Tumors of the Gastrointestinal tract
Programs Help Blacks Get Needed Colorectal Cancer Screening
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African-Americans are less likely than whites to be screened for colorectal cancer, and the disparity almost certainly contributes to higher mortality. A new review of studies identifies effective strategies for improving the situation, but suggests that work remains to be done.
“We have seen some success in interventions, and shown that it’s important to tailor approaches to African American individuals and to use multiple approaches, strategies, and communication media,” said review author Barbara Powe, Ph.D.
The studies’ lack of long term follow-up represents “a gap in research,” however. “We need to learn to design interventions to create patterns of screening that could enhance screening for other cancers as well,” said Powe, a registered nurse and director of Cancer Communication Science for the American Cancer Society.
Racial differences in cancer care still unexplained
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Even though black patients and white patients with rectal cancer are equally likely to consult with an oncologist, blacks are less likely to undergo additional treatment after surgery, according to research findings posted online by the Journal of the National Cancer Institute.
The lower rates of radiation and chemotherapy partially explain why long-term survival after rectal cancer surgery is up to 20 percent lower for black patients than for white patients. Dr. Arden M. Morris, at the University of Michigan in Ann Arbor, and her colleagues hypothesized that blacks may not be referred as often to medical and radiation oncologists.
Using information from a large national database, the researchers identified 2,716 patients 66 years of age or older who had undergone surgery for stage II or III rectal cancer.
Primary driver of stomach cancer development identified
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In a discovery that could lead to the development of new treatments for gastric cancer, scientists at the Melbourne Branch of the international Ludwig Institute for Cancer Research (LICR) have discovered what appears to be the primary driver of tumor development in the stomach. Results published today on-line in the Journal of Clinical Investigation show that inhibiting the signaling cascade initiated by the IL-11 protein prevented the development of inflammation, hyperplasia (an abnormal increase in the number of cells) and tumor formation in pre-clinical models of gastric cancer.
Gastric cancer is the second most common cause of cancer-related deaths around the world, and has been shown previously to be correlated with chronic inflammation. Persistent activation of the Stat3 protein, which is known to play roles in inflammation-associated carcinogenesis, is commonly found in gastric and many other types of cancer. Until now, however, the underlying cause of hyperactive Stat3 was unknown.
Birth control pills may lower colon cancer risk
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Women who have used birth control pills seem to have a slightly decreased risk of colon cancer as they age, a new study suggests.
Researchers found that among nearly 90,000 women ages 40 to 59, those who had ever used oral contraceptives were 17 percent less likely to develop colon cancer over the next 16 years.
The findings, which appear in the International Journal of Cancer, are in line with evidence suggesting that estrogen plays a role in colon cancer risk.
Pancreatic cancer
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Pancreatic cancer, primarily ductal adenocarcinoma, accounts for about 30,500 cases and 29,700 deaths in the US annually. Symptoms include weight loss, abdominal pain, and jaundice. Diagnosis is by CT. Treatment is surgical resection and adjuvant chemotherapy and radiation therapy. Prognosis is poor because disease is often advanced at the time of diagnosis.
Most pancreatic cancers are exocrine tumors that develop from ductal and acinar cells. Pancreatic endocrine tumors are discussed below.
Adenocarcinomas of the exocrine pancreas arise from duct cells 9 times more often than from acinar cells; 80% occur in the head of the gland. Adenocarcinomas appear at the mean age of 55 yr and occur 1.5 to 2 times more often in men. Prominent risk factors include smoking, a history of chronic pancreatitis, and possibly long-standing diabetes mellitus (primarily in women). Heredity plays some role. Alcohol and caffeine consumption do not appear to be risk factors.
