In　1979,　the　mechanism　of　chemical　carcinogenesis,　a　challenging　and　difficult　scientific　problem　pending　for　a　number　of　years,　was　explained　by　Dai　Qianhuan.　The　mechanism　named　di-region　theory　predicted　that　a　carcinogen　always　metabolizes　to　form　a　special　bi-functional　alkylating　agent.　This　agent　induces　cross-linkages　between　the　complementary　base　pairs　in　DNA　and　switches　on　initial　mutageneses　in　genomes　including　point　and　frameshift　mutations.　This,　in　turn,　induces　further　deep　mutageneses　including　the　production　of　various　chimeric　chromosomes,　deletions　and　other　aberrations　found　in　genomes.　In　the　end　this　initiates　carcinogenesis　of　the　whole　cell　through　the　reverse　transcription　mechanism　after　a　lengthy　incubation　period.　Recently,　this　laboratory　has　verified　that　physical　carcinogenesis,　including　the　oncogenesis　induced　by　radiation　and　asbestos　as　well　as　the　carcinogenesis　induced　by　endogenous　factors　such　as　estrogen　or　diethylstilbestrol　switch　on　carcinogenesis　by　inducing　the　formation　of　cross-linkages　between　the　complementary　base　pairs　in　DNA.　Di-region　theory　has　now　been　supported　by　many　experimental　observations　such　as　mutational　spectra　of　various　carcinogens.　The　potential　for　carcinogenesis,　teratogenesis,　sterility　and　mutagenesis　lumped　together　as　genetic　toxicity　appears　to　originate　almost　uniformly　from　the　cross-linking　between　complementary　bases,　i.e.　malignant　cross-linking,　which　is　in　accordance　with　di-region　theory.　Other　forms　of　cross-linking　between　non-complementary　bases,　benign　cross-linkings,　show　bi-functional　alkylation　anticancer　activity　but　lack　genetic　toxicity.　The　predictable　design　and　synthesis　of　a　high　selectivity　anticancer　agent　with　high　efficacy　and　low　genetic　toxicity,　a　goal　long　pursued　in　cancer　chemotherapy,　have　been　realized　for　the　first　time　in　this　laboratory　by　inhibiting　malignant　and　heightening　benign　cross-linking　using　the　principles　of　di-region　theory.　A　series　of　patented　new　anticancer　platinum　complexes　called　di-regioplatins,　based　on　the　above　predetermined　design,　have　been　reported.　In　these　cancer　cell　kill　rates,　tumor-inhibition　rates　and　the　ultimate　life-span　for　two　mouse　carcinoma　models　using　several　compounds　of　cis-di-substituted-benzylaminodihaloplatinum　(II)　are　notably　higher　than　those　of　cisplatin,　but　their　toxicities　all　are　much　lower　than　cisplatin.　Based　on　a　predictive　design　using　di-region　theory　and　group　theory,　a　new　anticancer　complex,　cis-diammine-cyclopentane-1,1-dicarboxylato-platinum　(II)　called　minoplatin,　has　been　synthesized　in　this　laboratory　by　making　the　minimal　structural　revision　of　adding　an　CH2　unit　on　the　four-member　ring　of　carboplatin.　The　water　solubility　of　minoplatin　is　almost　double　that　of　carboplatin,　yet　its　lipid　solubility　is　much　higher　than　carboplatin.　Animal　acute　toxicity　of　minoplatin　is　only　half　that　of　carboplatin,　and　the　curative　effect　of　minoplatin　in　a　rapid　growing　animal　tumor　model　of　the　ascites-type　is　remarkably　higher　than　that　of　carboplatin.　Genetic　toxicity　of　minoplatin　as　measured　by　reverse　mutagenesis　with　the　TA　102　strain　is　only　1/200　of　cisplatin　and　1/10　of　carboplatin.　Minoplatin,　as　opposed　to　cisplatin,　shows　no　teratogenesis　to　the　offspring　of　pregnant　female　mice.　Additionally,　some　recent　empirical　research　results　on　anticancer　platinum　complexes　have　been　explained　by　the　di-region　theory,　and　comments　from　the　perspective　of　predicting　the　selectivity　of　anticancer　agents　have　been　presented.　We　anticipate　that　future　clinical　testing　will　demonstrate　that　minoplatin　and　di-regioplatins　are　the　first　examples　in　a　class　consisting　of　highly　selective,　low　toxicity,　and　tailored　second　generation　anticancer　agents.