Monitoring of CA19-9 and SPan-1 can facilitate the earlier confirmation of progressing pancreatic cancer during chemotherapy

Tsutsumi, Keisuke; Kawamoto, Hirofumi; Hirao, Ken; Sakakihara, Ichiro; Yamamoto, Naoki; Noma, Yasuhiro; Fujii, Masazumi; Kato, Hironari; Ogawa, Tsuneyoshi; Ishida, Etsuji; Kuwaki, Kenji; Nouso, Kazuhiro; Okada, Hiroyuki; Yamamoto, Kazuhide

doi:10.1016/j.pan.2012.07.009

Cited by 19 publications

(15 citation statements)

References 21 publications

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“…The degree of CA19-9 response predicts how patients are responding to therapy. Post-treatment CA19-9 which has decreased by 25-90% is correlated with an improved median OS (11,(21)(22)(23)(24)).…”

Section: Discussionmentioning

confidence: 99%

Gemcitabine/nab-paclitaxel as second-line therapy following FOLFIRINOX in metastatic/advanced pancreatic cancer—retrospective analysis of response

Nguyen

Kalyan

Beasley

et al. 2017

J. Gastrointest. Oncol.

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Section: Discussionmentioning

confidence: 99%

Gemcitabine/nab-paclitaxel as second-line therapy following FOLFIRINOX in metastatic/advanced pancreatic cancer—retrospective analysis of response

Nguyen

Kalyan

Beasley

et al. 2017

J. Gastrointest. Oncol.

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“…Protein and carbohydrate tumor markers (e.g., CEA, CA19-9, CA125, alphafetoprotein, chromogranin A) have been used to monitor the effects of systemic therapy for specific tumor types [ 27 , 28 , 29 , 30 , 31 ]. The problem with protein biomarkers is that their abundance does not necessarily reflect alterations in cellular physiology.…”

Section: Biomarker-based Methods Of Responsementioning

confidence: 99%

Monitoring for Response to Antineoplastic Drugs: The Potential of a Metabolomic Approach

Rattner

Bathe

2017

Metabolites

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For most cancers, chemotherapeutic options are rapidly expanding, providing the oncologist with substantial choices. Therefore, there is a growing need to select the best systemic therapy, for any individual, that effectively halts tumor progression with minimal toxicity. Having the capability to predict benefit and to anticipate toxicity would be ideal, but remains elusive at this time. An alternative approach is an adaptive approach that involves close observation for treatment response and emergence of resistance. Currently, response to systemic therapy is estimated using radiographic tests. Unfortunately, radiographic estimates of response are imperfect and radiographic signs of response can be delayed. This is particularly problematic for targeted agents, as tumor shrinkage is often not apparent with these drugs. As a result, patients are exposed to prolonged courses of toxic drugs that may ultimately be found to be ineffective. A biomarker-based adaptive strategy that involves the serial analysis of the metabolome is attractive. The metabolome changes rapidly with changes in physiology. Changes in the circulating metabolome associated with various antineoplastic agents have been described, but further work will be required to understand what changes signify clinical benefit. We present an investigative approach for the discovery and validation of metabolomic response biomarkers, which consists of serial analysis of the metabolome and linkage of changes in the metabolome to measurable therapeutic benefit. Potential pitfalls in the development of metabolomic biomarkers of response and loss of response are reviewed.

