Pancreatic Cancer Medication

  • Author: Tomislav Dragovich, MD, PhD; Chief Editor: Jules E Harris, MD   more...
 
Updated: Sep 13, 2011
 

Medication Summary

The most active single agents for pancreatic cancer have been 5-fluorouracil (5-FU) and gemcitabine. Gemcitabine appears to be slightly more active than 5-FU. Objective responses, meaning actual regression of tumor, have been 20% or less.

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Antineoplastic agents

Class Summary

These agents inhibit cell growth and proliferation. They are used for chemotherapy.

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Gemcitabine (Gemzar)

 

A frequently quoted trial showed a small, but statistically significant, improvement in overall survival with gemcitabine versus 5-FU (5.7 vs 4.4 mo). Additionally, gemcitabine improved the quality of life in approximately 25% of patients.

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Fluorouracil (Adrucil, Efudex, Fluoroplex)

 

This is a fluorinated pyrimidine antimetabolite that inhibits thymidylate synthase (TS) and also interferes with ribonucleic acid (RNA) synthesis and function. Fluorouracil has some effect on DNA and is useful in symptom palliation for patients with progressive disease. It is commonly used in patients with gastrointestinal malignancies. Response rates are typically less than 20% in pancreatic cancer.

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Erlotinib (Tarceva)

 

This agent is pharmacologically classified as a human epidermal growth factor receptor type 1/epidermal growth factor receptor (HER1/EGFR) tyrosine kinase inhibitor. EGFR is expressed on the cell surface of normal cells and cancer cells. Erlotinib is has been approved by the FDA for use, in combination with gemcitabine, as a first-line treatment for locally advanced, unresectable, or metastatic pancreatic cancer.

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Capecitabine (Xeloda)

 

Capecitabine is a prodrug of fluorouracil that undergoes hydrolysis in liver and tissues to form the active moiety (fluorouracil), inhibiting thymidylate synthetase, which in turn blocks methylation of deoxyuridylic acid to thymidylic acid. This step interferes with DNA, and to a lesser degree with RNA synthesis.

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Contributor Information and Disclosures
Author

Tomislav Dragovich, MD, PhD  Associate Professor of Medicine, Director of Clinical Gastrointestinal Cancer Program, Arizona Cancer Center, University of Arizona College of Medicine

Tomislav Dragovich, MD, PhD is a member of the following medical societies: American Association for Cancer Research and American Society of Clinical Oncology

Disclosure: Nothing to disclose.

Coauthor(s)

Richard A Erickson, MD, FACP, FACG  Professor of Medicine, Division of Gastroenterology, Department of Internal Medicine, Texas A&M University Health Science Center; Director, Scott and White Clinic and Hospital

Richard A Erickson, MD, FACP, FACG is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, and American Society of Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Claire R Larson, MD  Staff Physician, Department of General Surgery, Texas A & M School of Medicine, Scott and White Hospital

Claire R Larson, MD is a member of the following medical societies: American College of Surgeons and American Medical Association

Disclosure: Nothing to disclose.

Mohsen Shabahang, MD, PhD, FACS  Assistant Professor of Surgery, Division of Surgical Oncology, Director of Surgical Residency, Texas A&M Health Science Center, Scott and White Clinic

Mohsen Shabahang, MD, PhD, FACS is a member of the following medical societies: American College of Surgeons, American Medical Association, Association for Academic Surgery, Society of Surgical Oncology, Texas Medical Association, and Western Surgical Association

Disclosure: Nothing to disclose.

Specialty Editor Board

Lodovico Balducci, MD  Professor of Oncology and Medicine, University of South Florida College of Medicine; Division Chief, Senior Adult Oncology Program, H Lee Moffitt Cancer Center and Research Institute

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Chief Editor

Jules E Harris, MD  Clinical Professor of Medicine, Division of Hematology/Medical Oncology, Department of Internal Medicine, University of Arizona College of Medicine; Consulting Staff, Arizona Cancer Center

Jules E Harris, MD is a member of the following medical societies: American Association for Cancer Research, American Association for the Advancement of Science, American Association of Immunologists, American Society of Hematology, and Central Society for Clinical Research

Disclosure: GlobeImmune Salary Consulting

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Pancreatic cancer. Gross section of an adenocarcinoma of the pancreas measuring 5 X 6 cm resected from the pancreatic body and tail. Although the tumor was considered to have been fully resected and had not spread to any nodes, the patient died of recurrent cancer within 1 year.
Pancreatic cancer. Hematoxylin and eosin stain of a pancreatic carcinoma. Note the intense desmoplastic response around the neoplastic cells. The large amount of fibrotic reaction in these tumors can make obtaining adequate tissue by fine-needle aspiration difficult.
Pancreatic cancer. T staging for pancreatic carcinoma. T1 and T2 stages are confined to the pancreatic parenchyma. T3 lesions invade local structures such as the duodenum, bile duct, and/or major peripancreatic veins, and T4 lesions invade surrounding organs (eg, stomach, colon, liver) or invade major arteries such as the superior mesenteric or celiac arteries.
Pancreatic cancer. Computerized tomographic scan showing a pancreatic adenocarcinoma of the pancreatic head. The gallbladder (gb) is distended because of biliary obstruction. The superior mesenteric artery (sma) is surrounded by tumor, making this an unresectable T4 lesion.
Pancreatic cancer. Abdominal CT scan of a small, vaguely seen, 2-cm pancreatic adenocarcinoma (mass) causing obstruction of both the common bile duct (cbd) and pancreatic duct (pd).
Pancreatic cancer. Endoscopic ultrasound of a 2.2-cm pancreatic adenocarcinoma of the head of the pancreas obstructing the common bile duct (CBD) but not invading the portal vein (PV) or superior mesenteric vein (SMV). Findings from endoscopic ultrasound–guided fine-needle aspiration revealed a moderately to poorly differentiated adenocarcinoma. Abdominal CT findings did not show this mass, and an attempt at endoscopic retrograde cholangiopancreatography at another institution was unsuccessful.
Algorithm for evaluation of a patient with suspected pancreatic cancer. CT scanning for definitive diagnosis and staging must be with thin-cut, multidetector, spiral CT scanning using dual-phase contrast imaging to allow for maximal information. This schema varies among institutions depending on local expertise, research interest, and therapeutic protocols for pancreatic carcinoma.
Pancreatic cancer. Tip of linear array echoendoscope (Pentax FG 36UX) with 22-gauge aspiration needle exiting from biopsy channel. Insert shows magnification of aspiration needle tip. Note that the needle exits from the biopsy channel such that it appears continuously in the view of the ultrasonic transducer on the tip of the echoendoscope.
Pancreatic cancer. Cytologic samples from fine-needle aspirations (rapid Papanicolaou stain) of pancreatic adenocarcinomas. (A) Well differentiated, (B) moderately differentiated, (C) moderate to poorly differentiated, (D) poorly differentiated tumor.
 
 
 
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