About: CA19-9 is a research topic. Over the lifetime, 5126 publications have been published within this topic receiving 148330 citations. The topic is also known as: CA 19-9 & carbohydrate antigen 19-9.
TL;DR: This work identified a highly tumorigenic subpopulation of pancreatic cancer cells expressing the cell surface markers CD44, CD24, and epithelial-specific antigen (ESA) that showed the stem cell properties of self-renewal, the ability to produce differentiated progeny, and increased expression of the developmental signaling molecule sonic hedgehog.
Abstract: Emerging evidence has suggested that the capability of a tumor to grow and propagate is dependent on a small subset of cells within a tumor, termed cancer stem cells. Although data have been provided to support this theory in human blood, brain, and breast cancers, the identity of pancreatic cancer stem cells has not been determined. Using a xenograft model in which primary human pancreatic adenocarcinomas were grown in immunocompromised mice, we identified a highly tumorigenic subpopulation of pancreatic cancer cells expressing the cell surface markers CD44, CD24, and epithelial-specific antigen (ESA). Pancreatic cancer cells with the CD44+CD24+ESA+ phenotype (0.2–0.8% of pancreatic cancer cells) had a 100-fold increased tumorigenic potential compared with nontumorigenic cancer cells, with 50% of animals injected with as few as 100 CD44+CD24+ESA+ cells forming tumors that were histologically indistinguishable from the human tumors from which they originated. The enhanced ability of CD44+CD24+ESA+ pancreatic cancer cells to form tumors was confirmed in an orthotopic pancreatic tail injection model. The CD44+CD24+ESA+ pancreatic cancer cells showed the stem cell properties of self-renewal, the ability to produce differentiated progeny, and increased expression of the developmental signaling molecule sonic hedgehog. Identification of pancreatic cancer stem cells and further elucidation of the signaling pathways that regulate their growth and survival may provide novel therapeutic approaches to treat pancreatic cancer, which is notoriously resistant to standard chemotherapy and radiation. [Cancer Res 2007;67(3):1030–7]
TL;DR: It is demonstrated that a subpopulation of migrating CD133(+) CX CR4(+) cancer stem cells is essential for tumor metastasis and strategies aimed at modulating the SDF-1/CXCR4 axis may have important clinical applications to inhibit metastasis of cancer stem Cells.
TL;DR: The combined of CEA, CA19-9 and CA72.4 had 62.0% sensitivity in the diagnosis of recurrence after radical surgery, and patients whose tumor markers continue to increase should be highly suspected for relapse.
Abstract: BACKGROUND/AIMS To explore the predictive value of markers in detection of recurrence after resection. METHODOLOGY This study was a case-control retrospective analysis; 521 patients underwent radical gastrectomy from April 2000 to January 2008, among whom 142 cases with complete data were involved. Seventy one were confirmed with recurrence, while the other 71 without recurrence were randomly selected from the database as control. We analyzed the popular serum marker change patterns and their correlation with imaging. RESULTS The two groups were well balanced in characteristics. Among the 3 markers, CA72.4 appeared highest in sensitivity (35.2%) while CEA had the lowest sensitivity. The sensitivity of triple-marker was 62.0%. We found that CEA, CA19-9 and CA72.4 elevated 2-4 months before imaging demonstration. If the cut-off values of CEA and CA19-9 were set twice as the upper limit of the normal, the specificities will increase to 98.6% and 94.4%, respectively. The sensitivity of single marker (CEA or CA 2.4) was 33.3% in predicting peritoneal metastasis, triple-marker had the highest sensitivity (66.7%). CONCLUSIONS The combined of CEA, CA19-9 and CA72.4 had 62.0% sensitivity in the diagnosis of recurrence after radical surgery. Patients whose tumor markers continue to increase should be highly suspected for relapse.
TL;DR: This work identified a highly tumorigenic subpopulation of pancreatic cancer cells expressing the cell surface markers CD44, CD24, and epithelial-specific antigen (ESA) that showed the stem cell properties of self-renewal, the ability to produce differentiated progeny, and increased expression of the developmental signaling molecule sonic hedgehog.
TL;DR: Data indicate that stellate cells have an important role in supporting and promoting pancreatic cancer, and the presence of HPSCs in tumors increases the growth and metastasis of these cells.
Abstract: Pancreatic adenocarcinoma is characterized by a dense background of tumor associated stroma originating from abundant pancreatic stellate cells. The aim of this study was to determine the effect of human pancreatic stellate cells (HPSC) on pancreatic tumor progression. HPSCs were isolated from resected pancreatic adenocarcinoma samples and immortalized with telomerase and SV40 large T antigen. Effects of HPSC conditioned medium (HPSC-CM) on in vitro proliferation, migration, invasion, soft-agar colony formation, and survival in the presence of gemcitabine or radiation therapy were measured in two pancreatic cancer cell lines. The effects of HPSCs on tumors were examined in an orthotopic murine model of pancreatic cancer by co-injecting them with cancer cells and analyzing growth and metastasis. HPSC-CM dose-dependently increased BxPC3 and Panc1 tumor cell proliferation, migration, invasion, and colony formation. Furthermore, gemcitabine and radiation therapy were less effective in tumor cells treated with HPSC-CM. HPSC-CM activated the mitogen-activated protein kinase and Akt pathways in tumor cells. Co-injection of tumor cells with HPSCs in an orthotopic model resulted in increased primary tumor incidence, size, and metastasis, which corresponded with the proportion of HPSCs. HPSCs produce soluble factors that stimulate signaling pathways related to proliferation and survival of pancreatic cancer cells, and the presence of HPSCs in tumors increases the growth and metastasis of these cells. These data indicate that stellate cells have an important role in supporting and promoting pancreatic cancer. Identification of HPSC-derived factors may lead to novel stroma-targeted therapies for pancreatic cancer.