Seemayer T A, Lagacé R, Schürch W, Tremblay G
Am J Surg Pathol. 1979 Dec;3(6):525-33. doi: 10.1097/00000478-197912000-00005.
After observing the presence of numerous stromal myofibroblasts in scirrhous mammary carcinomas, a series of invasive and metastatic carcinomas from diverse sites was examined by electron microscopy to determine whether myofibroblasts might also be present in their stroma. Myofibroblasts were identified in each instance and were most abundant in neoplasms which were hard, sclerotic, and retracted. This finding suggests that myofibroblasts represent a component of the stromal reaction to many carcinomas and contribute to the desmoplasia and retraction which characterize many of these neoplasms. The host commands several responses to neoplasia. As a result of the expression of tumor-associated antigens, the immune system contributes lymphocytes, macrophages, and antibodies, a reflection of immunologic surveillance against neoplasia. In contrast to experimental systems tumor neoantigens are poorly expressed or even lacking in many human neoplasms; thus, the immune system may be weakly stimulated or not activated at all. Tumor neovascularization induced by a tumor-angiogenesis factor represents a second host response, possibly deleterious, for it may facilitate tumor dissemination. The stromal myofibroblast reaction to many invasive and metastatic carcinomas may constitute a third, albeit more primitive response. The density of collagen produced and contractile state of such tissue may signify an attempt by the host stroma to contain the neoplasm and impede vascular invasion. If so, myofibroblast induction may complement immune surveillance or constitute a separate mechanism of response to invasive neoplasia in man.
在观察到硬癌性乳腺癌中存在大量基质肌成纤维细胞后，对一系列来自不同部位的浸润性和转移性癌进行了电子显微镜检查，以确定基质中是否也存在肌成纤维细胞。在每个病例中都鉴定出了肌成纤维细胞，并且在坚硬、硬化和回缩的肿瘤中最为丰富。这一发现表明，肌成纤维细胞是许多癌基质反应的一个组成部分，并且促成了许多此类肿瘤所特有的结缔组织增生和回缩。宿主对肿瘤会产生多种反应。由于肿瘤相关抗原的表达，免疫系统会贡献淋巴细胞、巨噬细胞和抗体，这是针对肿瘤的免疫监视的一种体现。与实验系统不同，肿瘤新抗原在许多人类肿瘤中表达不佳甚至缺乏；因此，免疫系统可能受到微弱刺激或根本未被激活。由肿瘤血管生成因子诱导的肿瘤新生血管形成是宿主的第二种反应，可能是有害的，因为它可能促进肿瘤扩散。基质肌成纤维细胞对许多浸润性和转移性癌的反应可能构成第三种反应，尽管更为原始。这种组织产生的胶原蛋白密度和收缩状态可能表明宿主基质试图限制肿瘤并阻止血管侵袭。如果是这样，肌成纤维细胞诱导可能补充免疫监视，或构成人类对浸润性肿瘤的一种单独反应机制。
