Host Resistance and Survival in Carcinoma of Breast: A Study of 104 Cases of Medullary Carcinoma in a Series of 1,411 Cases of Breast Cancer Followed for 20 years

Abstract

This paper deals with a special type of mammary carcinoma, generally of high-grade malignancy, which carries a remarkably good prognosis—the so-called “medullary carcinoma of the breast with lymphoid infiltrate.” Probably the increased lymphoid tissue seen in these tumours is concerned with cell-mediated and humoral immunological reactions and reflects a strong host-defence mechanism which is responsible for the remarkably high survival rates following radical treatment. Since the evidence for host resistance to malignant disease is based largely on animal data, the opportunity to study a group of patients followed for 20 years, in whom this type of defence reaction appears to exist, is of considerable clinical interest. Among 1,411 cases of breast cancer there were 104 with medullary carcinoma (7·4%), for which the corrected 5- to 20-year survival rates have been calculated. After 20 years 74% of cases with operable medullary tumours were alive, compared with 14% of cases with similar stage non-medullary cancer. In the presence of histologically proved axillary metastases the 20-year survival rate was 61% for medullary cases, compared with only 13% for other types of breast cancer. In 30 cases of medullary cancer in which the axilla was free, the corrected 20-year survival rate was 95% following a combination of radical operation and radiotherapy. No evidence could be found that axillary dissection or postoperative irradiation is harmful to women with operable highly malignant breast cancer in whom a well-marked host resistance is thought to be present. A combination of radical mastectomy and postoperative irradiation appears to be the most effective treatment for such cases. The present grounds for rejecting a radical approach to treatment of breast cancer, based on current immunological considerations, are regarded as being quite inadequate.