LWBK1006-20 LWW-Govindan-Review December 12, 2011 19:4
Chapter 20•Cancer of the Gastrointestinal Tract 247ANSWERS
Answer 20.2.1. The answer is C.
Tobacco smoke exposure plays a significant role in the development of
pancreatic adenocarcinoma. It has been estimated that tobacco smok-
ing contributes to the development of 20% to 30% of pancreatic cancers.
The strongest associations between cigarette smoking and pancreatic can-
cer have been observed when the smoking occurred within the previous
10 years. Smoking cessation can reduce this risk. Environmental tobacco
smoke contains the same toxins, irritants, and carcinogens, such as car-
bon monoxide, nicotine, cyanide, ammonia, benzene, nitrosamines, vinyl
chloride, arsenic, and hydrocarbons, as primary cigarette smoke. Host
etiologic factors associated with an increased risk of pancreatic cancer
include a history of diabetes mellitus (DM), chronic cirrhosis, pancreati-
tis, a high-fat/cholesterol diet, and prior cholecystectomy. Although not
all studies have supported a relationship between DM and pancreatic can-
cer, a meta-analysis of 20 epidemiologic studies confirms that the pooled
relative risk of pancreatic cancer in persons with DM for 5 years is dou-
ble (relative risk, 2.0; 95% confidence interval [CI], 1.2 to 3.2) the risk
of persons without DM. However, there is no association with a high-
protein diet. People of African American descent experience a higher rate
of pancreatic cancer than those of European ancestry in the United States,
with an annual incidence of 16.7 per 100,000 versus 10.9 per 100,000,
respectively. Death from pancreatic cancer is similarly elevated, with an
annual rate of 14.6 per 100,000 versus 10.6 per 100,000. The diagnosis is
slightly but significantly earlier in African Americans compared with Cau-
casians, with a median age of diagnosis of 68 and 73 years, respectively.
In developed countries, the incidence and mortality rates range from 7 to
9 per 100,000 for men and 4.5 to 6 per 100,000 for women.Answer 20.2.2. The answer is A.
CA 19-9 is a clinically useful tumor marker. The epitope of this antibody
is a sialylated lacto-N-fucopentaose II related to the Lewis-a blood group
antigen. Limitations of CA 19-9 are that it is not specific for pancreatic
cancer and has been found to be elevated in other tumor types, such
as biliary tract, colon, and stomach cancers. Ten percent of patients are
Lewis antigen-a or b negative and unable to synthesize this antigen, and
therefore may have undetectable levels of CA 19-9, even in the setting of
advanced pancreatic cancer. Cholestasis can falsely elevate serum CA 19-
9 levels; therefore, in patients who present with obstructive jaundice, an
elevated CA 19-9 is not specific for the presence of pancreatic malignancy.
Despite these caveats, serum CA 19-9 levels seem to have prognostic util-
ity, particularly when measured either preoperatively or postoperatively
in patients with resectable pancreatic cancer. Pancreatic ductal adenocar-
cinoma arises from ductal epithelial cells. Neoplasia arising from these
cells progresses from initial PanINs to invasive carcinomas. The evidence
that these lesions are precancerous includes the observation that after