Pancreatic Endocrine Tumors
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Pancreatic endocrine tumors arise from islet and gastrin-producing cells and often produce many hormones. They have two general presentations. Nonfunctioning tumors may cause obstructive symptoms of the biliary tract or duodenum, bleeding into the GI tract, or abdominal masses. Functioning tumors hypersecrete a particular hormone, causing various syndromes. These clinical syndromes can also occur in multiple endocrine neoplasia, in which tumors or hyperplasia affects two or more endocrine glands, usually the parathyroid, pituitary, thyroid, or adrenals.
Treatment for functioning and nonfunctioning tumors is surgical resection. If metastases preclude curative surgery, various antihormone treatments may be tried for functioning tumors. Because of tumor rarity, chemotherapy trials have not identified definitive treatment. However, streptozotocin has selective activity against pancreatic islet cells and is commonly used, either alone or in combination with 5-fluorouracil or doxorubicin. Some centers use chlorozotocin and interferon.
Insulinoma - Pancreatic cancers
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An insulinoma is a rare pancreatic β-cell tumor that hypersecretes insulin. The main symptom is fasting hypoglycemia. Diagnosis is by a 48- or 72-h fast with measurement of glucose and insulin levels, followed by endoscopic ultrasound. Treatment is surgery when possible. Drugs that block insulin secretion (eg, diazoxide, octreotide, Ca channel blockers, β-blockers, phenytoin) are used for patients not responding to surgery.
Of all insulinomas, 80% are single and may be curatively resected if identified. Only 10% of insulinomas are malignant. Insulinoma occurs in 1/250,000 at a median age of 50 yr, except in multiple endocrine neoplasia (MEN) type I (about 10% of insulinomas), when it occurs in the 20s. Insulinomas associated with MEN type I are more likely to be multiple.
Surreptitious administration of exogenous insulin can cause episodic hypoglycemia mimicking insulinoma.
Zollinger-Ellison Syndrom - Pancreatic cancers
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Zollinger-Ellison Syndrom -(Z-E Syndrome; Gastrinoma)
Zollinger-Ellison syndrome is caused by a gastrin-producing tumor usually located in the pancreas or the duodenal wall. Gastric acid hypersecretion and peptic ulceration result. Diagnosis is by measuring serum gastrin levels. Treatment is proton pump inhibitors and surgical removal.
Gastrinomas occur in the pancreas or duodenal wall 80 to 90% of the time. The remainder occur in the splenic hilum, mesentery, stomach, lymph node, or ovary. About 50% of patients have multiple tumors. Gastrinomas usually are small (< 1 cm in diameter) and grow slowly. About 50% are malignant. About 40 to 60% of patients with gastrinoma have multiple endocrine neoplasia.
Vipoma - Pancreatic cancers
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A vipoma is a non-β pancreatic islet cell tumor secreting vasoactive intestinal peptide (VIP), resulting in a syndrome of watery diarrhea, hypokalemia, and achlorhydria (WDHA syndrome). Diagnosis is by serum VIP levels, and tumor is localized with CT and endoscopic ultrasound. Treatment is surgical resection.
Of these tumors, 50 to 75% are malignant, and some may be quite large (7 cm) at diagnosis. In about 6%, vipoma occurs as part of multiple endocrine neoplasia.
Glucagonoma - Pancreatic cancers
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A glucagonoma is a pancreatic α-cell tumor that secretes glucagon, producing hyperglycemia and a characteristic skin rash. Diagnosis is by elevated glucagon levels and imaging studies. Tumor is localized with CT and endoscopic ultrasound. Treatment is surgical resection.
Glucagonomas are very rare but similar to other islet cell tumors in that the primary and metastatic lesions are slow-growing: 15-yr survival is common. Eighty percent of glucagonomas are malignant. The average age at symptom onset is 50 yr; 80% of patients are women. A few patients have multiple endocrine neoplasia type I.
Gastrointestinal stromal tumors
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Gastrointestinal stromal tumors (GIST) are tumors of the GI tract derived from mesenchymal precursor cells in the gut wall. They result from mutations of a growth factor receptor gene, C-KIT. Some are caused by previous radiation therapy to the abdomen for other tumors.
