Lack of healing reaction in the cancer wound.

Surgical wounds in cancer patients have a relatively high dehiscence rate. Although cancer resections are performed so as to include macroscopically non-involved tissues, some cancer cells can be present in the line of transection or surrounding tissues (R1 and R2 resections). The local healing process may facilitate proliferation of these localized cancer cells, and the high cytokine concentration within the healing wound may also attract cancer cells from distant sites to migrate into the wound area. The question arises how the tumor environment influences the wound healing process. The aim of the study was to monitor and compare, using immunohistochemical methods, the healing process of an incision wound performed through a metastatic liver tumor of colon cancer with the healing of a normal liver incision wound. The experiments were carried out on a CC531 colon cancer rat model. We observed impaired healing of cancer wounds at all stages of wound healing. Significantly fewer mononuclear cells infiltrated the cancer than the normal liver wounds. There were no significant differences in the phenotypes of infiltrating mononuclear cells. BrdU incorporation showed rapid proliferation of cancer but not infiltrating cells or fibroblasts in the cancer wounds. We observed no connective tissue formation and poor collagen deposition in cancer wounds. Additionally, cancer wounds were significantly deprived of newly formed vessels. We confirmed that the impaired migration and proliferation of inflammatory cells in cancer wounds and poor scar tissue formation contribute to impaired healing of cancer 'contaminated' wounds.

[Usefulness of preoperative assay CEA and CA 19-9 in colorectal cancer patients]. / Przydatnosc przedoperacyjnego oznaczania antygenów CEA i CA19-9 u chorych na raka jelita grubego.

Carcinoembryonic antigen (CEA) and carbohydrate antigen (CA19-9) are well known tumor markers expressed by colorectal cancer (CRC), particularly in advanced cases. In this study serological expression of CEA and CA19-9 concerning different clinicopathological factors and sensitivity of diagnosis of CRC by combination of both markers were evaluated. Eighty one patients with diagnosed CRC were in this study included. According to Dukes' classification there were 11 in stage A, 34 in stage B, 17 in stage C and 19 in stage D. Blood samples were collected before operation. CEA and CA19-9 were determined by MEIA (normal range 0-3 ng/ml for CEA and 0-37 U/ml for CA19-9). The statistical analysis revealed that the CEA well correlated with histological type, liver metastasis and term of symptoms. The CA19-9 well correlated with liver metastasis, peritoneal dissemination, nodal involvement and cancer localization. The levels of CEA and CA19-9 increased with stage of the tumor, but only in stage D the difference was statistically significant (for CEA p = 0.005, for CA19-9 p = 0.039). At time of diagnosis 50.6% of the patients had elevated serum levels of CEA and 29.6% of CA19-9. In combination of both antigens this elevation was in 54.3% of CRC patients. The common use of CEA and CA19-9 was more efficacious in identification of patients at high risk. The combination assay of CEA and CA19-9 did not cause a significant increase of sensitivity in diagnosis CRC.

[Problems with therapy for renovascular hypertension in Takayasu's arteritis--on the basis of two cases]. / Problemy terapii nadcisnienia tetniczego naczyniowo-nerkowego w przebiegu choroby Takayasu--na kanwie dwóch przypadków.

Takayasu's arteritis is non-specific vasculitis, affecting aorta and its main branches. Renal involvement is usually manifested by renovascular hypertension followed by ischemic nephropathy. Early start of immunosuppressive treatment can substantially improve prognosis and delay progress of dangerous organic complications. On the basis of two cases of Takayasu's arteritis with renal involvement, we paid the attention to progressive nature of disease with renovascular hypertension, requiring corrective operation of renal arteries, despite intensive immunosuppressive treatment.

[Surgical treatment of mediastinal tumors from personal material]. / Chirurgiczne leczenie guzów sródpiersia w materiale wlasnym.

90 patients with mediastinal tumors treated surgically was analysed. It was find, that tumor mostly was localized in anterior superior mediastinum, had benign character and in over half of cases was derived from thymus. 75% of mediastinal tumors were primary. In over 50% patients longitudinal sternotomy was performed. Radical excision of the tumor was possible nearly in 90% cases.

