Pendergrast W J, Futrell J W
Ann Surg. 1979 Feb;189(2):181-8. doi: 10.1097/00000658-197902000-00009.
The morphologic characteristics of a scar may render it an "immunologically privileged site" providing fertile ground for tumor occurrence and growth. We sought to extend this concept and to determine the effect of different stages of wound healing on tumor occurrence. Syngeneic strain-2 guinea pigs and a methylcholanthrene-induced liposarcoma (MCA-2) were used. Incisional flank wounds were created at appropriate intervals such that at the time of tumor inoculation each group of animals had a sequentially aged wound which was a) acute, b) three weeks old, c) nine weeks old, d) 11 weeks old, e) created one week after tumor injection, or f) no wound. Wounds which were three, nine, or 11 weeks old consistently caused a significant increase in tumor growth rate following inoculation of a single cell tumor suspension (<.001). The delayed wounds, or those created following after tumor injection, and the acute wounds did not promote increased tumor growth. This study demonstrates that the ability of a wound to amplify or retard tumor growth may vary with its age. As a postulate we suggest that the relative paucity of lymphatic regeneration within scar tissue may render it an "immunologically privileged site" such that early recognition and destruction of tumor cells within the scar may be delayed long enough for the tumor to grow to a "critical size." Subsequent to this regardless of the host's immunocompetence the tumor can no longer be destroyed by an immune mechanism. The general lack of progressive growth of tumor cells placed in acute wounds suggests that they were not protected from immunocompetent cells and were destroyed by the ongoing inflammatory response to injury. Therefore, different biologic characteristics of a surgical scar are important in potentiating or retarding tumor growth. Variations in such factors may account for the local recurrence of cancer in operative wounds.
瘢痕的形态学特征可能使其成为一个“免疫特惠部位”，为肿瘤的发生和生长提供了有利条件。我们试图扩展这一概念，并确定伤口愈合的不同阶段对肿瘤发生的影响。使用了同基因2系豚鼠和甲基胆蒽诱导的脂肪肉瘤（MCA - 2）。在适当的间隔时间在侧腹制造切口伤口，以便在接种肿瘤时，每组动物都有一个依次处于不同老化阶段的伤口，即：a）急性伤口，b）三周龄伤口，c）九周龄伤口，d）十一周龄伤口，e）在肿瘤注射后一周制造的伤口，或f）无伤口。接种单细胞肿瘤悬液后，三周龄、九周龄或十一周龄的伤口始终会导致肿瘤生长速率显著增加（<.001）。延迟伤口，即肿瘤注射后制造的伤口，以及急性伤口并未促进肿瘤生长增加。这项研究表明，伤口放大或延缓肿瘤生长的能力可能随其年龄而变化。作为一种假设，我们认为瘢痕组织内淋巴再生相对不足可能使其成为一个“免疫特惠部位”，这样瘢痕内肿瘤细胞的早期识别和破坏可能会延迟到足够长的时间，使肿瘤生长到“临界大小”。在此之后，无论宿主的免疫能力如何，肿瘤都不能再被免疫机制破坏。置于急性伤口中的肿瘤细胞普遍缺乏渐进性生长，这表明它们没有受到免疫活性细胞的保护，并被对损伤的持续炎症反应所破坏。因此，手术瘢痕的不同生物学特征在促进或延缓肿瘤生长方面很重要。这些因素的变化可能解释了手术伤口中癌症的局部复发。
