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Cancer of the Pancreas

Author: Ed Friedlander, M.D., Posted on Thursday, February 10 @ 10:38:49 IST by RxPG  

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CANCER OF THE PANCREAS ("cank of the pank", "the dismal disease", etc.; Lancet 363:1049, 2004)

Virtually all cancers of the pancreas are adenocarcinomas arising from the ducts.

Like adenocarcinomas anywhere else, you can spot them because they make little glands and/or are secretory- product (i.e., mucin)-positive.

Risk factors include (1) smoking (3x the normal risk), (2) exposure to chemicals (the disease is supposedly more common among both chemists and garage workers), and (3) hereditary pancreatitis (huge risk).

"Big Robbins" links it to the notable carcinogens naphthylamine and benzidine, and the hoopla over nitrosamines in food was related to their link to cancer of the pancreas in experimental animals.

This dread cancer accounts for about 5% of U.S. cancer deaths; the incidence has tripled in the past 50 years "because of smoking and chemicals" (I wonder).

* Famous victims in recent memory include Billy Carter, Jack Benny, Dizzy Gillespie, Rex Harrison, and Michael Landon.

* Truly hardcore future pathologists will want to read about MUC4 as a stainable marker for pancreatic neoplasia, especially as it grows nastier: Am. J. Clin. Path. 117: 791, 2002.

Future pathologists and surgeons: Cancer of the pancreas and chronic pancreatitis are hard to tell apart. A certain percentage of false-positive diagnoses of cancer of the pancreas, and a certain number of Whipple procedures for those without cancer of the pancreas, is acceptable: Br. J. Surg. 81: 585, 1994.

Future pathologists only: The in-situ evolution of pancreatic cancer has been well-studied. See Arch. Path. Lab. Med. 118: 227, 1994.

* For some reason, it is not uncommon to see real osteoclasts and even osseous metaplasia here (J. Clin. Path. 47: 372, 1994; Arch. Path. Lab. Med. 120: 306, 1996); these are still carcinomas.

Risk factors include (1) smoking (3x the normal risk), (2) exposure to chemicals (the disease is supposedly more common among both chemists and garage workers), and (3) hereditary pancreatitis (huge risk).

"Big Robbins" links it to the notable carcinogens naphthylamine and benzidine, and the hoopla over nitrosamines in food was related to their link to cancer of the pancreas in experimental animals.

* Questionable risk factors include alcohol consumption, high-fat diet ("cholecystokinin must be a promoter"; tough to believe if you think pancreatic acinar cells don't ordinarily divide), coffee drinking, obesity, and pernicious anemia. All of these are now pretty much discredited (see for example Cancer 67: 2664, 1991; the coffee crock discredited Cancer Epidem. 10: 429, 2001, several others uniformly negative).

Some cases seem to run in families, with no obvious pattern (Am. J. Gastroent. 85: 54, 1990). Blacks are at slightly greater risk.

Whatever the environmental "cause", most (or maybe all) cancers of the exocrine pancreas have mutated k-ras at hot-spot codon 12. This can be detected on fine-needle aspirate material, and by PCR in pancreatic fluid (Cancer 73: 1589, 1994; Am. J. Path. 144: 889, 1994) or stool (ooh, Cancer Res. 54: 3568, 1994) or smears (Am. J. Clin. Path. 105: 257 & 321, 1996). Smoking seems to cause this mutation (Cancer 85: 326, 1999).

There are presently seven familial pancreatic-cancer syndromes; however, the molecular biology remains elusive (Med. Clin. N.A. 84: 7409, 2000). Hereditary pancreatitis in particular gives at least a 40% risk of getting pancreatic cancer (Med. Clin. N.A. 84: 719, 2000).

* Stay tuned for more about the molecular genetics of pancreatic cancer. The animal model has mutant gastrin-cholecystokinin receptors (no surprise: Am. J. Surg. 167: 120, 1994), and cholecystokinin analog stimulates the growth of human pancreatic cancer cells (Dig. Dis. Sci. 39: 1007, 1994).

The distribution of cancers in "Big Robbins" is reasonable:
60% head
15% body
5% tail
20% too late to tell

Patients come in with back pain (why?), jaundice, weight loss, GI upsets, depression (very typical, and poorly understood), and/or migratory thrombophlebitis ("Trousseau's other sign"; the mechanism of the distinctive paraneoplastic problem is unknown).

The size of the cancer depends on the stage at which it is detected. Those in the head may be found early because they produce jaundice. Those in the body and tail will be detected late.

* Cytologic examination of the pancreatic juice is an excellent way to tell benign from malignant pancreatic tumors: Am. J. Clin. Path. 100: 497, 1993; Cancer 74: 826, 1994. Cancer cells in the peritoneal cavity in these patients is the kiss of death: Arch. Surg. 129: 639, 1994. Cytology on pancreatic cyst fluid: Am. J. Clin. Path. 101: 483, 1994.

There's a serum tumor marker, CA-19-9 (Gut 35: 707, 994, many others). * Another, for cyst fluid: CA-72-4 (Ann. Surg. 219: 131, 1994).

Future surgeons: Courvoisier's law states that a distended gall bladder in a patient with obstructive jaundice means cancer (pancreas, common bile duct). Obstruction due to a gallstone in the common bile duct will not result in a distended gallbladder, because the gallbladder would be heavily scarred-up from years of cholelithiasis. This works most of the time, though you would never rely on it.

Gung-ho surgeons may try to resect a tumor in the head of the pancreas ("Whipple procedure"; * for the pylorus-sparing technique see J. Am. Col. Surg. 178: 443, 1994; for the Hopkins study, which hails 11 cures out of 201 surgeries as an enormous improvement, see Ann. Surg. 221: 721, 1995. Desperate diseases require desperate remedies).

The overall 5-year survival rate in cancer of the pancreas is about 1%; typical survival is about six months (Gut 31: 494, 1990; J. Am. Col. Surg. 179: 38, 1994).

These patients often have diabetes, and the cause is insulin resistance. This now appears to be due to massive production of amylin (IAPP, see below) by the tumor (NEJM 330: 313, 1994; Gastroenterology 114: 130, 1998). This probably explains the well-known "link" between pancreatic cancer and diabetes, and it now appears that only new-onset (i.e., less than three years) diabetes is a "risk factor" (NEJM 331: 81, 1994).

* A recent British euthanasia case involved intractable pain from cancer of the pancreas: Lancet 335: 719, 1990 ("not guilty"; in my opinion this is a triumph of humanity and common sense; you may disagree).

Adenocarcinoma of the pancreas typically metastasizes to lymphatics, and blood-borne metastases to the liver are typically massive.

* Acinar carcinoma of the pancreas is a rare PAS-positive tumor, usually of younger people. It presents stippled cells which stain for amylase, lipase, and chymotrypsin, and often elaborates lipase into the blood (which may produce subcutaneous fat necrosis!) Molecular genetics: Am. J. Path. 160: 953, 2002.
Author: Ed Friedlander, M.D., Pathologist, Pathguy.com

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