Tumors are slow growing, and malignant potential varies from minimal to significant. Most (60 to 70%) occur in the stomach, 20 to 25% in the small bowel, and a small number in the esophagus, colon, and rectum. Average age at presentation is 50 to 60.
Small-bowel tumors
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Small-bowel tumors account for 1 to 5% of GI tumors.
Benign tumors include leiomyomas, lipomas, neurofibromas, and fibromas. All may cause abdominal distention, pain, bleeding, diarrhea or, if obstruction develops, vomiting. Polyps are not as common as in the colon.
Polyps of the Colon and rectum
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An intestinal polyp is any mass of tissue that arises from the bowel wall and protrudes into the lumen. Most are asymptomatic except for minor bleeding, which is usually occult. The main concern is malignant transformation; most colon cancers arise in a previously benign adenomatous polyp. Diagnosis is by endoscopy. Treatment is endoscopic removal.
Polyps may be sessile or pedunculated and vary considerably in size. Incidence of polyps ranges from 7 to 50%; the higher figure includes very small polyps (usually hyperplastic polyps or adenomas) found at autopsy. Polyps, often multiple, occur most commonly in the rectum and sigmoid and decrease in frequency toward the cecum. Multiple polyps may represent familial adenomatous polyposis. About 25% of patients with cancer of the large bowel also have satellite adenomatous polyps.
Adenomatous (neoplastic) polyps are of greatest concern. Such lesions are classified histologically as tubular adenomas, tubulovillous adenomas (villoglandular polyps), or villous adenomas. The likelihood of malignancy in an adenomatous polyp at the time of discovery is related to size, histologic type, and degree of dysplasia; a 1.5-cm tubular adenoma has a 2% risk of containing a malignancy, vs. 35% risk in 3-cm villous adenomas.
Familial adenomatous polyposis
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Familial adenomatous polyposis is a hereditary disorder causing numerous colonic polyps and resulting in colon carcinoma by age 40. Patients are usually asymptomatic but may have heme-positive stool. Diagnosis is by colonoscopy and genetic testing. Treatment is colectomy.
Familial adenomatous polyposis (FAP) is an autosomal dominant disease in which ≥ 100 adenomatous polyps carpet the colon and rectum. The disorder occurs in 1 in 8,000 to 14,000 people. Polyps are present in 50% of patients by age 15, and 95% by 35. Malignancy develops before age 40 in nearly all untreated patients.
Patients also can develop various extracolonic manifestations (previously termed Gardner’s syndrome), both benign and malignant. Benign manifestations include desmoid tumors, osteomas of the skull or mandible, sebaceous cysts, and adenomas in other parts of the GI tract. Patients are at increased risk for malignancy in the duodenum (5 to 11%), pancreas (2%), thyroid (2%), brain (medulloblastoma in < 1%), and liver (hepatoblastoma in 0.7% of children < 5).
Stomach cancer
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Etiology of stomach cancer is multifactorial, but Helicobacter pylori plays a significant role. Symptoms include early satiety, obstruction, and bleeding but tend to occur late in the disease. Diagnosis is by endoscopy, followed by CT and endoscopic ultrasound for staging. Treatment is mainly surgery; chemotherapy may provide a temporary response. Long-term survival is poor except for those with local disease.
Stomach cancer accounts for about 21,000 cases and 12,000 deaths in the US annually. Gastric adenocarcinoma accounts for 95% of malignant tumors of the stomach; less common are localized gastric lymphomas and leiomyosarcomas. Stomach cancer is the 2nd most common cancer worldwide, but the incidence varies widely; it is extremely high in Japan, Chile, and Iceland. In the US, incidence has declined in recent decades to the 7th most common cause of death from cancer. In the US, it is most common in blacks, Hispanics, and American Indians. Its incidence increases with age; > 75% of patients are > 50 yr.
