eMedicine Specialties > Oncology > Carcinomas of the Gastrointestinal Tract

Pancreatic Cancer

Author: 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
Coauthor(s): Claire R Larson, MD, Staff Physician, Department of General Surgery, Texas A & M School of Medicine, Scott and White Hospital; 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
Contributor Information and Disclosures

Updated: Apr 7, 2009

Introduction

Background

Pancreatic cancer is the fourth leading cause of death among both men and women, comprising 6% of all cancer-related deaths. The incidence of pancreatic cancer has risen slowly over the years. The disease is notoriously difficult to diagnose in its early stages. At the time of diagnosis, 52% of all patients have distant disease and 26% have regional spread. The relative 1-year survival is only 24% and the overall 5-year survival rate for this disease is less than 5%. 

Pancreatic cancer. Gross section of an adenocarci...

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.

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Pancreatic cancer. Gross section of an adenocarci...

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.


Pathophysiology

Pancreatic cancers can arise from both the exocrine and endocrine portions of the pancreas. Of pancreatic tumors, 95% develop from the exocrine portion of the pancreas, including the ductal epithelium, acinar cells, connective tissue, and lymphatic tissue. Approximately 75% of all pancreatic carcinomas occur within the head or neck of the pancreas, 15-20% occur in the body of the pancreas, and 5-10% occur in the tail.

Typically, pancreatic cancer first metastasizes to regional lymph nodes, then to the liver, and, less commonly, to the lungs. It can also directly invade surrounding visceral organs such as the duodenum, stomach, and colon or metastasize to any surface in the abdominal cavity via peritoneal spread. Ascites may result, and this has an ominous prognosis. Pancreatic cancer may spread to the skin as painful nodular metastases. Pancreatic cancer uncommonly metastasizes to bone. It is rare for pancreatic cancer to spread to the brain. It can, however, produce meningeal carcinomatosis.

The molecular genetics of pancreatic adenocarcinoma have been well studied.1,2,3 Of these tumors, 80-95% have mutations in the KRAS2 gene, and 85-98% have mutations, deletions, or hypermethylation in the CDKN2 gene. Of these cancers, 50% have mutations in p53 and about 55% have homozygous deletions or mutations of Smad4. Some of these mutations can also be found in high-risk precursors of pancreatic cancer. For example, in chronic pancreatitis, 30% of patients have detectable mutations in p16 and 10% have K-ras mutations.

Families with BRCA-2 mutations, which are associated with a high risk of breast cancer, also have an excess of pancreatic cancer.4 Assaying pancreatic juice for the genetic mutations associated with pancreatic adenocarcinoma is invasive but may be useful for the early diagnosis of the disease;5 this approach is problematic as genetic mutations in the pancreatic juice may be found associated with inflammatory pancreatic disease.

Certain precursor lesions have been associated with pancreatic tumors arising from the ductal epithelium of the pancreas.  The main morphologic form associated with ductal adenocarcinoma of the pancreas has been pancreatic intraepithelial neoplasia or PIN. These lesions arise from specific genetic mutations and cellular alterations that all contribute to the development of invasive ductal adenocarcinoma. The initial alterations appear to be related to KRAS2 gene mutations and telomere shortening. Thereafter p16/CDKN2A is inactivated. Finally, the inactivation of TP53 and MAD4/DPC4 occur. These mutations have been correlated with increasing development of dysplasia, and thus the development of ductal carcinoma of the exocrine pancreas.

As in other organs, chronic inflammation appears to be a predisposing factor in the development of pancreatic cancer. Patients with chronic pancreatitis from alcohol and especially those with familial chronic pancreatitis have much higher incidence and an earlier age of onset of pancreatic carcinoma.

Frequency

United States

In 2008, an estimated 37,680 new cases of pancreatic cancer (18,770 in men and 18,910 in women) will have been diagnosed in the United States; 34,290 persons (17,500 men and 16,790 women) will have died of the disease in 2008.6

The overall incidence of pancreatic cancer is approximately 8-10 cases per 100,000 persons per year.7,8 Although the overall incidence of pancreatic cancer has been relatively stable for decades, the incidence of pancreatic cancer in males has been slowly dropping over the past 2 decades, while the incidence in females has increased slightly. These trends probably represent the effect of changing smoking rates for men and women.

International

Worldwide, pancreatic cancer ranks 13th in incidence but 8th as a cause of cancer death.7 The highest incidence rate is approximately 13 cases per 100,000 persons per year in black males in the United States. Native Hawaiian males and men of Korean, Czech, Latvian, and New Zealand Maori ancestry also have high incidence rates, that is, 11 cases per 100,000 persons per year. Most other countries have incidence rates of 8-12 cases per 100,000 persons per year. In some areas of the world, pancreatic cancer is quite infrequent; for example, the incidence in India is less than 2 cases per 100,000 persons per year.

