Hull C C, Galloway P, Gordon N, Gerson S L, Hawkins N, Stellato T A
Department of Surgery, Case Western Reserve University School of Medicine, Cleveland, OH.
Arch Surg. 1988 Apr;123(4):462-4. doi: 10.1001/archsurg.1988.01400280072012.
The influence of a functional spleen on induction and growth of cancer is unknown. Both beneficial and detrimental results have been observed in tumor-bearing hosts following splenectomy. We examined the effect of splenectomy, splenic autotransplantation, and splenic preservation on the induction and growth of 1,2-dimethylhydrazine (DMH)-induced murine colon cancer. Following splenectomy there was a significant increase in malignant tumors but no increase in benign tumors. To rule out the possibility that splenectomy increased the carcinogenicity of DMH by decreasing the capacity for DNA repair in colon cells, the units of 06-alkylguanine DNA alkyltransferase were measured in tumor-free and malignant colon tissue from both splenectomized and control rats. This repair protein was chosen because it is known to protect cells from the mutagenic effects of methylating agents. There was no significant difference in the alkyltransferase activity of tumor-free colon vs malignant tumor or between treatment regimens. Thus, the ability of the spleen to protect rats from the induction of malignant colon tumors induced by DMH is most likely due to preservation of immunologic surveillance in the host.
功能性脾脏对癌症诱导和生长的影响尚不清楚。在荷瘤宿主中,脾切除术后观察到了有益和有害的结果。我们研究了脾切除术、自体脾移植和脾保留对1,2-二甲基肼(DMH)诱导的小鼠结肠癌的诱导和生长的影响。脾切除术后,恶性肿瘤显著增加,但良性肿瘤没有增加。为了排除脾切除术通过降低结肠细胞DNA修复能力而增加DMH致癌性的可能性,我们在脾切除大鼠和对照大鼠的无肿瘤和恶性结肠组织中测量了06-烷基鸟嘌呤DNA烷基转移酶的单位。选择这种修复蛋白是因为已知它能保护细胞免受甲基化剂的诱变作用。无肿瘤结肠与恶性肿瘤之间或治疗方案之间的烷基转移酶活性没有显著差异。因此,脾脏保护大鼠免受DMH诱导的恶性结肠肿瘤的能力很可能是由于宿主免疫监视的保留。