Morphologic Progression of Pedunculated Submucosal Invasive Colon Cancer

To clarify the morphologic progression ofpedunculated submucosal invasive colon cancers, weassessed the morphologic changes in 50 such cancersaccording to the volume of cancer in the submucosallayer. The shape of the head of the polyp was definedat the widest slice as round, concave, or semicircularwith a horizontal head (SHH). As the cancer invaded thesubmucosa, the peduncle of the submucosal invasive cancer thickened and the structure of the headprogressively collapsed, causing its shape to changefrom round to concave to SHH. The proliferating cellnuclear antigen (PCNA) expression (labeling index, LI), determined at the deepest point ofsubmucosal invasion, showed a significant correlationwith the morphologic progression among round, concave,and SHH cancers as 36.4 ± 12.1%, 42.3 ±11.8%, and 62.1 ± 12.5%, respectively (P <0.05). Results indicate that the PCNA-LI may be a usefulmarker for the morphologic progression of pedunculatedsubmucosal invasive colon cancers.     

Submucosal Colonic Edema—Urticaria of the Colon

Radiographically, colonic urticaria presents a non-specific pattern of submucosal edema. Previously unreported diverticulitis with colonic distention resulting in the flat, polygonal, mosaic pattern typical of this entity is described.     

Ameboma Mimicking Submucosal Tumor of the Colon in an Elderly

Ameboma is a rare presentation of intestinal amebiasis, which is caused by infection with Entamoeba histolytica. Amebomas are generally concentric and can be difficult to differentiate from carcinoma in the gastrointestinal tract, which are commonly seen in elderly patients. Radiological studies or colonoscopy can be difficult to provide the diagnosis. We present an elderly man with an ameboma in the ascending colon, which manifested as a submucosal tumor in the radiological or endoscopic studies. His serum antiamebic serology test was positive. He received surgery because of poor response to medical treatment. A full course of antiamebic therapy followed by a luminal agent were given and he had a smooth postoperative course without relapse of amebic infection. Although the elderly population has a higher incidence of colonic malignancy, ameboma should be considered in the differential diagnosis of submucosal tumors in the colon, especially in patients with an insidious onset of disease.     

Gastrin and Colon Cancer

The classical peptide hormone gastrin was identified originally as a stimulant of gastric acid secretion, but is now known to also act as a growth factor for the gastrointestinal mucosa. In an earlier review the existing evidence that gastrin and related peptides act as growth factors for the normal colonic mucosa and for colorectal carcinomas was summarised. In this review I will highlight some recent developments in the field.     

Obesity Potentiates AOM-Induced Colon Cancer

Obesity and diet affect the incidence and severity of various types of cancer, including colon cancer. It is not known whether obesity, independent of diet, is a risk factor for colon adenocarcinoma. We used azoxymethane (AOM) to induce colon cancer in mature genetically obese male Zucker rats (fa/fa) on low-fat crude diet (LFC, 10% fat) and their lean counterparts (Fa/fa and Fa/fa) on high-fat crude diet (HFC, 40% fat) for three months. At death visible tumors, histopathology, and colonic aberrant crypt (AC) formation were studied by blinded investigators. At death the obese animals were heavier (719 ± 19 g; mean ± sem) than lean animals regardless of diet or genotype (Fa/fa-LFC:451 ± 6 g; Fa/fa-HFC:441 ± 10 g; Fa/Fa-HFC:412 ± 9 g; P < 0.001 vs fa/fa by ANOVA). All AOM-treated rats developed AC, compared to none of the saline-injected controls. Macroscopic adenocarcinoma developed in 8/9 obese rats on LFC (P < 0.001), compared to none in lean rats regardless of diet. Obese rats had significantly more AC (876 ± 116) than any of the lean rats (Fa/fa-LFC:550 ± 99; Fa/fa-HFC:325 ± 37; Fa/Fa-HFC:360 ± 36; P < 0.05 vs fa/fa). We conclude that obesity more than exposure to high-fat diet was associated with colon carcinogenesis in these rats.