PubMed · 196166
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B Bouvier. 1977-06-18. Problems in breast reconstruction.. https://doi.org/10.5694/j.1326-5377.1977.tb131258.x
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The purpose of this study was to determine the relationship between 2-[(11)C]thymidine positron emission tomography (PET) in vivo-derived parameters and the ex vivo Ki-67 index of proliferation in human tumors. The study comprised 17 treatment-naïve patients with advanced intra-abdominal malignancies. Tumor thymidine kinetics were measured using 2-[(11)C]thymidine PET. Tissue data were analyzed to give the standardized uptake value, the area under the time activity curve, and the fractional retention of thymidine (FRT) obtained by kinetic modeling. For the latter, the contribution of labeled metabolites was accounted for by measuring thymidine metabolites in arterial plasma. To examine the influence of tumor blood flow on the thymidine PET data, a perfusion scan using inhaled [(15)O]CO(2) was carried out in a subset of 11 patients. Biopsies were stained with a MIB1 antibody to obtain a Ki-67 index, and correlations with the PET-derived parameters were investigated. There was no relationship between tumor blood flow and the thymidine PET data, showing that the retention of 2-[(11)C]thymidine in tumors was independent of tumor perfusion. There was no correlation between the Ki-67 index and either standard uptake value or area under the curve. There was a correlation between the Ki-67 index and FRT (r = 0.58; P = 0.01). The correlation between the Ki-67 index and FRT in this dataset was not influenced by the interval between biopsy and imaging (0.1-126 weeks), the origin of the biopsy for Ki-67 staining (primary tumor or metastasis), or whether the biopsy was from an imaged or a nonimaged tumor. This is the first report in human tumors showing that 2-[(11)C]thymidine PET-derived parameters correlate with the level of tumor proliferation measured using Ki-67 immunohistochemistry. The study shows that the in vivo measurement of 2-[(11)C]thymidine in tumors using PET can provide a surrogate marker of proliferation and supports the potential use of the technique in the early assessment of response to antiproliferative cancer treatment.
BACKGROUND: Case reports of patients developing tumor metastases at port sites following laparoscopic surgery have prompted the development of preventive strategies to address this potential problem, including local excision of the port sites. While it has been suggested that this strategy could be used clinically, its efficacy has not been established. METHODS: Twenty four immune-competent Dark Agouti rats underwent laparoscopy and standardized intraperitoneal laceration of an implanted abdominal flank tumor, using an established laparoscopic cancer model. Rats were randomized to either control (n = 12) or wound excision (n = 12) groups. Both groups underwent laparoscopy using carbon dioxide (CO2) insufflation and two mini-laparoscopy ports. In the wound excision group, one of the port site wounds was excised following desufflation of the abdominal cavity. One week later, the port site wounds were excised for histological examination. RESULTS: Wound involvement with tumor was significantly more common following wound excision than with untreated control wounds (nine of 12 vs two of 12, p = 0.002). In the wound excision group, tumor metastases arose preferentially in the excised port site wound. CONCLUSION: This study suggests that excision of laparoscopy port site wounds following laparoscopic surgery for cancer does not prevent the subsequent development of port site tumors. Furthermore, the excision of port sites may actually increase the risk of tumor metastases arising in port sites, suggesting that the clinical application of this strategy should be avoided pending further evaluation.
BACKGROUND: Radiation enteritis is one of the most feared complications of abdominal and pelvic radiation. Once its occurs, the process is relentless and may result in the patient's death. Available treatment is only supportive. Recent progress in molecular biology has shed some light on the pathogenesis of radiation enteritis and other diseases that are characterized by excessive fibrosis. New treatment modalities may be devised to improve the outcome of patients who are affected with this complication. METHODS: A literature search was used to identify the common denominator between many radiation-induced fibrotic conditions and other sclerotic diseases. Factors that affect the disease process and possible therapeutic interventions were evaluated. RESULTS: The hyperstimulation of transforming growth factor beta1 (TGF-beta1) leads to increased fibrosis and, ultimately, organ failure. Interferon gamma (IFN-gamma) inhibits the effects of TGF-beta1 in the nucleus. The fibrotic process may be reverted by IFN-gamma in various pathologic conditions. CONCLUSIONS: Radiation enteritis and other radiation-induced, long-term complications are characterized by excessive stimulation of TGF-beta1. Preliminary studies suggest that IFN-gamma may be effective in the treatment of patients with radiation-induced cutaneous fibrosis. IFN-gamma should be considered in Phase I-II studies to assess its toxicity and efficacy in the treatment of patients with radiation enteritis.