The evaluation of CA 19-9 antigen level in the early detection of pancreatic cancer: A prospective study of 866 patients

Frébourg, Thierry; Bercoff, É.; Manchon, N. D.; Sénant, J; Basuyau, Jean-Pierre; Breton, Pascal; Janvresse, A.; Brunelle, P; Bourreille, J

doi:10.1002/1097-0142(19881201)62:11<2287::aid-cncr2820621103>3.0.co;2-h

Cited by 96 publications

(38 citation statements)

References 23 publications

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“…3,4 In the series by Homma and Tsuchiya, 4 mass screening of 10,162 patients age Ͼ 40 years yielded only 4 patients (0.04%) with pancreatic carcinoma using serum CA19-9 and elastase-1 in combination with ultrasonography, whereas 85 of 4506 outpatients (1.9%) with gastrointestinal complaints or jaundice had pancreatic carcinoma. Many reports emphasized the correlation between pancreatic carcinoma and diabetes mellitus, [5][6][7][8] but pancreatic carcinoma is not frequent, even in patients with diabetes.…”

Section: Discussionmentioning

confidence: 99%

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A prospective pancreatographic study of the prevalence of pancreatic carcinoma in patients with diabetes mellitus

Ogawa

Tanaka

Inoue

et al. 2002

Cancer

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BACKGROUNDThe correlation between diabetes mellitus and pancreatic carcinoma is well documented, but no criteria have been established for the efficient selection of a high‐risk group among patients with diabetes mellitus.METHODSEighty‐seven patients were selected prospectively from outpatients with diabetes and underwent endoscopic retrograde pancreatography (ERP) according to the authors' original criteria, including the onset of diabetes after age 55 years, deterioration of diabetes or loss of body weight despite strict medical control, elevation of serum amylase and/or CA19‐9 levels, and pancreatobiliary abnormalities on routine ultrasonography. The patients were divided into two groups according to the time from the onset of diabetes to ERP: Patients in Group A had recent‐onset diabetes (within 3 years), and Group B patients had diabetes for > 3 years.RESULTSA total of 86 patients (excluding 1 patient with unsuccessful ERP who had undergone previous Billroth‐2 gastrectomy) were enrolled. There were 33 males and 53 females, age 40–90 years, with a mean age of 65.1 years. ERP demonstrated pancreatic carcinoma, although it was advanced disease in all patients, at an extremely high rate of 7.0% (6 of 86 patients) with no serious complications. The prevalence of pancreatic carcinoma in Group A (13.9%; 5of 36 patients) was significantly greater compared with Group B (2.0%; 1 of 50 patients; P = 0.0442). ERP with an indwelling balloon catheter and subsequent pancreatic juice sampling was performed in 49 patients, yielding positive cytology in 1 patient with pancreatic tail carcinoma, whereas measurements of carcinoembryonic antigen and CA19‐9 levels in pancreatic juice were of no use in the diagnosis of pancreatic carcinoma.CONCLUSIONSSelective ERP in patients with diabetes who were at high risk did not lead to the early diagnosis of pancreatic carcinoma, although this study showed that the 3‐year period after the onset of diabetes was critical. A more aggressive diagnostic approach within this period in diabetic patients with the authors' criteria may contribute to the earlier diagnosis of pancreatic carcinoma. Cancer 2002;94:2344–9. © 2002 American Cancer Society.DOI 10.1002/cncr.10493

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Section: Discussionmentioning

confidence: 99%

“…In this study, ERP was used as a gold standard for the diagnosis of pancreatic carcinoma despite its invasiveness, 9 because no other prospective studies using noninvasive diagnostic modalities have achieved acceptable results. 3,4 …”

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confidence: 99%

A prospective pancreatographic study of the prevalence of pancreatic carcinoma in patients with diabetes mellitus

Ogawa

Tanaka

Inoue

et al. 2002

Cancer

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“…Also, in patients with chronic pancreatitis, the most important control group for pancreatic cancer, the specificity of CAM 17.1 was significantly higher than the specificity of CA 19-9 (90% and 78%; P>0.05). The combined evaluation of CAM 17.1 and CA 19-9 in patients with pancreatic cancer or chronic 10 000 (Frebourg et al, 1988;Haglund et al, 1986;Lucarotti et al, 1991;Magnani et al, 1983;Ohshio et al, 1990;Von Rossen et al, 1993;Safi et al, 1986;Toshkov et al, 1994). The monoclonal antibody CAM 17.1 detects a mucus glycoprotein with a high specificity for intestinal mucus, particularly in the colon, small intestine, biliary tract and pancreas (Makin et al, 1984;Raouf et al, 1991).…”

Section: Immunohistochemistrymentioning

confidence: 99%

“…Mucins are also often detectable in the serum of patients suffering from pancreatic cancer; these include the blood group antigen sialylated Lewisa, which is the epitope for the antibody detecting CA19-9 (Magnani et al, 1983) and ThomsenFriedenreich antigen (galactose , Rhodes, 1988, 1990), which is the epitope for the lectin peanut agglutinin (PNA). Many reports have evaluated the practicality of using tumour markers such as CA19-9, CEA, CA50, CA242, CA494 and others for the serological diagnosis of pancreatic cancer and the follow-up of patients after tumour resection for pancreatic cancer (Frebourg et al, 1988;Freiss et al, 1993;Habib et al, 1986;Haglund et al, 1986;Kalser et al, 1978;Lucarotti et al, 1991;Nilsson et al, 1992;Ohshio et al, 1990;Von Rosen et al, 1993;Safi et al, 1986;Toshkov et al, 1994). In 1992, Parker et al firstly reported a new enzyme-linked antibody sandwich assay (CAM 17.1/WGA) using the monoclonal antibody CAM 17.1, which was generated after immunisation with Coll 2 -23 colorectal cancer cells.…”

