RETARDATION OF METASTATIC TUMOR-GROWTH AFTER IMMUNIZATION WITH METASTASIS-SPECIFIC MONOCLONAL-ANTIBODIES

被引：82

作者：

REBER, S

MATZKU, S

GUNTHERT, U

PONTA, H

HERRLICH, P

ZOLLER, M

机构：

[1] GERMAN CANC RES CTR,INST RADIOL & PATHOPHYSIOL,NEUENHEIMER FELD 280,W-6900 HEIDELBERG 1,GERMANY

[2] UNIV KARLSRUHE,INST GENET,W-7500 KARLSRUHE,GERMANY

[3] KERNFORSCHUNGSZENTRUM KARLSRUHE GMBH,INST GENET & TOXICOL,W-7500 KARLSRUHE 1,GERMANY

来源：

INTERNATIONAL JOURNAL OF CANCER | 1990年 / 46卷 / 05期

关键词：

D O I：

10.1002/ijc.2910460528

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

The influence of 4 murine monoclonal antibodies (MAbs) directed against surface determinants of a metastasizing rat adenocarcinoma (BSp73ASML) on metastatic spread was evaluated and compared to their in vivo binding as well as to the induction of a humoral anti‐MAb response, especially with respect to the development of anti‐idiotypic (ID) antibodies of the internal image type. In a protocol of explicit immunization, all 4 MAbs transiently inhibited metastatic growth. Survival was prolonged only with one MAb (4.4ASML). With another MAb (1.1ASML), directed against a new variant form of CD44, metastatic growth was accelerated after transient retardation. Retardation of metastatic growth correlated with the humoral anti‐MAb response. This accounted for the isotype‐ as well as for the idiotype‐specific response. An exception was noted after immunization with MAb 1.1ASML. Rats with high levels of anti‐1.1ASML antibodies, which inhibited binding to the tumor cells (internal image‐type antibodies) showed accelerated metastatic spread. Data are interpreted to mean that MAb‐induced inhibition of metastatic spread may be based on 2 independent mechanisms: blockade of metastasis‐associated epitopes (i. e., with MAb 1.1ASML) and induction of an anti‐mouse lg response. In the latter case it was irrelevant whether the response was isotype‐ or idiotype‐specific. Copyright © 1990 Wiley‐Liss, Inc., A Wiley Company

引用

页码：919 / 927

页数：9

共 65 条

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