Mortality/Morbidity

Pancreatic cancer is the fourth leading cause of death among both men and women, comprising 6% of all cancer-related deaths. The incidence of pancreatic cancer has risen slowly over the years. The death rate has risen from 5 per 100,000 population in 1930 to more than 10 per 100,000 in 2003. The disease is notoriously difficult to diagnose in its early stages. At the time of diagnosis, 52% of all patients have distant disease and 26% have regional spread. 

The relative 1-year survival is only 24%, and the overall 5-year survival rate for this disease is less than 5%. This number has not changed significantly over the years. A 5-year survival in pancreatic cancer is no guarantee of cure; patients who survive for 5 years after successful surgery may still die of recurrent disease years after the 5-year survival point. The occasional patient with metastatic disease or locally advanced disease who survives beyond 2-3 years may die of complications of local spread, such as bleeding esophageal varices.

Pancreatic carcinoma is unfortunately usually a fatal disease. The collective median survival time of all patients is 4-6 months. Most patients eventually succumb to the consequences of local invasion and metastatic cancer, and true long-term cures are rare. However, neuroendocrine and cystic neoplasms of the pancreas such as mucinous cystadenocarcinomas or intraductal papillary mucinous neoplasms (IPMN) have much better survival rates than pancreatic adenocarcinoma.

In patients able to undergo a successful curative resection (only about 20% of patients), median survival time ranges from 12-19 months, and the 5-year survival rate is 15-20%. The best predictors of long-term survival after surgery are a tumor diameter of less than 3 cm, no nodal involvement, negative resection margins, and diploid tumor DNA content.

Race

  • The incidence rate of pancreatic cancer for black males in the United States from 2000 to 2003 was 16.2 cases per 100,000 persons per year, and the incidence for black females was 13.7 cases per 100,000 persons per year9 .
  • For white males in the United States, the incidence is 12.7 cases per 100,000 persons per year, and for white females the incidence is 9.8 cases per 100,000 persons per year.
  • The reasons for the 1.3 to 1.4 increase in pancreatic cancer in African Americans are unclear. Certainly, differences in dietary habits and the frequency of cigarette smoking are recognized among different groups. Obesity has been identified as a possible risk factor for pancreatic cancer and may contribute to the higher incidence of this disease among blacks. However, these variations may also be related to the underlying frequency of predisposing genetic mutations for pancreatic cancer or to other unknown factors.

Sex

In the United States, slightly more women than men are diagnosed each year with pancreatic cancer; slightly more men than women die of the disease.

Age

  • Age is the most significant risk factor for pancreatic cancer.
  • In the absence of predisposing conditions, such as familial pancreatic cancer and chronic pancreatitis, pancreatic cancer is unusual in persons younger than 45 years. After age 50 years, the frequency of pancreatic cancer increases linearly. At age 70, mortality incidence due to pancreatic cancer is approximately 60 deaths per 100,000 persons per year.
  • The median age at diagnosis is 69 years in whites and 65 years in blacks; some single institution data reported from large cancer centers suggest that the median age at diagnosis in both sexes has fallen to 63 years of age.

Clinical

History

The early clinical diagnosis of pancreatic cancer is fraught with difficulty. Unfortunately, the initial symptoms are often quite nonspecific and subtle in onset.