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CAM 17.1 - A new diagnostic marker in pancreatic cancer

Gansauge

Gansauge²,

Parker³

et al. 1996

Br J Cancer

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CAM 17.1-Ab is a recently described monoclonal antibody that detects a mucus glycoprotein with high specificity for intestinal mucus, particularly in the colon, small intestine, biliary tract and pancreas. We investigated the expression and release of CAM 17.1 in pancreatic carcinoma cell lines and tissue specimens of normal pancreas, chronic pancreatitis and pancreatic cancer. CAM 17.1 was weakly expressed on normal ductal cells and chronic pancreatitis, whereas it was overexpressed in pancreatic cancer. Serum analysis using a new enzyme-linked antibody sandwich assay (CAM 17.1/WGA) of patients with chronic pancreatitis, pancreatic cancer or other gastrointestinal cancer and of healthy blood donors revealed a high sensitivity (67%) and excellent specificity (90%) of CAM 17.1/WGA assay in pancreatic cancer. In comparison with the tumour marker CA19-9, the sensitivity of the CAM 17.1/WGA assay was similar to the sensitivity of CA 19-9 (67% and 76%, P = 0.22), whereas the specificity of CAM 17.1/WGA assay was higher than in CA 19-9 (90% compared with 78% in chronic pancreatitis, P > 0.05). Images Figure 2

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“…In addition, patients who are negative for Lewis antigen A or B (∼10% of patients with PDA) do not synthesize CA 19-9 and have undetectable levels, even in the advanced stages of the disease. 24 A promising discovery of biomarkers for the early diagnosis of PDA came from a serological proteome approach, which identified autoantibodies as a potential diagnostic marker in patients with PDA, in a genetically engineered mouse (GEM) model of PDA and in a prediagnostic cohort. These autoantibodies recognize the cytoskeletal protein Ezrin 25 and the phosphorylated α-enolase (ENO1), a glycolytic enzyme, which also functions as a plasminogen receptor.…”

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Pancreatic cancer vaccine: a unique potential therapy

Cappello¹,

Principe²,

Novelli³

2015

GICTT

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Pancreatic ductal adenocarcinoma (PDA) is a lethal disease and is one of the cancers that is most resistant to traditional therapies. Historically, neither chemotherapy nor radiotherapy has provided any significant increase in the survival of patients with PDA. Despite intensive efforts, any attempts to improve the survival in the past 15 years have failed. This holds true even after the introduction of molecularly targeted agents, chosen on the basis of their involvement in pathways that are considered to be important in PDA development and progression. Recently, however, FOLFIRINOX (5-fluorouracil, leucovorin, irinotecan, and oxaliplatin) treatment has provided a limited survival advantage in patients with advanced PDA. Therefore, effective therapeutic strategies are urgently needed to improve the survival rate of patients with PDA. Results from the last 10 years of research in the field of PDA have helped to identify new immunological targets and develop new vaccines that are capable of stimulating an immune response. In addition, the information obtained about the role of the tumor microenvironment in suppressing the immune response and the possibility of targeting PDA microenvironment to limit immune suppression and enhance the response of effector T-cells has opened new avenues for treating this incurable disease. The time is ripe for developing new therapeutic approaches that are able to effectively counteract the progression and spreading of PDA. This review discusses the potential prospects in the care of patients with pancreatic cancer through vaccination and its combination therapy with surgery, chemotherapy, targeting of the tumor microenvironment, and inhibition of immunological checkpoints. Keywords: pancreatic cancer, vaccines, T-cells, antibody, immunotherapy Pancreatic cancerAlthough lung, breast, prostate, and colorectal cancers are considered to be the "big four" cancer types in the USA, pancreas and liver cancers are expected to surpass breast, prostate, and colorectal cancers to become the second and third leading causes of cancer-related deaths by 2030, respectively.1 Pancreatic ductal adenocarcinomas (PDAs) arise from the exocrine pancreas and account for 95% of pancreatic cancers. In the USA, there were an estimated 48,960 cases of new-onset pancreatic cancer in 2015, which led to 40,560 deaths, with a 5-year survival rate of ∼7%.3 PDA is nearly universally lethal; ,20% of patients are suitable candidates for surgery at the time of diagnosis, and the median survival rate is 3.5 months and 12.6 months for nonresected patients and resected patients, respectively.2,4 PDA evolves from noninvasive precursor lesions that do not invade the basement membrane. [5][6][7] Three precursors have been characterized, namely, pancreatic intraepithelial neoplasias (PanINs), intraductal papillary mucinous neoplasms, and mucinous cystic neoplasms.

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The evaluation of CA 19-9 antigen level in the early detection of pancreatic cancer: A prospective study of 866 patients

Cited by 96 publications

References 23 publications

A prospective pancreatographic study of the prevalence of pancreatic carcinoma in patients with diabetes mellitus

A prospective pancreatographic study of the prevalence of pancreatic carcinoma in patients with diabetes mellitus

CAM 17.1 - A new diagnostic marker in pancreatic cancer

Pancreatic cancer vaccine: a unique potential therapy

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