Interleukin 6 (IL-6) levels in the monitoring of surgical trauma. A comparison of serum IL-6 concentrations in patients treated by cholecystectomy via laparotomy or laparoscopy.

Interleukin 6 (IL-6) is involved in the processes of inflammation and tissue repair. We have been looking for the correlation between IL-6 concentration in patient's serum and the other factors related to the gravity of surgical trauma. Out of 25 patients with acute cholecystitis, 11 were randomly selected for laparoscopic cholecystectomy and the other 14 for open (laparotomic) cholecystectomy. The diagnostic and prognostic factors, age, and duration of disease did not differ significantly in either group. IL-6 serum levels were monitored by using commercially available ELISA tests throughout 72 h following the surgery. In patients who underwent laparoscopy, average IL-6 serum levels were significantly (up to fourfold) lower than in their laparotomy-treated counterparts, and the monitoring of IL-6 serum levels seems to be useful in the evaluation of the extent of trauma caused by surgery.

Colony-stimulating factor 1-dependent resident macrophages play a regulatory role in fighting Escherichia coli fecal peritonitis.

Osteopetrotic op/op mice have less than 5% of the normal number of macrophages in the peritoneal cavity (W. Wiktor-Jedrzejczak, A. Ahmed, C. Szczylik, and R.R. Skelly, J. Exp. Med. 156:1516-1527, 1982). Fecal peritonitis was induced by intraperitoneal injection of 0.5 ml of 5% autoclaved feces in saline along with Escherichia coli grown from feces of mice of the same colony and added in doses ranging between 10 and 10(6) CFU. Such infection led to a septic shock and either was lethal within 24 h or became cured without additional treatment of the mice. The op/op mice survived administration of 30-times-smaller doses of bacteria compared with their normal littermates. Analysis of the kinetics of cellular changes in the peritoneal cavity associated with such infection revealed that this increased susceptibility of macrophage-deficient mice cannot be explained by a direct role of macrophages in combating the infection. Instead, it appeared that the increased susceptibility to fatal fecal peritonitis was most likely due to delayed and impaired recruitment of neutrophils to the site of infection in mutant mice. The increased susceptibility of the op/op mice to E. coli fecal peritonitis was not due to their possible increased sensitivity to endotoxin, since the mutant mice tolerated lipopolysaccharide doses more than twice those tolerated by control littermates. On the other hand, their susceptibility to exogenous tumor necrosis factor alpha and interleukin-1 alpha was increased. Both mutant op/op and control mice were able to survive secondary challenge with 10(6) E. coli (administered along with feces) lethal for both types of mice on primary challenge. These data suggest that colony-stimulating factor 1-dependent resident peritoneal macrophages play a role in controlling primary infection by recruiting neutrophils and are not required for efficient response to secondary infection.

Impaired tumor growth in colony-stimulating factor 1 (CSF-1)-deficient, macrophage-deficient op/op mouse: evidence for a role of CSF-1-dependent macrophages in formation of tumor stroma.

Macrophages have been suggested to play a major role in the immune response to cancer. They have also been suggested to stimulate the formation of tumor stroma and to promote tumor vascularization. The availability of the op/op mouse, which has no endogenous colony-stimulating factor 1 (CSF-1) and which possesses a profound macrophage deficiency, provides a new model to verify these notions. Subcutaneous growth of transplantable Lewis lung cancer (LLC) is markedly impaired in the op/op mice compared with normal littermates. Treatment of tumor-bearing op/op mice with human recombinant CSF-1 corrects this impairment. Histological analysis of tumors grown in op/op and normal mice revealed marked differences. Tumors grown in op/op mice display a decreased mitotic index and pronounced necrosis, particularly hemorrhagic. Moreover, particularly in the op/op tumors, peculiar sinusoid-like abortive vessels (not filled with blood) have been observed. These tumors, in contrast to tumors grown in normal mice, are almost deprived of regular arteries and veins. In contrast to tumors grown in normal mice, they exhibit almost no Sirius red-stained collagenous fibers and Gomori silver-stained reticular fibers. Our data suggest that the CSF-1-dependent macrophage subpopulation missing in op/op mice plays a primary role in supporting tumor stroma formation and tumor vascularization in murine LLC tumors.