  • Patients typically report the gradual onset of nonspecific symptoms such as anorexia, malaise, nausea, fatigue, and mid-epigastric or back pain.
  • Significant weight loss is a characteristic feature of pancreatic cancer.
  • These initial symptoms can be easily attributed to other processes unless a physician has a high index of suspicion for the possibility of underlying pancreatic carcinoma. Delayed diagnosis is a common problem in patients with pancreatic cancer, with fewer than a third of patients in the past being diagnosed within 2 months of the onset of their symptoms. The availability of CT scans has shortened that interval.
  • Pain is the most common presenting symptom in patients with pancreatic cancer. Typically, it is mid epigastric in location, with radiation of the pain sometimes occurring to the mid- or lower-back region. Back radiation of the pain is a worrisome sign indicating retroperitoneal invasion of the splanchnic nerve plexus by the tumor. Often, the pain is unrelenting in nature with night-time pain often being a predominant complaint. Some patients may note increased discomfort after eating. The pain may be worse when the patient is lying flat. About one third of patients may not have pain at the time of initial presentation; one third of patients have moderate pain and one third of patients have severe pain. All patients experience pain at some point in their clinical course.
  • Weight loss may be related to cancer associated anorexia and/or subclinical malabsorption from pancreatic exocrine insufficiency caused by pancreatic duct obstruction by the cancer. Patients with malabsorption usually complain about diarrhea and malodorous, greasy stools. Nausea and early satiety from gastric outlet obstruction and delayed gastric emptying from the tumor may also contribute to weight loss.
  • The onset of diabetes mellitus within the previous year is sometimes associated with pancreatic carcinoma. However, only about 1% of cases of new-onset diabetes mellitus in adults are actually related to occult pancreatic cancer.10 However, pancreatic cancer should be at least thought of in a patient older than 70 years with a new diagnosis of diabetes without any other diabetic risk factors.
  • The most characteristic sign of pancreatic carcinoma of the head of the pancreas is painless obstructive jaundice.
    • Patients with this sign may come to medical attention before their tumor grows large enough to cause abdominal pain.
    • These patients usually notice a darkening of their urine and lightening of their stools before they or their families notice the change in skin pigmentation. Physicians can usually recognize clinical jaundice when the total bilirubin reaches 2.5-3 mg%. Patients and their families do not usually notice clinical jaundice until the total bilirubin reaches 6-8 mg%. Urine darkening, stool changes, and pruritus are often noticed by patients before clinical jaundice.
    • Pruritus may accompany and often precedes clinical obstructive jaundice. Pruritus can often be the patient's most distressing symptom.
  • Depression is reported to be more common in patients with pancreatic cancer than in patients with other abdominal tumors. In some patients, depression may be the most prominent presenting symptom. This may be, in part, secondary to the high frequency of delayed diagnosis with this disease. In addition, although patients may not communicate it to their families, they are often aware that some serious illness, like cancer, is occurring in them.
  • Migratory thrombophlebitis (ie, Trousseau sign) and venous thrombosis also occur with higher frequency in patients with pancreatic cancer and may be their first presentation. Marantic endocarditis may develop in pancreatic cancer occasionally being confused with subacute bacterial endocarditis.

Physical

The physical examination findings in a patient with pancreatic cancer usually involves evidence of significant weight loss and some mild-to-moderate midepigastric tenderness together with other more specific signs. 

  • Patients with clinical jaundice may also have a palpable gallbladder (ie, Courvoisier sign) and may have evidence of skin excoriations from unrelenting pruritus.
  • Patients presenting with or developing advanced intraabdominal disease may have ascites, a palpable abdominal mass, hepatomegaly from liver metastases, or splenomegaly from portal vein obstruction.
  • Subcutaneous metastases (referred to as a Sister Mary Joseph nodule or nodules) in the paraumbilical area signify advanced disease.
  • A metastatic mass in the rectal pouch may be palpable on rectal examination (Blumer's shelf).
  • A metastatic node may be palpable behind the medial end of the left clavicle (Virchow's node). However, other nodes in the cervical area may also be involved. Indeed, prior to the advent of CT scanners to assess intraabdominal disease, pancreas cancer accounted for some 25% of adenocarcinoma of the cervical nodes, primary site unknown.

Causes

Overall, estimates indicate that 40% of pancreatic cancer cases are sporadic in nature. Another 30% are related to smoking, and 20% may be associated with dietary factors. Only 5-10% are hereditary in nature. Fewer than 5% of all pancreatic cancers are related to underlying chronic pancreatitis.

