Post-transplant malignant lymphoma with monoclonal immunoglobulin gene rearrangement and polyclonal Epstein-Barr virus episomes.
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This report describes the case of an 8 year old boy who developed ileocecal B cell lymphoma after liver transplantation. The patient underwent orthotopic liver transplantation for biliary atresia and had been given immunosuppressive drugs--cyclosporin A and tacrolimus hydrate. Six years after the liver transplantation, the patient had a sudden onset of fever and abdominal pain. Necropsy revealed an ileocecal mass that was a B cell lymphoma. Epstein-Barr virus (EBV) encoded RNA 1 was demonstrated in lymphoma cells and hyperplastic follicular germinal centre cells in various tissues. Although monoclonal immunoglobulin gene rearrangement was detected in the liver, EBV episomes were of polyclonal origin and lytic forms of EBV were also demonstrated by Southern blotting. Immunohistochemically, lymphoma cells were positive for p53 but negative for latent membrane protein 1 and EBV nuclear antigen 2. These findings suggested that this B cell lymphoma might have occurred sporadically, regardless of EBV infection. (+info)
Circulating insulin-like growth factor-I levels regulate colon cancer growth and metastasis.
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It has been shown previously that slight elevations in serum levels of insulin-like growth factor-I (IGF-I) are correlated with an increased risk for developing prostate, breast, colon, and lung cancer. The aim of this study was to determine the role of serum IGF-I levels in the process of stimulating tumor growth and metastasis in a mouse model of colon cancer. Colon 38 adenocarcinoma tissue fragments were orthotopically transplanted by attachment to the surface of the cecum in control and liver-specific IGF-I-deficient (LID) mice in which serum IGF-I levels are 25% of that in control mice. A total of 156 male mice at 5 weeks of age (74 control mice and 82 LID mice) received tumor transplants. Mice were divided randomly into two groups; one group was injected i.p. with recombinant human IGF-I (2 mg/kg) twice daily for 6 weeks, and the other group received saline injections. IGF-I treatment increased the serum levels of IGF-I and IGFBP-3 in both control and LID mice. In the saline-injected group, the incidence of tumor growth on the cecum as well as the frequency of hepatic metastasis was significantly higher in control mice as compared with LID mice. Both control and LID mice treated with recombinant human IGF-I displayed significantly increased rates of tumor development on the cecum and metastasis to the liver, as compared with saline-injected mice. The number of metastatic nodules in the liver was significantly higher in control mice as compared with LID mice. The expression of vascular epithelial growth factor (VEGF) as well as vessel abundance in the cecum tumors was dependent on the levels of serum IGF-I. This study supports the hypothesis that circulating IGF-I levels play an important role in tumor development and metastasis. (+info)
Comments on the epidemiology of large bowel cancer.
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Available evidence strongly suggests that there are at least two epidemiological subentities of large bowel cancer. Tumors of the intermediate portions display a socioeconomic gradient not observed for cancer of the cecum or lower rectum. Dietary factors are the most plausible etiological candidates. High-fat intake may be a prominent factor, but other dietary constituents could be relevant and may be studied in populations in which stomach and large bowel cancer are infrequent. The eqidemiological usefulness of precursor lesions is emphasized. (+info)
Longitudinal variation in O(6)-alkylguanine DNA-alkyltransferase activity in the human colon and rectum.
(12/130)
In a systematic study of O(6)-alkylguanine DNA-alkyltransferase activity in the human colon and rectum, tumours were found to occur in regions of low activity. These results are consistent with the hypothesis that O(6)-alkylguanine DNA-alkyltransferase levels and alkylating agent exposure may be important determinants of large bowel tumorigenesis. (+info)
Colonic carcinoma with granulomatous (sarcoid) reaction.
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A 74 year old man had a right hemicolectomy for a caecal adenocarcinoma. Microscopic examination also revealed non-caseating epithelioid granulomatas within the adjacent stroma and some of these granulomata contained centrally located malignant cells. Granulomatous inflammation was not present within the lymph nodes and the importance of this rare occurrence is discussed. (+info)
Appendicitis caused by caecal carcinoma: report of a case.
