Anastasis, a new mechanism driving cell survival and evolution

描述(由申请者提供)：我们最近发现了一种新的生物现象，我们称之为Anastsis(希腊语，“复活”的意思)。推翻了目前认为细胞死亡是不可逆转的教条，我们发现各种正常和癌细胞类型都可以逆转这一过程，存活和增殖。这种可逆性甚至发生在细胞经历了被广泛认为是不归路的事件之后，包括caspase酶的激活和广泛的DNA损伤。值得注意的是，虽然大多数细胞完全恢复和修复其受损的DNA，但一些细胞保留了突变，这增加了致癌转化的频率。阿纳斯塔西的发现至少有五个范式转换的含义。第一, 我们认为ANASTASIS代表了一种以前未知的癌症原因，因此抑制ANASTASIS应该可以预防癌症。ANASTASIS也可以为长期观察到的反复损伤会增加癌症发病率提供解释。其次，我们认为转移可以使肿瘤细胞逃脱化疗并产生耐药性。因此，抑制复发可能会增强化疗和放射治疗的有效性，并防止复发。第三，通过Anastasis挽救濒临死亡的细胞可能会限制由于短暂的环境压力或毒素暴露而造成的永久性组织损伤。因此，加强转移可能会促进组织再生。第四，我们假设再生是一种细胞生存机制，保护难以替代的细胞，如成年大脑或心肌细胞中的神经元，因此促进再生可以预防或减缓退行性疾病。第五，我们认为，通过Anastsis获得突变的生殖细胞的存活提供了一种机制，当动物暴露在应激环境条件下时，它恰恰提供了一种增强遗传多样性的机制。这可能会加速适应进化过程中不断变化的环境。在这里，我们建议对这些想法进行测试。我们设计了一种生物传感器

DESCRIPTION (provided by applicant): We recently discovered a new biological phenomenon, which we call anastasis (Greek for "rising to life"). Overturning the current dogma that cell death is irreversible, we found that a variety of normal and cancer cell types can reverse the process, survive, and proliferate. This reversibility takes place even after cells experience events widely believed to be points of no return, including activation of caspase enzymes and widespread DNA damage. Notably, while most cells fully recover and repair their damaged DNA, some cells retain mutations, and this increases the frequency of oncogenic transformation. The discovery of anastasis has at least five paradigm-shifting implications. First, we suggest that anastasis represents a previously unknown cause of cancer, so inhibiting anastasis should prevent cancer. Anastasis could also offer an explanation for the longstanding observation that repeated injury increases the incidence of cancer. Second, we propose that anastasis allows tumor cells to escape chemotherapy and evolve drug resistance. Therefore, inhibiting anastasis may enhance the effectiveness of chemo- and radiation therapies and prevent relapses. Third, salvaging cells on the brink of death via anastasis may limit permanent tissue injury due to transient environmental stresses or toxin exposures. Consequently, enhancing anastasis may promote tissue regeneration. Fourth, we posit that anastasis is a cell survival mechanism that protects cells that are difficult to replace such as neurons in the adult brain or heart muscle cells, so promoting anastasis could prevent or slow degenerative diseases. Fifth, we propose that the survival of germ cells with mutations acquired through anastasis provides a mechanism to enhance genetic diversity precisely when animals are exposed to stressful environmental conditions. This could accelerate adaptation to changing environments during evolution. Here we propose to test these ideas. We designed a biosen