  • Smoking
    • Smoking is the most common environmental risk factor for pancreatic carcinoma.
    • People who smoke have at least a 2-fold increased risk for pancreatic cancer. Current smokers with over a 40 pack-year history of smoking may have up to a 5-fold increase risk of the disease. Smokeless tobacco also increases the risk of pancreatic cancer. It takes 5-10 years of discontinued smoking to reduce the increased risk of smoking to approximately that of nonsmokers.
  • Dietary factors
    • Alcohol consumption does not appear to be an independent risk factor for pancreatic cancer unless it is associated with chronic pancreatitis.
    • In a number of studies, obesity, especially central, has been associated with a higher incidence of pancreatic cancer. The incidence is lower in those with a diet rich in fresh fruits and vegetables. Fruits and vegetables rich in folate and lycopenes (such as tomatoes) may be especially good at reducing the risk of developing pancreatic cancer. Red meat consumption, especially processed, is associated with a higher risk of pancreatic cancer. Poultry and dairy product consumption does not increase the risk of this disease. Supplemental antioxidants such as vitamin C or E do not appear to decrease the risk of pancreatic cancer or other gastrointestinal cancers and may actually be associated with excess mortality.
    • Despite early reports to the contrary, coffee consumption is not associated with an increased risk of pancreatic cancer. 
  • Diabetes mellitus
    • Numerous studies have examined the relative risk of pancreatic cancer in persons with diabetes mellitus.
    • Meta-analysis of 30 studies concluded that patients with diabetes mellitus of at least 5-years' duration have a 2-fold increased risk of developing pancreatic carcinoma. Pancreatic cancer may follow 18-36 months after a diagnosis of diabetes mellitus in elderly patients with no family history of diabetes mellitus.
  • Chronic pancreatitis
    • Long-standing chronic pancreatitis is a substantial risk factor for the development of pancreatic cancer. A multicenter study of more than 2000 patients with chronic pancreatitis showed a 26-fold increase in the risk of developing pancreatic cancer. This risk increased linearly with time, with 4% of patients who had chronic pancreatitis for 20 years' duration developing pancreatic cancer.
    • The risk of pancreatic cancer is even higher in patients with hereditary pancreatitis. The mean age of development of pancreatic cancer in these patients is approximately 57 years. The relative risk of pancreatic cancer in hereditary pancreatitis is increased more than 50-fold, and the cumulative risk rate of pancreatic cancer by age 70 years is 40%. This cumulative risk increases to 75% in those families with a paternal inheritance pattern.
  • Genetic factors
    • Approximately 5-10% of patients with pancreatic carcinoma have some genetic predisposition to developing the disease.11
    • The inherited disorders that increase the risk of pancreatic cancer include hereditary pancreatitis, multiple endocrine neoplasia (MEN), hereditary nonpolyposis rectal cancer (HNPCC), familial adenomatous polyposis (FAP) and Gardner syndrome, familial atypical multiple mole melanoma (FAMMM) syndrome, von Hippel-Lindau syndrome (VHL), and germline mutations in the BRCA1 and BRCA2 genes. Hereditary pancreatitis has been associated with a cumulative risk of developing pancreatic cancer at 40%.12  MEN-1 and VHL are other genetic syndromes associated with pancreatic endocrine tumor development. 
      • Patients with MEN-1 develop symptomatic pancreatic endocrine tumors about 50% of the time, and these pancreatic tumors are noted to be the leading cause of disease-specific mortality.13  von Hippel-Lindau syndrome has been associated with malignancy in 17% of masses found in the pancreas in people with this syndrome.14  
      • Syndromes associated with increased risk of the development of colon cancer such as HNPCC and FAP (and Gardner syndrome) have also shown an increased correlation with existence of pancreatic cancer but the statistics unfortunately have not been impressive. One cohort study of 1391 patients with FAP only showed 4 to develop pancreatic adenocarcinoma, and in patients with HNPCC, no statistics are currently available to show incidence of pancreatic cancer in these patients.15 FAMMM has been shown to increase relative risk of developing pancreatic cancer by 13- to 22-fold and incidence in sporadic cases to be 98%. Germline mutations in BRCA1 and BRCA2 have only been shown to moderately increase risk of developing pancreatic cancer by 2.3- to 3.6-fold, but BRCA2 has been associated more commonly with pancreatic cancer at an incidence of 7%.11
    • The above disorders have specific genetic abnormalities associated with the noted increased risk of pancreatic cancer. Pancreatic cancer in hereditary pancreatitis is associated with a mutation in the PRSS1 gene. Pancreatic cancer appearing in FAP and HNPCC has been associated with a mutation in the APC gene and MSH2 and MLH1 genes respectively. FAMMM and pancreatic cancer has been associated with a mutation in CDKN2A. Endocrine tumors of the pancreas associated with VHL are thought to develop by way of the inactivation of the VHL tumor suppressor gene.11

More on Pancreatic Cancer

Overview: Pancreatic Cancer
Differential Diagnoses & Workup: Pancreatic Cancer
Treatment & Medication: Pancreatic Cancer
Follow-up: Pancreatic Cancer
Multimedia: Pancreatic Cancer
References
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Further Reading

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Keywords

pancreatic cancer, pancreas cancer, pancreatic carcinoma, pancreas carcinoma, gastrointestinal cancer, GI cancer, gastrointestinal carcinoma, GI carcinoma, pancreas tumor, pancreatic tumor, malignancy, exocrine, endocrine, pancreatic adenocarcinoma, chronic pancreatitis from alcohol

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Contributor Information and Disclosures

Author

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.

Coauthor(s)

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.

Medical Editor

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.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Benjamin Movsas, MD, Vice-Chairman, Department of Radiation Oncology, Fox Chase Cancer Center
Benjamin Movsas, MD is a member of the following medical societies: American College of Radiology, American Radium Society, and American Society for Therapeutic Radiology and Oncology
Disclosure: Nothing to disclose.

CME Editor

Rajalaxmi McKenna, MD, FACP, Consulting Staff, Department of Medicine, Southwest Medical Consultants, SC, Good Samaritan Hospital, Advocate Health Systems
Rajalaxmi McKenna, MD, FACP is a member of the following medical societies: American Society of Clinical Oncology, American Society of Hematology, and International Society on Thrombosis and Haemostasis
Disclosure: Nothing to disclose.

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 at Tucson; 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; Amplimed Consulting fee Consulting

 
 
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