Pancreatic cancer is the third leading cause of cancer death in the United States, and the 5-year relative survival for patients diagnosed with pancreatic cancer is less than 10%. Early intervention is the key to a better survival outcome. Currently, there are no biomarkers that can reliably detect pancreatic cancer at an early stage or identify precursors that are destined to progress to malignancy. The National Cancer Institute in partnership with the Kenner Family Research Fund and the Pancreatic Cancer Action Network convened a Data Jamboree on Biomarkers workshop on December 5, 2016, to discuss and evaluate existing or newly developed biomarkers and imaging methods for early detection of pancreatic cancer. The primary goal of this workshop was to determine if there are any promising biomarkers for early detection of pancreatic cancer that are ready for clinical validation. The Alliance of Pancreatic Cancer Consortia for Biomarkers for Early Detection, formed under the auspices of this workshop, will provide the common platform and the resources necessary for validation. Although none of the biomarkers evaluated seemed ready for a large-scale biomarker validation trial, a number of them had sufficiently high sensitivity and specificity to warrant additional research, especially if combined with other biomarkers to form a panel.
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http://dx.doi.org/10.1097/MPA.0000000000000973 | DOI Listing |
JCO Clin Cancer Inform
January 2025
Machine Learning Department, H. Lee Moffit Cancer Center and Research Institute, Tampa, FL.
Purpose: Adaptive radiotherapy accounts for interfractional anatomic changes. We hypothesize that changes in the gross tumor volumes identified during daily scans could be analyzed using delta-radiomics to predict disease progression events. We evaluated whether an auxiliary data set could improve prediction performance.
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January 2025
Department of Radiation Oncology, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu Province, China.
Background: The role of adjuvant radiotherapy in pancreatic cancer following radical surgery remains a subject of of controversy. This study aimed to more accurately screen pancreatic patients who benefit from adjuvant radiotherapy.
Methods: Clinicopathologic characteristics of patients with resectable pancreatic cancer were collected from the Surveillance, Epidemiology, and End Results (SEER) database (2004-2015).
PLoS One
January 2025
Cardiovascular Outcomes Research Laboratories (CORELAB), University of California, Los Angeles, Los Angeles, CA, United States of America.
Purpose: Patients with chronic kidney disease (CKD) and end-stage renal disease (ESRD) have been noted to face increased cancer incidence. Yet, the impact of concomitant renal dysfunction on acute outcomes following elective surgery for cancer remains to be elucidated.
Methods: All adult hospitalizations entailing elective resection for lung, esophageal, gastric, pancreatic, hepatic, or colon cancer were identified in the 2016-2020 National Inpatient Sample.
Cancer Res
January 2025
Tsinghua University, Beijing, China.
Pancreatic ductal adenocarcinoma (PDAC) is highly aggressive and lacks effective therapeutic options. Cancer cells frequently become more dependent on splicing factors than normal cells due to increased rates of transcription. Terminal uridylyltransferase 1 (TUT1) is a specific terminal uridylyltransferase for U6 small nuclear RNA (snRNA), which plays a catalytic role in the spliceosome.
View Article and Find Full Text PDFCell Rep
January 2025
MOE Key Laboratory of Biosystems Homeostasis & Protection, and Zhejiang Provincial Key Laboratory of Cancer Molecular Cell Biology, Life Sciences Institute, Zhejiang University, Hangzhou, Zhejiang 310058, China; Center for Life Sciences, Shaoxing Institute, Zhejiang University, Shaoxing, Zhejiang 321000, China; Cancer Center, Zhejiang University, Hangzhou, Zhejiang 310058, China; The Second Affiliated Hospital, Zhejiang University, Hangzhou, Zhejiang 310009, China. Electronic address:
Transforming growth factor β (TGF-β) is well known to play paradoxical roles in tumorigenesis as it has both growth-inhibitory and pro-metastatic effects. However, the underlying mechanisms of how TGF-β drives the opposing responses remain largely unknown. Here, we report that ERBB4, a member of the ERBB receptor tyrosine kinase family, specifically promotes TGF-β's metastatic response but not its anti-growth response.
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