A cancer DNA phenotype in healthy prostates, conserved in tumors and adjacent normal cells, implies a relationship to carcinogenesis - PubMed (original) (raw)

A cancer DNA phenotype in healthy prostates, conserved in tumors and adjacent normal cells, implies a relationship to carcinogenesis

Donald C Malins et al. Proc Natl Acad Sci U S A. 2005.

Abstract

A cancer DNA phenotype, identical to the DNA structure of tumors, has been identified in the prostate glands of certain healthy men over 55 years of age. We now show that the same DNA signature exists in normal tissues adjacent to tumors. This finding implies that the phenotype is maintained in normal prostate cells from its inception through tumor development. The presence of the phenotype in tumors, adjacent normal cells, and in the normal prostate cells of certain older men suggests that it is a potentially critical factor in tumor development and may serve as an early biomarker for cancer risk assessment. Intervention to inhibit the development of the phenotype in healthy men, or to eliminate it once formed, may suppress or even prevent tumor formation.

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Figures

Fig. 1.

Fig. 1.

Significant differences in the base and backbone structures exist between the DNA of the younger men and that of the older men with the cancer DNA phenotype. (A) Comparison of FT-IR spectra of the DNA of younger men (black line; n = 9) and the cancer DNA phenotype in the older men (magenta line; n = 5). (B) Corresponding P values.

Fig. 2.

Fig. 2.

PC plots of FT-IR spectra of DNA show complete discrimination between prostate groups. (A) PC4 (P < 0.01) vs. PC10 (P < 0.01) for the cancer DNA phenotype in the older men (▴; n = 5) and the older men without the phenotype (▵; n = 7). (B) PC7 (P = 0.03) vs. PC9 (P = 0.02) for the cancer DNA phenotype in the older men (▴; n = 5), the older men without the phenotype (▵; n = 7), and the younger men (•; n = 9).

Fig. 3.

Fig. 3.

P values resulting from comparisons of FT-IR spectra of DNA from the following prostate tissues show no significant differences (P < 0.05), thus establishing the structural similarity between the groups: (A) tumor (n = 9) vs. the cancer DNA phenotype in the older men (n = 5); and (B) histologically normal tissues surrounding tumors (n = 9) vs. the cancer DNA phenotype in the older men.

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