Prognostic value of CA 19-9 levels in patients with inoperable adenocarcinoma of the pancreas treated with gemcitabine

Ziske, Carsten; Schlie, Christin; Gorschlüter, Marcus; Glasmacher, Axel; Mey, Ulrich; Strehl, John; Sauerbruch, Tilman; Schmidt‐Wolf, Ingo G.H.

doi:10.1038/sj.bjc.6601263

Cited by 149 publications

(107 citation statements)

References 22 publications

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“…Whether serum CA 19-9 levels can be used as a surrogate marker of response to chemotherapy has been studied in a variety of clinical settings [41,44,[53][54][55][56][57][58][59][60][61][62][63][64]. Willett et al measured CA 19-9 serum levels in 42 resectable pancreatic cancer patients receiving neoadjuvant treatment with 5-flourouracil and external beam radiation prior to planned pancreaticoduodenectomy.…”

Section: Ca 19-9 Serum Levels As a Biomarker For Chemotherapy Responsmentioning

confidence: 99%

“…Nearly all studies have demonstrated that a treatment related decline in CA 19-9 serum levels is associated with prolonged survival and is an independent predictor of overall survival [41,44,[53][54][55][56][57][58][59][60][61][62][63][64] (Table 5). Reni et al compared basal CA 19-9 serum levels in 247 advanced pancreatic cancer patients enrolled in five consecutive chemotherapy trials (G, gemcitabine; PEFG, cisplatin, epirubicin, 5-fluorouracil, and gemcitabine; PDXG, cisplatin, docetaxel, capecitabine, and gemcitabine) [60].…”

Section: Ca 19-9 Serum Levels As a Biomarker For Chemotherapy Responsmentioning

confidence: 99%

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Serum CA 19-9 as a Biomarker for Pancreatic Cancer—A Comprehensive Review

Ballehaninna

Chamberlain

2011

Indian J Surg Oncol

213

161

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Section: Ca 19-9 Serum Levels As a Biomarker For Chemotherapy Responsmentioning

confidence: 99%

Section: Ca 19-9 Serum Levels As a Biomarker For Chemotherapy Responsmentioning

confidence: 99%

Serum CA 19-9 as a Biomarker for Pancreatic Cancer—A Comprehensive Review

Ballehaninna

Chamberlain

2011

Indian J Surg Oncol

213

161

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“…Serial CA19-9 measurements have been shown to predict survival in patients treated with gemcitabine-based chemotherapy (Stemmler et al, 2003;Ziske et al, 2003) and fluorouracil-based chemoradiation (Micke et al, 2003). More recently, in a cohort of 154 patients treated with either PVI 5-FU, gemcitabine with or without capecitabine, patients with low baseline CA19-9 (HR: 0.56, P ¼ 0.0004) or 20% decrease from baseline with treatment (HR: Weeks since treatment start Difference in Ln CA19-9 Gastrazole (JB95008) 5FU Figure 6 Difference in log CA19-9 level compared to baseline in trial B with 95% confidence interval.…”

Section: Discussionmentioning

confidence: 99%

Gastrazole (JB95008), a novel CCK2/gastrin receptor antagonist, in the treatment of advanced pancreatic cancer: results from two randomised controlled trials

et al. 2006

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Gastrin has been shown to be a growth stimulant in pancreatic cancer cells. Gastrazole is a potent and selective gastrin receptor antagonist. Two randomised blinded trials were conducted to assess the effect of gastrazole in advanced pancreatic cancer. Patients with biopsy-proven, inoperable pancreatic carcinoma were recruited. Trial A compared protracted venous infusion (PVI) gastrazole with PVI placebo, whereas trial B compared PVI gastrazole with PVI fluorouracil (5-FU). Eighteen patients were randomised in trial A. Gastrazole produced significantly better survival compared to placebo (median 7.9 months vs 4.5 months; 1-year survival: 33 vs 11%, respectively; log rank P ¼ 0.02). No difference in toxicity was seen between gastrazole and placebo, except central venous catheter and pump complications. Ninety-eight patients were randomised in trial B. No significant survival difference was detected between gastrazole and 5-FU (median: 3.6 vs 4.2 months; 1-year survival: 13.2 vs 26.2%, respectively; log rank P ¼ 0.42). Toxicity of gastrazole was mild with significantly less diarrhoea (P ¼ 0.03), stomatitis (Po0.001) and hand -foot syndrome (Po0.001) compared to 5-FU. Quality of life (QoL) assessment showed similar QoL between gastrazole and 5-FU at baseline and no significant differences occurred with treatment either between arms or within arms. Compared to placebo, patients with advanced pancreatic cancer treated with gastrazole appeared to live longer, albeit in a very small trial and will require confirmation with large-scale randomised data. However, it did not produce survival advantage over PVI 5-FU. Lack of toxicity for gastrazole may allow its combination with cytotoxic drugs.

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“…GEM does not always induce a complete response in all types of tumors; however, many studies have shown its clinical efficacy in the treatment of pancreatic cancer (7,8). GEM is phosphorylated and metabolized and then incorporated into cellular DNA.…”

Section: Introductionmentioning

confidence: 99%

“…In the present study, we used cDNA microarray technology to investigate the mechanism that underlies the inhibition of cell proliferation by GEM in pancreatic cancer. Given the previous findings that clinical efficacy does not require cytotoxic doses of GEM (7,8), we focused on the effects of lower concentrations of GEM.…”

Section: Introductionmentioning

confidence: 99%

Molecular features linked to the growth-inhibitory effects of gemcitabine on human pancreatic cancer cells

Toshimitsu

Iizuka²,

Yamamoto³

et al. 2006

Oncol Rep

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Abstract. Although gemcitabine (GEM) is widely used in the treatment of pancreatic cancers, the molecular mechanisms that underlie its anti-tumor effects are not fully understood. To clarify the anti-tumor mechanism(s) of GEM, we studied a human pancreatic cancer cell line, YPK-1, that showed a 50% inhibitory concentration (IC50) of GEM of 6.3x10 -3 μg/ml after 72 h of exposure. Cell proliferation was perturbed by 6 to 72 h of exposure to GEM concentrations equal to one-half or one-quarter of the IC50. We used cDNA microarrays containing 2976 genes to identify genes with expression affected by exposure to GEM. The self-organizing map identified nine clusters, including 85 and 87 genes, that showed differential expression in response to exposure to one half and one quarter IC50 GEM, respectively. Of these, 24 genes were common to cells exposed to the two different concentrations of GEM. Most are signal transduction or transcription-related genes. The microarray data for two of these genes, SPARC and RPS8, were validated by RT-PCR. Although further studies are needed to examine whether the changes in expression profiles of these genes are specific to cells exposed to GEM, the present data provide insights into the anti-tumor effects of GEM on pancreatic cancers.

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Prognostic value of CA 19-9 levels in patients with inoperable adenocarcinoma of the pancreas treated with gemcitabine

Cited by 149 publications

References 22 publications

Serum CA 19-9 as a Biomarker for Pancreatic Cancer—A Comprehensive Review

Serum CA 19-9 as a Biomarker for Pancreatic Cancer—A Comprehensive Review

Gastrazole (JB95008), a novel CCK2/gastrin receptor antagonist, in the treatment of advanced pancreatic cancer: results from two randomised controlled trials

Molecular features linked to the growth-inhibitory effects of gemcitabine on human pancreatic cancer cells

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