Welcome to Peter Duesberg's CANCER research web site. Peter H. Duesberg, Ph.D. is a professor of Molecular and Cell Biology at the University of California, Berkeley.

He isolated the first cancer gene through his work on retroviruses in 1970, and mapped the genetic structure of these viruses. This, and his subsequent work in the same field, resulted in his election to the National Academy of Sciences in 1986. He was also the recipient of a seven-year Outstanding Investigator Grant from the National Institute of Health.

In 1987 he claimed that HIV is not the cause of AIDS.¹⁾

Biography - University of California, Berkley - Professor of Biochemistry and Molecular Biology Department of Molecular & Cell Biology genetic structure of retroviruses, carcinogenesis, aneuploidy, virology, HIV-AIDS

Description

Research in Carcinogenesis; Aneuploidy, an abnormal balance of chromosomes is (i) ubiquitous in cancer, is (ii) proportional to the degree of malignancy of cancer, and (iii) inevitably generates abnormal phenotypes, because it alters the dosages and expression of thousands of normal genes. Take Down syndrome, a trisomy of chromosome 21, as an example. In view of this we have recently proposed that aneuploidy is sufficient to cause cancer.

Our hypothesis proposes that cancer-specific chromosome combinations, or aneusomies, cause cancer-specific phenotypes. According to this hypothesis carcinogens initiate carcinogenesis with a random aneuploidy. Aneuploidy then renders chromosome segregation and maintenance error-prone because it unbalances teams of spindle proteins, repair enzymes, and even centrosome numbers. The resulting chain reaction of chromosome reassortments then generates cancer-specific aneuploidy and further random aneuploidy autocatalytically.

The aneuploidy-cancer hypothesis predicts all peculiar aspects of carcinogenesis, particularly those that have remained paradoxical according to the competing gene-mutation hypothesis: For example, 1) The ubiquity of aneuploidy in cancer. In contrast, the mutation hypothesis predicts diploid cancers.

2) Carcinogens function as aneuploidogens. This was confirmed with non-mutagenic and mutagenic carcinogens. For example, 100% of Chinese hamster cells transformed in vitro by the non-mutagenic polycyclic aromatic hydrocarbons (PAHs) were aneuploid. But non-mutagenic carcinogens are a paradox of the mutation hypothesis.

3) Aneuploidy prior to carcinogenesis. This has been confirmed by us and others.

4) The slow kinetics of carcinogenesis, from experimental or accidental carcinogen to cancer. This is explained by the low probability of evolving cancer-specific aneuploidies by random chromosome assortments _ a process analogous to phylogenesis. By contrast, the mutation hypothesis predicts carcinogenesis without lag, because mutation is instantaneous.

5) The genetic instability and the corresponding heterogeneous phenotypes of cancer. These are based on the inherent instability of the aneuploid karyotype. But, stable phenotypes are predicted by the mutation hypothesis because gene mutations are stable.

6) The ability of cancer cells to become resistant against a selected, chemotherapeutic drug, and simultaneously against many unselected drugs. This is also explained by aneuploidy-catalyzed reassortments of chromosomes, encoding selected and un-selected resistances in the same chromosomes. This hypothesis also explains the failure of diploid cells of cancer patients to become drug-resistant.

7) The low risk of transformation of human cells by carcinogens, compared to rodent cells, is thought to reflect the high resistance of human cells to aneuploidization. This is currently tested experimentally.

The aneuploidy-cancer hypothesis predicts improvements in cancer prevention by eliminating aneuploidogens from food and drugs, and in therapy by early detection of preneoplastic cells, eg. Pap smears, based on the presence of aneuploidy.

Research in Virology; A thorough audit of the HIV-AIDS hypothesis leads to the conclusion that the various AIDS epidemics of the US, Europe and Africa have chemical bases, namely toxic, recreational drugs, DNA-chain terminators prescribed as anti-HIV drugs and malnutrition.²⁾