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免疫能力处于不同状态的小鼠中致癌物诱导的皮肤肿瘤的发展

Development of carcinogen-induced skin tumors in mice with varied states of immune capacity.

作者信息

Outzen H C

出版信息

Int J Cancer. 1980 Jul 15;26(1):87-92. doi: 10.1002/ijc.2910260114.

DOI:10.1002/ijc.2910260114
PMID:7239715
Abstract

The incidence of tumor formation in MCA-treated skin grafted onto maximally immunosuppressed mice that had been restored to varying extents with normal spleen cells was significantly greater in the mice with intermediate immune capacities than in those that had either minimal or maximal capacities. A similar biphasic tumor incidence curve was observed when MCA-treated skin was grafted onto mice of varying immune capacities, produced by thymectomy and varying doses of whole-body irradiation. Significantly more tumors occurred in the mice given moderate doses of irradiation than in tohse given higher or lower doses. That both of these procedures were actually able to induce discrete levels of immunocompetence was demonstrated by measuring skin allograft rejection times. The immunomodulated mice were observed to have skin graft rejection times which strongly correlated with the number of immunologically competent spleen cells transferred into them. The outgrowth potential of syngeneic normal mammary epithelial cells grafted into cleared mammary fat pads was similar in both immunologically altered and normal control mice, showing that immunoaltered and normal control mice were equally able to support the growth of transplanted normal tissues. These results, which conform with the predictions of the immunostimulation hypothesis, suggest that the immune response is able to stimulate as well as inhibit oncogenesis.

摘要

将经甲基胆蒽(MCA)处理的皮肤移植到已用正常脾细胞不同程度恢复的最大程度免疫抑制小鼠身上,免疫能力处于中等水平的小鼠中肿瘤形成的发生率显著高于免疫能力最低或最高的小鼠。当将经MCA处理的皮肤移植到通过胸腺切除和不同剂量全身照射产生的具有不同免疫能力的小鼠身上时,观察到了类似的双相肿瘤发生率曲线。接受中等剂量照射的小鼠中出现的肿瘤明显多于接受高剂量或低剂量照射的小鼠。通过测量皮肤同种异体移植排斥时间证明,这两种方法实际上都能够诱导不同水平的免疫能力。观察到免疫调节小鼠的皮肤移植排斥时间与转移到它们体内的免疫活性脾细胞数量密切相关。将同基因正常乳腺上皮细胞移植到清除的乳腺脂肪垫中,在免疫改变的小鼠和正常对照小鼠中的生长潜力相似,这表明免疫改变的小鼠和正常对照小鼠同样能够支持移植的正常组织生长。这些结果与免疫刺激假说的预测相符,表明免疫反应既能刺激也能抑制肿瘤发生。

相似文献

1
Development of carcinogen-induced skin tumors in mice with varied states of immune capacity.免疫能力处于不同状态的小鼠中致癌物诱导的皮肤肿瘤的发展
Int J Cancer. 1980 Jul 15;26(1):87-92. doi: 10.1002/ijc.2910260114.
2
In vitro reactivity of splenic lymphocytes from normal and UV-irradiated mice against syngeneic UV-induced tumors.正常小鼠和紫外线照射小鼠的脾淋巴细胞对同基因紫外线诱导肿瘤的体外反应性。
J Immunol. 1977 Apr;118(4):1483-7.
3
Influence of immune status of host on immunogenicity of tumors induced with two doses of methylcholanthrene.宿主免疫状态对两剂量甲基胆蒽诱导肿瘤免疫原性的影响。
Cancer Immunol Immunother. 1982;13(3):194-7. doi: 10.1007/BF00205388.
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Evidence for immunological surveillance during skin carcinogenesis. Inflammatory foci in immunologically competent mice.皮肤癌发生过程中免疫监视的证据。免疫功能正常小鼠中的炎症病灶。
Isr J Med Sci. 1971 Jan;7(1):52-65.
5
Accelerated growth of syngeneic tumors in mice treated with methylcholanthrene.用甲基胆蒽处理的小鼠中同基因肿瘤的加速生长。
Int J Cancer. 1978 Apr 15;21(4):511-5. doi: 10.1002/ijc.2910210418.
6
[Methylcholanthrene sensitization in skin tumor induction].[甲基胆蒽致敏在皮肤肿瘤诱导中的作用]
Vopr Onkol. 1977;23(11):75-9.
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[Development of drug-induced tumors in mice depending on the activity of the immunocompetent systems of the body].[药物诱导小鼠肿瘤的发生与机体免疫活性系统的活性的关系]
Patol Fiziol Eksp Ter. 1978 Mar-Apr(2):26-9.
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Failure of long-term immunologic control of 3-methylcholanthrene-induced skin tumors in the autochthonous host.在同种宿主中,对3-甲基胆蒽诱导的皮肤肿瘤长期免疫控制失败。
J Reticuloendothel Soc. 1971 Jul;10(1):120-30.
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Evidence of the nonimmune regression of chemically induced papillomas in mouse skin.
J Natl Cancer Inst. 1971 Sep;47(3):653-65.
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Neonatal thymectomy and tumor induction with methylcholanthrene in mice.新生小鼠胸腺切除术及用甲基胆蒽诱导肿瘤
J Natl Cancer Inst. 1966 Mar;36(3):513-21.

引用本文的文献

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A new kink in an old theory of carcinogenesis.致癌作用旧理论中的一个新转折。
Theor Biol Med Model. 2013 Feb 18;10:12. doi: 10.1186/1742-4682-10-12.
2
The early antitumor immune response is necessary for tumor growth: Re-visiting Prehn's hypothesis in the human melanoma system.早期抗肿瘤免疫反应对肿瘤生长至关重要:在人类黑色素瘤系统中重新探讨普雷恩假说。
Oncoimmunology. 2012 Sep 1;1(6):930-934. doi: 10.4161/onci.21455.
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Does the immune reaction cause malignant transformation by disrupting cell-to-cell or cell-to-matrix communications?
免疫反应是否通过破坏细胞间或细胞与基质间的通讯而导致恶性转化?
Theor Biol Med Model. 2007 May 4;4:16. doi: 10.1186/1742-4682-4-16.
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An immune reaction may be necessary for cancer development.免疫反应可能是癌症发展所必需的。
Theor Biol Med Model. 2006 Feb 3;3:6. doi: 10.1186/1742-4682-3-6.
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On the nature of cancer and why anticancer vaccines don't work.论癌症的本质及抗癌疫苗为何无效。
Cancer Cell Int. 2005 Aug 1;5(1):25. doi: 10.1186/1475-2867-5-25.
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Revisiting immunosurveillance and immunostimulation: Implications for cancer immunotherapy.重新审视免疫监视与免疫刺激:对癌症免疫治疗的启示。
J Transl Med. 2005 Feb 8;3(1):8. doi: 10.1186/1479-5876-3-8.
7
Tumor immunogenicity: how far can it be pushed?肿瘤免疫原性:其可被提升到何种程度?
Proc Natl Acad Sci U S A. 1993 May 15;90(10):4332-3. doi: 10.1073/pnas.90.10.4332.
8
Pathology of aging female SENCAR mice used as controls in skin two-stage carcinogenesis studies.在皮肤两阶段致癌研究中用作对照的衰老雌性SENCAR小鼠的病理学
Environ Health Perspect. 1986 Sep;68:81-9. doi: 10.1289/ehp.866881.
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Immunotoxicology.免疫毒理学
Clin Exp Immunol. 1985 Aug;61(2):219-23.