Intraperitoneal cancer dissemination: Mechanisms of the patterns of spread

被引:160
作者
C. Pablo Carmignani
Tessa A. Sugarbaker
Christina M. Bromley
Paul H. Sugarbaker
机构
[1] Surgical Oncology, Washington Cancer Institute, Washington, DC
[2] Marin County General Hospital, Marin County, CA
[3] Biostat Solutions Inc., Damascus, MD 20872
关键词
Appendix cancer; Mucinous carcinoma; Ovarian cancer; Peritoneal carcinomatosis; Sarcoma;
D O I
10.1023/A:1023791229361
中图分类号
学科分类号
摘要
Background: Well known patterns govern the distribution of hematogenous and lymphatic metastasis of cancer. In the past the distribution of cancer cells free within abdominal cavity received little attention and was thought to be a random event. However, surgical observation led the authors to generate and test hypotheses regarding patterns of spread that vary with tumor type, with the intraperitoneal environment, and with the physiology of the peritoneal surface tissues. Methods: The distribution and volume of peritoneal surface malignancy was prospectively recorded in 129 patients with 5 different types of tumors at the time of cytoreductive surgery. The malignancies studied included pseudomyxoma peritonei (PMP) of appendiceal origin, colonic mucinous adenocarcinoma (MA), non-mucinous colonic adenocarcinoma (NMA), ovarian carcinoma (OV) and sarcoma (SA). The abdominal and pelvic cavity was divided into 3 horizontal sectors, 9 regions and 25 sites. The incidences of tumor implants in these designated areas were statistically analyzed for each tumor type and comparisons between tumor types studied. Results: The magnitude of intraperitoneal cancer dissemination was similar for mucinous tumors, including PMP and MA and significantly higher than for non-mucinous tumors. Also the mucinous cancers were more likely to be present in the upper horizontal sector than were non-mucinous. When NMA was compared to PMP and MA the epigastric region was significantly less likely to contain tumor. For all cancer diagnoses the colon, greater omentum and cul-de-sac of Douglas were most often affected. The ileocecal valve region was more likely to have large tumor masses on its surface than small bowel surface or small bowel mesentery. Conclusions: Peritoneal carcinomatosis had a wider distribution when mucinous fluid was present; this cancer distribution by intraperitoneal fluid hydrodynamics occurred regardless of histologic aggressiveness. The organs that have peritoneal fluid resorption (omentum and omental appendages) have a high incidence of implants. Small bowel and its mesentery free to move by peristalsis had a reduced incidence of implants as compared to the ileocecal area, which is fixed to the retroperitoneum. These observations may facilitate efforts to treat peritoneal surface malignancy.
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页码:465 / 472
页数:7
相关论文
共 12 条
[1]  
Cole W., The mechanisms of spread of cancer, Surgery, Gynecology & Obstetrics, 137, pp. 853-871, (1973)
[2]  
Viadana E., Bross I.D., Pickren J.W., The metastatic spread of cancers of the digestive system in man, Oncology, 35, pp. 114-126, (1978)
[3]  
Sugarbaker P.H., Observations concerning cancer spread within the peritoneal cavity and concepts supporting an ordered pathophysiology, Peritoneal Carcinomatosis: Principles of Management, pp. 80-99, (1995)
[4]  
Fortner J.G., Inadvertent spread of cancer at surgery, J Surg Oncol, 53, pp. 191-196, (1993)
[5]  
Solomon M.J., Egan M., Roberts R.A., Philips J., Russell P., Incidence of free colorectal cancer cells on the peritoneal surface, Dis Colon Rectum, 40, pp. 1294-1298, (1997)
[6]  
Manual for Staging of Cancer. Fourth Ed., (1992)
[7]  
Jacquet P., Sugarbaker P.H., Current methodologies for clinical assessment of patients with peritoneal carcinomatosis, J Exp Clin Cancer Res, 15, pp. 49-58, (1996)
[8]  
Weyn B., Jacob W., Da Silva V.D., Montironi R., Hamilton P.W., Thompson D., Bartels H.G., Van Daele A., Dillon K., Data representation and reduction for chromatin texture in nuclei from premalignant prostatic, esophageal, and colonic lesions, Cytometry, 41, pp. 133-138, (2000)
[9]  
Autio V., The spread of intraperitoneal infection, Acta Chirurgica Scandinavica, S, 321, pp. 5-31, (1964)
[10]  
Lopes Cardozo A.M., Gupta A., Koppe M.J., Meijer S., Van Leeuwen P.A., Beelen R.J., Bleichrodt R.P., Metastatic pattern of CC531 colon carcinoma cells in the abdominal cavity: An experimental model of peritoneal carcinomatosis in rats, Eur J Surg Oncol, 27, pp. 359-363, (2001)