Effects From Specific References

References

-Diplochromosome tetraploidy occurrence:

[4] [5] [6] [7] [12] [13] [14] [15] [26] [33] [52] [69] [71]

-4n-skewed division-system (4n-SDS) and 90˚ nuclear turn:

[6] [7] [10] [12] [13] [14] [21] [30]

-Accepted provisions for cancer beginning from normal human cells:

[2] [3] [16]

-Cancer hallmark: gain of fitness, not in MT, but positive in 4n-SDS

[9] [22] [24] [28] [35] [36] [37] [45] [46] [51]

-Origin of genetics for fitness-gain, the ontogeny of 4n-SDS

[1] [4] [5] [6] [100]

-4n-SDS and fragile site (dark DNAs) deletion-repair = genome instability

[1] [27] [28] [43] [70] [71] [72] [79] [80] [81] [89] [90] [100]

-Consequences from the above in cancers:

-Gross chromosomal: aberrations, B-F-B cycles, HSRs or DMs

[74] [75] [76] [83] - [88]

-Molecular: mutations of high frequency mutated genes (p53, Rb)

[1] [91] [93] [94] & herein

-Molecular special: copy number variance/alterations (CNVs/CNAs)

[77] [78] [79] [80] [81] [93] [94]

-Why special? Oncogene CNVs (HSRs) with assumed gain in gene activity from hundreds or more gene amplified is an explanation for their drug resistant therapy

[47] [48] [84] [87] [96]

-WRONG! Drosophila cytogenetics of salivary polytene chromosomes, demonstrate inactivation of gene-function when duplicated (see text books citing BAR phenotype)

[11] [82]

-In new therapy program, gene inactivation from PE [11] must also be considered, herein suggested to inactivate the high frequency mutations, because of their close location to satellite DNAs, which are forms of heterochromatin, the culprit in PE (see conclusion).

Hematological cancers, dependent on genomic damage in normal cells:

[58] [59] [60] [61]

Location of nuclear domains relative to each other; special significance:

[62] [63] [64]

Presence of diplochromosomal tetraploidy (4n-SDS) in leukemia:

[69]

which replaces leukemogenesis with molecular mutations

4n-SDS to same type molecular lesions and resultant mutations:

[68] [96] [98]

New discoveries: bone marrow density increase (?) and laminar protein anomalies:

[58] [59]

Same therapy questions (above), except for leukemic haploidization:

[22] [23] [24] [43] [44] [103]