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“…Thus CA19-9 is considered the standard for monitoring response to chemotherapy and recurrence following surgical resection in patients with pancreatic cancer, but not for the initial diagnosis of the disease. Due to the inability of CA19-9 to identify early potentially curable disease, several other serologic markers have been studied, including carcinoembryonic antigenrelated cell adhesion molecule 1 (CEACAM1) [69], MIC1 [70], carcinoembryonic antigen (CEA) [71], alpha-fetoprotein (AFP) [72], pancreatic associated antigen (SPan-1) [73], CA50 antigen, DU-PAN-2, alpha4GnT, cytokeratin-19 (CK-19) mRNA, elastase-1, tissue polypeptide antigen and tissue polypeptide-specific antigen. Unfortunately, none of these markers have achieved the levels of sensitivity and specificity necessary to be recommended as a screening tool for asymptomatic patients in the general population.…”

Section: Biomarkersmentioning

confidence: 99%

The Pathogenesis, Diagnosis, and Management of Pancreatic Cancer

Malhotra¹,

Ahn²,

Bloomston

2015

J Gastrointest Dig Syst

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Pancreatic cancer is an aggressive and devastating disease accounting for 44,000 new cases per year in US. It is characterized by invasiveness, rapid progression and profound resistance to treatment. The majority of cases are diagnosed above age 65 with about 60% of cases at an advanced stage and 5 year survival less than 10%. Advances in molecular biology have greatly improved our understanding of pathogenesis of pancreatic cancer. Many patients have mutations of K-ras oncogene and various tumor suppressor genes are also investigated. Radical surgery remains the only curative treatment option for pancreatic cancer in early stages. For locally advanced, unresectable and metastatic disease, treatment is palliative, in form of adjuvant or neoadjuvant chemotherapy with or without radiotherapy. Gemcitabine based combinations have essentially failed to provide a substantial prolongation of survival and constitute treatment option only in patients with a good performance status. This article provides an overview of epidemiology; risks factors, molecular genetics, biomarkers, diagnostic modality and evidence based therapeutic options for resectable and palliative options for unresectable disease. Keywords: Pancreatic cancer; Diagnosis EpidemiologyPancreatic cancer is one of the most lethal human cancers and is the fourth leading cause of cancer-related deaths in the United States [1,2]. It is estimated that 38,460 of 45,220 people diagnosed with pancreatic cancer in the United States in 2013 will die of their disease, representing approximately 6% of total U.S. cancer deaths [1]. Typically a cancer of the elderly, only 13% of cases occur in patients younger than 55 years, whereas 69% of cases occur in those older than 65. There is a slight predilection for men over women in most countries. Furthermore the incidence of pancreatic cancer in the United States increased from 1999 to 2008, possibly because of the increasing prevalence of obesity and other unknown factors [1,[3][4][5]. Mortality rates have remained largely unchanged [6].The etiology of pancreatic cancer remains unclear, thus making specific risk factors allusive. Still, accepted associated risk factors include smoking, family history of chronic pancreatitis, advancing age, male gender, diabetes mellitus, obesity, non-O blood group, occupational exposures (to chlorinated hydrocarbon solvents and nickel), African American ethnic origin, a high-fat diet, diets high in meat and low in vegetables and folate, and possibly Helicobacter pylori infection and periodontal disease [7]. Findings of preliminary studies suggest that metformin could protect against development of pancreatic cancer [8,9]. A retrospective analysis of 302 patients with pancreatic cancer and diabetes found that metformin use was associated with increased survival at 2 years (30.1% vs. 15.4%; P=0.004) and increased overall survival (OS) (15.2 months vs. 11.1; P=0.009). The OS difference was significant only in patients without distant metastases and remained significant when insulin user...

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Monitoring of CA19-9 and SPan-1 can facilitate the earlier confirmation of progressing pancreatic cancer during chemotherapy

Abstract: ABSTRACT:Background: Measurement of objective response to chemotherapy using imaging modalities is sometimes

Cited by 19 publications

References 21 publications

Gemcitabine/nab-paclitaxel as second-line therapy following FOLFIRINOX in metastatic/advanced pancreatic cancer—retrospective analysis of response

Gemcitabine/nab-paclitaxel as second-line therapy following FOLFIRINOX in metastatic/advanced pancreatic cancer—retrospective analysis of response

Monitoring for Response to Antineoplastic Drugs: The Potential of a Metabolomic Approach

The Pathogenesis, Diagnosis, and Management of Pancreatic Cancer

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