorts. Subsequently, an integrated survival decision tree and a scoring nomogram were constructed to improve prognostic stratification and predictive accuracy for individual patients. In addition, gseaGO and gseaKEGG pathway analyses were performed on genes in the key module by the R package.ResultsOverall survival and the objective response rate (ORR) of patients with pancreatic body/tail cancer were markedly superior to those with pancreatic head cancer. In addition, distinct immune characteristics and gene patterns were observed between the two groups. Then, we screened 5 biomarkers related to the prognosis of pancreatic cancer and constructed a more powerful novel SRS model to predict prognosis.ConclusionsOur research shed some light on the revelation of gene patterns, immune and mutational landscape characterizations, and their relationships in different PDAC locations.
| S-EPMC9213676 | biostudies-literature
Project description:The association between pancreatic ductal adenocarcinoma (PDAC) location (head vs. Body/Tail (B/T)) and clinical outcome remains controversial. We collected clinicopathological and gene expression data from 249 resected PDAC samples from public data sets, and we compared data between 208 head and 41 B/T samples. The 2-year overall survival (OS) was better for the head than for the B/T PDACs (44 vs. 27%, p = 0.043), especially when comparing tumors with similar TNM classification (T3/4N0M0: 67% vs. 17%, p = 0.002) or from the same molecular class (squamous subtype: 31% vs. 0%, p < 0.0001). Bailey's molecular subtypes were differentially distributed within the two groups, with the immunogenic subtype being underrepresented in the "B/T" group (p = 0.005). Uni- and multivariate analyses indicated that PDAC anatomic location was an independent prognostic factor. Finally, the supervised analysis identified 334 genes differentially expressed. Genes upregulated in the "head" group suggested lymphocyte activation and pancreas exocrine functions. Genes upregulated in the "B/T" group were related to keratinocyte differentiation, in line with the enrichment for squamous phenotype. We identified a robust gene expression signature (GES) associated with B/T PDAC location, suggesting that head and B/T PDAC are different. This GES could serve as an indicator for differential therapeutic management based on PDAC location.
| S-EPMC6520848 | biostudies-literature
Project description:Pancreatic ductal adenocarcinoma (PDAC) of the head (H) and body/tail (B/T) differ in embryonic origin, cell composition, blood supply, lymphatic and venous drainage, and innervation. We aimed to compare the molecular and tumor immune microenvironment (TIME) profiles of PDAC of the H vs. B/T. A total of 3499 PDAC samples were analyzed via next-generation sequencing (NGS) of RNA (whole transcriptome, NovaSeq), DNA (NextSeq, 592 genes or NovaSeq, whole exome sequencing), and immunohistochemistry (Caris Life Sciences, Phoenix, AZ). Significance was determined as p values adjusted for multiple corrections (q) of <0.05. Anatomic subsites of PDAC tumors were grouped by primary tumor sites into H (N = 2058) or B/T (N = 1384). There were significantly more metastatic tumors profiled from B/T vs. H (57% vs. 44%, p < 0.001). KRAS mutations (93.8% vs. 90.2%), genomic loss of heterozygosity (12.7% vs. 9.1%), and several copy number alterations (FGF3, FGF4, FGF19, CCND1, ZNF703, FLT4, MUTYH, TNFRS14) trended higher in B/T when compared to H (p < 0.05 but q > 0.05). Expression analysis of immuno-oncology (IO)-related genes showed significantly higher expression of CTLA4 and PDCD1 in H (q < 0.05, fold change 1.2 and 1.3) and IDO1 and PDCD1LG2 expression trended higher in B/T (p < 0.05, fold change 0.95). To our knowledge, this is one of the largest cohorts of PDAC tumors subjected to broad molecular profiling. Differences in IO-related gene expression and TIME cell distribution suggest that response to IO therapies may differ in PDAC arising from H vs. B/T. Subtle differences in the genomic profiles of H vs. B/T tumors were observed.
| S-EPMC10998911 | biostudies-literature
Project description:Single-cell RNA sequencing of pancreatic islets from adult male mice. To disect islet heterogeneity we sorted cells based on anatomical location and maturity marker (Fltp).
