第二次看到这个理论，不由自主相信了，也许验证了生命的产生和群体扩张的一系列过程。
染色体畸变，产生不同于人类的基因组，具有自我复制能力，自我繁殖，属于新的生命。
寄生于人体，吸取人体，有自我觅食的能力。
癌细胞群体在扩张的时候满足孟德尔群体遗传的模型，
逼迫自己不得不重新审视这个神奇的家伙!
如果是新生的生命力强的物种也许会带来治疗思想上的变革。
任何一种生命力强的东西，想使其灭绝，困难实在太大，
带来直接的后果是绝地反弹，和系统的崩溃。
也许像拦洪大堤一样，不能堵死，总要留一个缺口。
总要给他人留条生路。
Is carcinogenesis a form. of speciation?
Since cancers have individual clonal karyotypes, are immortal
and evolve from normal cells treated by carcinogens only after exceedingly long
latencies of many months to decades—we deduce that carcinogenesis may be a form.
of speciation. This theory proposes that carcinogens initiate carcinogenesis by
causing aneuploidy, i.e., losses or gains of chromosomes. Aneuploidy
destabilizes the karyotype, because it unbalances thousands of collaborating
genes including those that synthesize, segregate and repair chromosomes. Driven
by this inherent instability aneuploid cells evolve ever-more random karyotypes
automatically. Most of these perish, but a very small minority acquires
reproductive autonomy—the primary characteristic of cancer cells and species.
Selection for autonomy stabilizes new cancer species against the inherent
instability of aneuploidy within specific margins of variation. The speciation
theory explains five common characteristics of cancers: (1) species-specific
autonomy; (2) karyotypic and phenotypic individuality; (3) flexibility by
karyotypic variations within stable margins of autonomy; (4) immortality by
replacing defective karyotypes from constitutive pools of competent variants or
subspecies generated by this flexibility; and (5) long neoplastic latencies by
the low probability that random karyotypic alterations generate new autonomous
species. Moreover, the theory explains phylogenetic relations between cancers of
the same tissue, because carcinogenesis is restricted by tissue-specific
transcriptomes. The theory also solves paradoxes of other cancer theories. For
example, “aneuploidy” of cancers is now said to be a “paradox” or “cancer’s
fatal flaw,” because aneuploidy impairs normal growth and development. But if
the “aneuploidies” of cancers are in effect the karyotypes of new species, this
paradox is solved.