Pancreatic cancer: Epidemiology

Gender and age

The US National Center for Health Statistics estimates the number of new cases of PC in 2020 will be 30,400 in men and 27,200 in women, accounting for 3% of all cancers in the US. The US population risk for PC is 14.0 per 100,000 for men and 10.7 per 100,000 for women. Women in high development index countries have 5 times greater risk of PC than women in lower development index countries. A systematic review of 15 studies found no reproductive factors associated with the risk of developing PC in women.

In the US, the peak incidence of PDAC occurs in the seventh and eighth decades of life. ^, The main risk factor for PC is advancing age. Between 2007 and 2011, the median age at diagnosis for cancer of the pancreas was 71 years, and the median age at death was 73 years according to Surveillance, Epidemiology, and End Results (SEER) data. More than 60% of new PDAC cases occur between the ages of 65 and 84 years. The peak age of incidence varies between countries; for example, in India, the peak age is the sixth decade. An emerging age-specific trend has been identified in individuals 20 to 29 years old and in those persons over the age of 80 years in the US.

Race and ethnicity

The incidence of PDAC remains highest for black Americans, with rates of 17.2 per 100,000 in men and 14.2 per 100,000 in women. The lowest risk of pancreatic cancer is among Asian/Pacific Islander men and women (10.7 and 8.9 per 100,000, respectively). African Americans have the highest death rates from cancer and the shortest survival period of all racial groups. ^, African American males specifically have higher incidence rates for all cancers combined and also for the most common cancers (prostate, lung, colorectal, and pancreas). Death rates, per 100,000 population, from PDAC are 15.5 for African American men and 12.6 for African American women, compared with 12.4 for white men and 9.3 for white women. African Americans of lower socioeconomic status are more likely to be diagnosed with advanced stage pancreatic cancer and are less likely to undergo surgery or to receive chemotherapy. Other known risk factors for PDAC (such as obesity, diabetes, and pancreatitis) are more common in African Americans.

It has been reported that, among smokers, serum cotinine levels, the primary metabolite of nicotine, are consistently higher in African Americans than in Whites and Mexican Americans, even after adjustment for the number of cigarettes smoked per day, the number of smokers in the home, the number of hours of environmental tobacco smoke (ETS) exposure at work, the number of rooms in the home, and the region of the country where the subject lived. This suggests that genetic differences in cigarette product metabolism may influence rates of PDAC.

Familial pancreatic cancer and inherited genetic disorders (see Chapter 9D )

PC is generally considered to be familial if two or more first-degree relatives (mother, father, sister, brother) have a confirmed diagnosis of pancreatic cancer. A more stringent definition used at some institutions requires three first-degree relatives to have PC to be considered familial cases. A family history is found in about 5% to 10% of PC cases. Just having a family history of PC confers a 9-fold greater risk for PC than not having a family history.

Findings from the 2017 Australian Pancreatic Cancer Genome Initiative found that 10% to 20% of PCs likely have an inherited component. This is a higher percentage than previously estimated and relates to deleterious mutations in BRCA1, BRCA2, MLH1, ATM, PALB2 , and CDK2NA, as well as mismatch repair gene mutations found in families with Lynch syndrome (see Chapter 9D ). Germline mutations have also been detected in 7% of patients unselected for a family history of PDAC. In the classic prospective studies of family members of PC kindreds from the National Familial Pancreas Tumor Registry at Johns Hopkins Hospital, a 2-fold increased risk of PC was found in the first-degree relatives of persons with sporadic PC and a 9-fold increased risk in first-degree relatives of those with familial PC. ^, Germline mutations of BRCA2 are found in 6% to 19% of familial pancreatic cancer patients. When a more stringent definition of familial PC is used, a 57-fold increased risk of PC was reported in kindreds with three or more family members affected with PC. This corresponds to a notably high incidence rate of 301 cases per 100,000 per year, compared with the SEER age-adjusted rate for the entire US population of only 8.8 cases per 100,000 per year. A recent report identified a germline truncating mutation of the PALB2 gene in 3% of familial pancreatic cancer patients. ^, Despite these many advances in the understanding of the mutations involved in the pathogenesis of PC, no single “pancreatic cancer gene” has been identified.

Two recent studies have documented an increased risk of PC in persons with A, B, and AB blood types. ^, This risk has been attributed to an ABO single nucleotide polymorphism, rs505922. Overall, 56% of the population has a non-O blood group and the proportion of PDAC because of non-O blood group is 13% to 19%.

Six genetic syndromes associated with pancreatic ductal adenocarcinoma (see Chapter 9D )

Six genetic familial syndromes and their respective predisposing genes have been identified and linked to the development of PC; these are described briefly later ( Table 61.3 ). Although individuals with these syndromes have an increased risk of developing PC, collectively these syndromes account for less than 5% of the familial aggregation of PC. The mean age of onset of familial PC is similar to that of nonfamilial cases: 65.8 years versus 65.2 years. Familial cases have also been noted to have a somewhat increased incidence of secondary primary cancers (23.8%) when compared with their nonfamilial counterparts (18.9%).