CA19-9 for detecting recurrence of pancreatic cancer

Abstract

CA19-9 values are regularly measured in patients with pancreatic cancer. Certainly, its potential as a biomarker has been compromised by false negative results in CA19-9 negative patients and false positive results in benign pancreatico-biliary diseases. For detection of PDAC recurrence, however, CA19-9 might play an important role. The aim of this study is to analyze the accuracy of CA19-9 for detecting recurrence of pancreatic cancer. All included patients were treated either at the University Medical Center Goettingen, or at the Department of Interdisciplinary Oncology and Pneumonology, DRK-Kliniken Nordhessen, Kassel. We analyzed data of 93 patients with pancreatic cancer in the training set and 41 in the validation set, both retrospectively. Pre- and postoperative CA19-9 values and results of imaging techniques were compared. We performed ROC-analysis. The association between longitudinally measured CA19-9 values and relapse was studied with a joint model between a random effects model for the longitudinal CA19-9 measurements and a Cox proportional hazards models for the survival data. In the test set (n = 93 patients) the median follow-up time was 644 days (22 months). Overall, 71 patients (76.3%) developed recurrence during follow-up. Patients with CA19-9 values of <10kU/l were considered as CA19-9 negative patients (n = 11) and excluded from further analysis. Among the rest, approximately 60% of the patients showed significantly elevated CA19-9 prior to detection of recurrence by imaging techniques. Recurrence was shown by 2.45 times elevated CA19-9 values with 90% positive predictive value. In the validation set, 2.45 times elevated CA19-9 values showed recurrence with 90% sensitivity and 83,33% specificity, with an area under the curve of 95%. Based on measured CA19-9 values during follow-up care, the joint model estimates in recurrence-free patients the probability of recurrence-free survival. CA19-9 elevation is an early and reliable sign for PDAC recurrence. On the strength of a very high accuracy in CA19-9 positive patients, it should be considered to use CA19-9 for therapy decision even without a correlate of imaging technics. Using the joint model, follow-up care of PDAC patients after curative therapy can be stratified.

A Prognostic Score for Predicting Survival in Patients With Pancreatic Head Adenocarcinoma and Distal Cholangiocarcinoma

“…Similarly in regard to pancreatic density, we assumed that a low pancreatic density (<40 HU) may allow local cancer spread; however, this hypothesis was only partially confirmed because pancreatic density <40 UH was significantly related to an unfavorable prognosis only at 3 years (Table IV). We confirmed that a high serum CA19.9 level is an important factor predictive of poor survival, as already highlighted by others, and a significant marker of locally advanced tumor and cancer recurrence (11,(33)(34)(35).…”

Current Status of Circulating Tumor DNA Liquid Biopsy in Pancreatic Cancer

“…While 13 of 13 patients with postoperatively detectable ctDNA relapsed, only 10 of 22 patients with undetectable postoperative ctDNA had recurrences at 38 months post-resection [ 92 ]. CA19-9 has traditionally been used as a surveillance tool, but has its limitations, namely low sensitivity and the fact that 5–10% of the population are incapable of producing CA19-9, rendering it useless in these patients [ 93 , 94 ]. ctDNA can be used for monitoring throughout treatments including surgery and chemotherapy [ 95 , 96 , 97 , 98 , 99 ].…”

Current status of targeted microbubbles in diagnostic molecular imaging of pancreatic cancer

“…However, tumor development is slow and colony maintenance is costly. Carcinogen-induced PDAC in miceThe administration of carcinogens via a combination of DNAdamaging agents(7,anthracene, DMBA and 12-O-tetradecanoyl-phorbol-13-acetate, TPA) is another way to induce pancreatic cancer in animal models. Mechanistically, tumor initiation is achieved by DMBA administration that generates a point of mutation in Ha-Ras, an oncogene encoding a protein called H-RAS primarily involved in the regulating cell division 158.…”