Meng Xiaolong, Riordan Neil H
Bio-Communications Research Institute, 3100 N. Hillside, Wichita, KS 67219, USA.
Med Hypotheses. 2006;66(3):486-90. doi: 10.1016/j.mehy.2005.09.041. Epub 2005 Nov 15.
When a wound occurs, growth and repair genes (GR genes, such as oncogenes, proto-oncogenes, etc.) in surrounding cells are activated and secretion of growth and repair factors (GR factors, such as growth, stem cell, and stimulating factors, etc.) is induced to heal the wound. However, if the wound is persistent due to chronic physical (radiation, electromagnetic field, trauma, particles, etc.), chemical (carcinogens, toxic chemicals, heavy metals etc.) or biological (aging, free radicals, inflammation, nutrient deficiency, bacteria and virus infections, stress, etc.) damage, amplification of GR gene activation in surrounding cells may lead to a clinical cancer. Based on the commonalities between cancer and wound healing, a new hypothesis of cancer is presented: malignancies are not passive mutated useless masses; rather, they are functional tissues produced by GR gene activation to secrete GR factors in an effort to heal persistent wounds in the body. Based on the hypothesis, current cancer treatments aimed at killing cancer cells only may be misguided. The logical extension of the hypothesis is that cancer treatment focused on wound healing by limiting causes of persistent wounds, providing repair cells, GR factors, and substrates required by repair cells may yield more fruitful results than treatments focused on killing cancer cells alone. Spontaneous regressions of cancer, although rare, may be successful examples of serendipitous spontaneous wound healing. Standard therapies aimed at killing cancer cells, should be limited to adjuvant status for limiting symptoms or buying time for completion of the wound healing process. Attempts to destroy cancer cells without healing underlying persistent wounds will allow for eventual recurrence.
当伤口出现时，周围细胞中的生长和修复基因（GR基因，如癌基因、原癌基因等）被激活，并诱导生长和修复因子（GR因子，如生长因子、干细胞因子和刺激因子等）的分泌以愈合伤口。然而，如果由于慢性物理（辐射、电磁场、创伤、颗粒等）、化学（致癌物、有毒化学物质、重金属等）或生物（衰老、自由基、炎症、营养缺乏、细菌和病毒感染、压力等）损伤导致伤口持续存在，周围细胞中GR基因激活的放大可能会导致临床癌症。基于癌症与伤口愈合之间的共性，提出了一种新的癌症假说：恶性肿瘤并非被动突变的无用肿块；相反，它们是由GR基因激活产生的功能性组织，通过分泌GR因子来努力愈合身体中持续存在的伤口。基于这一假说，目前仅旨在杀死癌细胞的癌症治疗方法可能是错误的。该假说的合理延伸是，通过限制持续性伤口的病因、提供修复细胞、GR因子以及修复细胞所需的底物来专注于伤口愈合的癌症治疗可能比仅专注于杀死癌细胞的治疗产生更丰硕的成果。癌症的自发消退虽然罕见，但可能是意外自发伤口愈合的成功例子。旨在杀死癌细胞的标准疗法应限于辅助地位，以限制症状或为完成伤口愈合过程争取时间。在未愈合潜在持续性伤口的情况下试图摧毁癌细胞将导致最终复发。
