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Core Signaling Pathways in Human Pancreatic Cancers Revealed by Global Genomic Analyses
It is found that pancreatic cancers contain an average of 63 genetic alterations, the majority of which are point mutations, which defined a core set of 12 cellular signaling pathways and processes that were each genetically altered in 67 to 100% of the tumors.
International Cancer of the Pancreas Screening (CAPS) Consortium summit on the management of patients with increased risk for familial pancreatic cancer
Screening is recommended for high-risk individuals, but more evidence is needed, particularly for how to manage patients with detected lesions, particularly at high-volume centres with multidisciplinary teams.
An Illustrated Consensus on the Classification of Pancreatic Intraepithelial Neoplasia and Intraductal Papillary Mucinous Neoplasms
The purpose of this meeting was to define an international acceptable set of diagnostic criteria for PanINs and IPMNs and to address a number of ambiguities that exist in the previously reported classification systems for these neoplasms.
Recurrent GNAS Mutations Define an Unexpected Pathway for Pancreatic Cyst Development
It is determined that the presence of mutations in two oncogenes can identify the cysts that are likely to progress to carcinoma and so are good candidates for surgical removal, and suggest that GNAS mutations can inform the diagnosis and management of patients with cystic pancreatic lesions.
Detection of Circulating Tumor DNA in Early- and Late-Stage Human Malignancies
The ability of circulating tumor DNA (ctDNA) to detect tumors in 640 patients with various cancer types was evaluated and suggested that ctDNA is a broadly applicable, sensitive, and specific biomarker that can be used for a variety of clinical and research purposes.
Detection and localization of surgically resectable cancers with a multi-analyte blood test
A blood test that combines protein and DNA markers may allow earlier detection of eight common cancer types through assessment of the levels of circulating proteins and mutations in cell-free DNA.
Progression model for pancreatic cancer.
- R. Hruban, M. Goggins, J. Parsons, S. Kern
- MedicineClinical cancer research : an official journal of…
- 1 August 2000
A progression model for colorectal neoplasia was proposed in which it was hypothesized that the progression from normal colonic epithelium, to small adenomatous polyps, to infiltrating adenocarcinoma is associated with the activation.
Prevalence of the alternative lengthening of telomeres telomere maintenance mechanism in human cancer subtypes.
Tumor-suppressive pathways in pancreatic carcinoma.
This type of multigenic analysis in human tumors may serve to substantiate experimental tumor models and thus increase the understanding of the truly physiologically relevant tumor-suppressive pathways that are abrogated during human tumorigenesis.
Presence of somatic mutations in most early-stage pancreatic intraepithelial neoplasia.
It is shown that more than 99% of the earliest-stage, lowest-grade, pancreatic intraepithelial neoplasm-1 lesions contain mutations in KRAS, p16/CDKN2A, GNAS, or BRAF, which could improve the understanding of the development and progression of these premalignant lesions.