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Appendicitis can rarely occur in association with carcinoma of the caecum, particularly in elderly patients. We report a case of acute appendicitis provoked by an adenocarcinoma of the caecum which obstructs the lumen of the appendix in a 58-year-old man. The patient underwent an ileocaecal resection with lymph node dissection. The difficulties of identifying a small tumor at laparotomy and the implication for optimal treatment are emphasized. (+info)
Colliding / concomitant tumors of the intestine: report of 3 cases.
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Collision/concomitant tumors of the intestine involving lymphomas are very rare. For these cases molecular genetic analyses are valuable diagnostic adjuncts. We report one collision tumor of the rectum (adenocarcinoma and peripheral T-cell lymphoma, unspecified), and two cases of concomitant tumors (carcinoma in the cecum and lymphoma in the ileum; carcinoma in the sigmoid and lymphoma in the ileum). The collision tumor (poorly differentiated adenocarcinoma and a peripheral T-cell lymphoma, unspecified) showed a variable proportion of the anaplastic tumor cells expressing lymphatic markers as well as cytokeratin. Only polymerase chain reaction (PCR) analysis revealing T-cell monoclonality of the anaplastic part of the colliding tumor allowed the correct diagnosis. In the second case, a moderately differentiated adenocarcinoma in the cecum with a concomitant B-cell Non-Hodgkin lymphoma in the ileum, PCR analysis was non contributory. In the third case (adenocarcinoma in the sigmoid colon and a follicular center lymphoma in the ileum) PCR analysis revealed gene rearrangement of the immunoglobulin heavy chain gene. We would like to emphasize that collision and concomitant tumors of the gut are rare and that molecular genetic analysis may be mandatory for correct diagnosis. It is our impression, that these tumors may be diagnosed more often in the intestinal tract if molecular genetic analysis and immunohistochemistry are used routinely, at least for all anaplastic tumors. (+info)
In vivo imaging of cellular proliferation in colorectal cancer using positron emission tomography.
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BACKGROUND: and aims: Positron emission tomography (PET) using (18)F labelled 2-fluoro-2-deoxy-D-glucose ((18)FDG) is an established imaging tool, although the recent development of a biologically stable thymidine analogue [18F] 3'-deoxy-3-fluorothymidine ((18)FLT) has allowed PET to image cellular proliferation by utilising the salvage pathway of DNA synthesis. In this study, we have compared uptake of (18)FLT and (18)FDG with MIB-1 immunohistochemistry to evaluate the role of PET in quantifying in vivo cellular proliferation in colorectal cancer (CRC). PATIENTS AND METHODS: Patients with resectable, primary, or recurrent CRC were prospectively studied. Thirteen lesions from 10 patients (five males, five females), median age 68 years (range 54-87), were evaluated. Patients underwent (18)FDG and (18)FLT PET scanning. Tracer uptake within lesions was quantified using standardised uptake values (SUVs). Histopathological examination and MIB-1 immunohistochemistry were performed on all lesions, and proliferation quantified by calculating a labelling index (% of MIB-1 positively stained nuclei within 1500 tumour cells). RESULTS: Histology confirmed adenocarcinoma in 12 of 13 lesions; the remaining lesion was reactive. All eight extrahepatic lesions were visualised using both (18)FLT and (18)FDG. Three of the five resected liver metastases were also avid for (18)FLT and showed high proliferation, while the remaining two lesions which demonstrated no uptake of (18)FLT had correspondingly very low proliferation. There was a statistically significant positive correlation (r =0.8, p<0.01) between SUVs of the tumours visualised with (18)FLT and the corresponding MIB-1 labelling indices. No such correlation was demonstrated with (18)FDG avid lesions (r =0.4). CONCLUSIONS: (18)FLT PET correlates with cellular proliferation markers in both primary and metastatic CRC. This technique could provide a mechanism for in vivo grading of malignancy and early prediction of response to adjuvant chemotherapy. (+info)