Abstract
Permanent changes in the endocrine status of female SJL/J and CR mice were induced by masculinization, ablation of endocrine glands, inoculation of hormones, or feeding of the chemical carcinogen DMBA. All these procedures resulted in modification of the host hormonal milieu, as shown by blood hormone determination. Masculinization reduced drastically the onset of lymphosarcoma and increased the incidence of systemic neoplasms respectively in DMBA-treated female SJL/J and CR mice. Continued administration of gonadotrophins increased the incidence of systemic neoplasia in CR mice. A direct correlation is suggested between onset of lymphosarcoma or other tumours in mice and a specific shift to an abnormal hormonal environment.
Highlights
Summary.-Permanent changes in the endocrine status of female SJL/J and Charles River (CR) mice were induced by masculinization, ablation of endocrine glands, inoculation of hormones, or feeding of the chemical carcinogen DMBA
Specific endocrine disorders have recently been found in SJL/J mice (Pierpaoli et al, 1974), a strain developing a high incidence of spontaneous reticulum-cell neoplasms (Murphy, 1963), classified as Type B (RCN-B) by Dunn (1954)
The findings in this investigation do not supply a definitive proof that a well-defined, congenital or induced hormonal derangement is directly related to carcinogenesis (Pierpaoli et al, 1974). They suggest a prominent role for induced long-term endocrine imbalance in leukaemogenesis, and permit the identification of some of the hormones which are primarily involved and changed in response to DMBA
Summary
On the basis of the abnormal endocrine pattern present in SJL/J mice, it has been proposed that chronic congenital or induced endocrine derangements (Pierpaoli et al, 1974; Pierpaoli and HaranGhera, 1975) might be determinants in the emergence and proliferation of " dormant " pre-leukaemic cells and the type of systemic neoplasms that ensue. Such an association between endocrine derangements and leukaemogenesis had already been strengthened by recent data showing a striking decrease in the incidence of leukaemia in mice whose hypophyseal function had been inhibited or depressed by antiadenohypophysis (anti-AH) antibodies (Pierpaoli and Haran-Ghera, 1975). Permanent hormonal derangements have been induced in mice by various means, and the correlation between a particular abnormal hormonal status and onset of LS and RCN has been studied
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