2022-12-23 | GSE211796 | GEO
Project description:Pancreatic ductal adenocarcinoma (PDAC), one of the most lethal human cancers, can be divided into head and body/tail cancers anatomically. We previously reported a prognostic relevance of tumour location in resectable PDAC. This study aimed to further explore the mechanism underlying the molecular diversity between the head and body/tail of PDACs. We detected tumour genomes in 154 resectable (surgery) and non-resectable (biopsy) PDACs using a next-generation sequencing panel. Wilcoxon's rank test or Fisher's exact test was used for evaluating associations between clinical characteristics, mutation frequency and survival probability between the two cohorts. Compared with pancreatic head cancers, pancreatic body/tail cancers showed significantly more enriched genomic alterations in KRAS (97.1% vs 82.4%, P = 0.004) and SMAD4 (42.0% vs 21.2%, P = 0.008). At early stages (I-II), the SMAD4 mutation rate was significantly higher in pancreatic body/tail cancers than pancreatic head cancers (56.0% vs 26.5%, P = 0.021). At late stages (III-IV), pancreatic body/tail cancers presented significantly higher KRAS mutation rate (100.0% vs 75.8%, P = 0.001), higher frequency of MAPK pathway mutation (100% vs 87.8%, P = 0.040) and lower rates of druggable genomic alterations (30.8% vs 57.6%, P = 0.030) than pancreatic head cancers. Our work points out that pancreatic body/tail cancer seems to be more malignant than pancreatic head cancer at late stages.
| S-EPMC7875914 | biostudies-literature
Project description:Molecular subtypes in pancreatic adenocarcinoma
| PRJNA311745 | ENA
Project description:BackgroundMain pancreatic duct (MPD) dilation is a high-risk stigmata/worrisome feature of malignancy in intraductal papillary mucinous neoplasms (IPMNs). The threshold of MPD diameter in predicting malignancy may be related to the lesion location. This study aimed to separately identify the thresholds of MPD for malignancy of IPMNs separately for the head-neck and body-tail.Materials and methodsA total of 185 patients with pathologically confirmed IPMNs were included. Patient demographic information, clinical data, and pathological features were obtained from the medical records. Those IPMNs with high-grade dysplasia or with associated invasive carcinoma were considered as malignant tumor. Radiological data including lesion location, tumor size, diameter of the MPD, mural nodule, and IPMN types (main duct, MD; branch duct, BD; and mixed type, MT), were collected on computed tomography or magnetic resonance imaging. Serum carbohydrate antigen 19-9 levels, serum carcinoembryonic antigen levels, and the medical history of diabetes mellitus, chronic cholecystitis, and pancreatitis were also collected.ResultsMalignant IPMNs were detected in 31.6% of 117 patients with lesions in the pancreatic head-neck and 20.9% of 67 patients with lesions in the pancreatic body-tail. In MPD-involved IPMNs, malignancy was observed in 54.1% of patients with lesions in the pancreatic head-neck and 30.8% of patients with lesions in the pancreatic body-tail (p < 0.05). The cutoff value of MPD diameter for malignancy was 6.5 mm for lesions in the head-neck and 7.7 mm for lesions in the body-tail in all type of IPMNs. In MPD-involved IPMNs, the threshold was 8.2 mm for lesion in pancreatic head-neck and 7.7 mm for lesions in the body-tail. Multivariate analysis confirmed that MPD diameter ≥ 6.5 mm (pancreatic head-neck) and MPD diameter ≥ 7.7 mm (pancreatic body-tail) were independent predictors of malignancy (p < 0.05). Similar results were observed in MPD-involved IPMNs using 8.2 mm as a threshold.ConclusionThe thresholds of the dilated MPD may be associated with IPMNs locations. Thresholds of 6.5 mm for lesions in the head-neck and 7.7 mm for lesions in the body-tail were observed. For MPD-involved IPMNs alone, threshold for lesions in the head-neck was close to that in the body-tail.
| S-EPMC9675150 | biostudies-literature
Project description:The goal of the study was to examine the transcriptional profile of pancreatic cancer cell lines and assess if the molecular subtypes observed in tumor samples were represented in existing cell line models. Cell line models allow us to investigate if the molecular subtype observed in tumor have unique sensitivity profiles to anticancer drugs. 29 pancreatic cancer cell lines were compared to a mixed reference pool of 30 pancreatic cancer cell lines to identify cell line specific gene expression.
2016-06-01 | E-GEOD-77850 | biostudies-arrayexpress
Project description:Aberrant regulation of angiogenesis involves in the growth and metastasis of tumors, but angiogenesis inhibitors fail to improve overall survival of pancreatic cancer patients in previous phase III clinical trials. A comprehensive knowledge of the mechanism of angiogenesis inhibitors against pancreatic cancer is helpful for clinical purpose and for the selection of patients who might benefit from the inhibitors. In this work, multi-omics analyses (transcriptomics, proteomics and phosphoproteomics profiling) were carried to delineate the mechanism of anlotinib, a novel angiogenesis inhibitor, against pancreatic cancer cells.
2021-09-09 | PXD023345 | Pride