Abstract:SummaryTwenty-five patients with advanced metastatic breast cancer were treated with the combination of methotrexate 60 mg/M2 and 5-fluorouracil 700 mg/M2 intravenously on the first and eighth days, and cyclophosphamide 100 mg/M2 and prednisone 40 mg/M2 by mouth daily for the first 14 days of a 28-day cycle. The patients had had no previous chemotherapy or extensive radiotherapy and all but two had not responded to hormonal therapy or endocrine ablation. The major metastatic lesions were: lung (12 patients), l… Show more
“…The median duration of objective remissions in our study was 9.5 (range 5-21) months and com pares well with that given for palliative CMF chemotherapy in general [9][10][11][12], There were no statistically significant differ ences in remission rates in different catagories of patients according to the predominant localisa tion of disease, ER-status and menopausal status. However, the subgroups of patients were small.…”
Section: Discussionmentioning
confidence: 57%
“…Remission rates for CMF in chemotherapy naive patients are reported as 45-53% in litera ture data between 1976 and 1991, covering our w observation time [9][10][11][12].…”
“…The median duration of objective remissions in our study was 9.5 (range 5-21) months and com pares well with that given for palliative CMF chemotherapy in general [9][10][11][12], There were no statistically significant differ ences in remission rates in different catagories of patients according to the predominant localisa tion of disease, ER-status and menopausal status. However, the subgroups of patients were small.…”
Section: Discussionmentioning
confidence: 57%
“…Remission rates for CMF in chemotherapy naive patients are reported as 45-53% in litera ture data between 1976 and 1991, covering our w observation time [9][10][11][12].…”
“…К со-жалению, подобные эффекты почти всегда носили неполный и непродолжительный характер [7,8]. Пер-вые послевоенные десятилетия были отмечены разра-боткой нескольких цитостатических препаратов, показавших многообещающие результаты при лечении РМЖ; опять же, в подавляющем большинстве случаев выраженность ответа опухоли на лечение была уме-ренной, при этом комбинирование нескольких цито-статиков зачастую приводило к значительному увели-чению эффектов [9]. Неудивительно, что сразу после появления лекарственных способов эндокринной абляции опухоли, в частности тамоксифена [10], поя-вились ожидания, что сочетанное назначение антаго-ниста ER и химиопрепаратов приведет к многократ-ному усилению противоопухолевого воздействия.…”
Section: истина рождается как ересь а умирает как предрассудок г гunclassified
“…Schabel, 1975) that the whole tumour burden, including micrometastases, is reduced progressively by chemotherapy according to first-order kinetics, describes well the responses of some transplanted tumours, and has provided a satisfactory explanation for the treatment protocols which have proved so successful in the cure of a substantial proportion of children with acute lymphoblastic leukaemia (ALL) who require long periods of maintenance treatment after complete remission has been achieved. (Lister et al, 1981 (Canellos et al, 1974). These findings suggest that clinically evident disease can respond better to antiproliferative chemotherapy than residual disease.…”
A serious limitation of chemotherapy for acute myeloid leukaemia (AML), Hodgkins disease and some classes of breast cancer is that, even when clinically evident disease responds well, the same chemotherapy when given during remission does not affect the rate of relapse after chemotherapeutic or surgical ablation of the primary disease. This cannot, in general, be caused by genetic adaptation of the residual cancer cells which renders them resistant to specific drugs, because after relapse further remissions can be obtained with the same drugs that were ineffective by chronic administration in prolonging remission. The resistance of the residual cells may arise from mechanisms such as inaccessibility for anatomical or other reasons, or because of a change in metabolic state which causes these cells temporarily to cease division, when they cannot be harmed by cycle-dependent drugs and repair damage sustained from cycle-independent drugs. Limited differentiation has been shown capable of reversal and this may be a mechanism which leads to quiescence and associated “resistance”, particularly in the case of AML. Where such resistance occurs treatment during remission—or as an adjuvant to surgery and radiotherapy—may have to rely on mechanisms which are independent of cellular proliferation such as processes associated with graft-versus-host-disease or the induction of terminal differentiation. A model for studying the nature of resistance of residual cancer and for testing treatments that might be active against cancer cells in this state may be dormant metastases. The latter are malignant cells which appear to be in peaceful co-existence with their host and which in experimental systems have been induced to grow into lethal metastases by perturbation of the host by surgical trauma, by hormonal manipulation or by immunosuppression.
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