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  • 1.
    Islam, Quamrul
    et al.
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Cell biology.
    Islam, Khaleda
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Cell biology.
    A new functional classification of tumor-suppressing genes and its therapeutic implications2000In: Bioessays, ISSN 0265-9247, E-ISSN 1521-1878, Vol. 22, no 3, p. 274-285Article in journal (Refereed)
    Abstract [en]

    Cell fusion studies have demonstrated that malignancy can be suppressed by a single dose of malignancy suppressor genes (MSGs), indicating that malignancy is a recessive phenotype. Correspondingly, it is widely believed that mutational inactivation of both alleles of tumor suppressor genes (TSGs), in familial and sporadic tumors, is the formal proof of the recessive nature of malignancy. Evidence presented here, however, shows that unlike MSGs, identified solely through cell fusion studies with no gene of this class yet cloned, many well-known TSGs have gene dosage effects and inhibit cellular growth in vitro. Moreover, homozygous inactivation of a growth-inhibitory TSG (GITSG) is not directly correlated with malignancy. An alternative interpretation is provided for the loss of wild-type alleles of these genes in the tumors. It is concluded that the MSGs and the GITSGs do not belong to the same class of genes. The functional classification of tumor-suppressing genes has important implications for developing effective cancer therapies. (C) 2000 John Wiley and Sons, Inc.

  • 2.
    Los, Marek Jan
    et al.
    Interfaculty Institute for Biochemistry, University of Tübingen, Germany; BioApplications Enterprises, Winnipeg, MB, Canada.
    Maddika, Subbareddy
    Department of Therapeutic Radiology, Yale School of Medicine, New Haven, USA.
    Erb, Bettina
    Interfaculty Institute for Biochemistry, University of Tübingen, Tübingen, Germany.
    Schulze-Osthoff, Klaus
    Interfaculty Institute for Biochemistry, University of Tübingen, Germany.
    Switching Akt: from survival signaling to deadly response2009In: Bioessays, ISSN 0265-9247, E-ISSN 1521-1878, Vol. 31, no 5, p. 492-495Article, review/survey (Refereed)
    Abstract [en]

    Akt, a protein kinase hyperactivated in many tumors, plays a major role in both cell survival and resistance to tumor therapy. A recent study,1 along with other evidences, shows interestingly, that Akt is not a single-function kinase, but may facilitate rather than inhibit cell death under certain conditions. This hitherto undetected function of Akt is accomplished by its ability to increase reactive oxygen species and to suppress antioxidant enzymes. The ability of Akt to down-regulate antioxidant defenses uncovers a novel Achilles' heel, which could be exploited by oxidant therapies in order to selectively eradicate tumor cells that express high levels of Akt activity.

  • 3.
    Maklakov, Alexei A.
    et al.
    Uppsala University, Uppsala, Sweden.
    Rowe, Locke
    University of Toronto, Toronto, ON, Canada.
    Friberg, Urban
    Linköping University, Department of Physics, Chemistry and Biology, Biology. Linköping University, The Institute of Technology.
    Why organisms age: Evolution of senescence under positive pleiotropy?2015In: Bioessays, ISSN 0265-9247, E-ISSN 1521-1878, Vol. 37, no 7, p. 802-807Article in journal (Refereed)
    Abstract [en]

    Two classic theories maintain that aging evolves eitherbecause of alleles whose deleterious effects are confinedto late life or because of alleles with broad pleiotropiceffects that increase early-life fitness at the expense oflate-life fitness. However, empirical studies often revealpositive pleiotropy for fitness across age classes, andrecent evidence suggests that selection on early-lifefitness can decelerate aging and increase lifespan, therebycasting doubt on the current consensus. Here, we brieflyreview these data and promote the simple argument thataging can evolve under positive pleiotropy between earlyandlate-life fitness when the deleterious effect ofmutations increases with age. We argue that thishypothesis makes testable predictions and is supportedby existing evidence.

  • 4.
    Pagano, G.
    et al.
    Italian National Cancer Institute, G. Pascale Foundation, Paediatric Oncology Research Centre, Mercogliano (AV), Italy, Istituto Nazionale Tumori, Fondazione G. Pascale, v. M. Semmola, I-80131 Naples, Italy.
    Youssoufian, H.
    Clinical Discovery, Bristol-Myers Squibb Company, Princeton, NJ, United States.
    Anak, S.S.
    Dept. of Paediat. Haematol./Oncolog., Istanbul Univ. School of Medicine, Istanbul, Turkey.
    Brunk, Ulf
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Health Sciences, Pharmacology .
    Calzone, R.
    Department of Genetics, Elena d'Aosta Hospital, Naples, Italy.
    Clarke, A.A.
    Department of Haematology, St. George's Hosp. Medical School, University of London, London, United Kingdom.
    Degan, P.
    Italian National Cancer Institute, Genoa, Italy.
    D'Ischia, M.
    Department of Organic Chemistry, Federico II Naples University, Naples, Italy, Department of Physiology, Valencia University, Valencia, Spain.
    Dunster, C.
    Division of Life Sciences, King's College, London, United Kingdom.
    Giudice, A.
    Italian National Cancer Institute, Genoa, Italy.
    Iaccarino, M.
    Italian National Cancer Institute, Genoa, Italy.
    Hirsch-Kauffmann, M.
    Kelly, F.J.
    Division of Life Sciences, King's College, London, United Kingdom.
    Lloret, A.
    Department of Organic Chemistry, Federico II Naples University, Naples, Italy, Department of Physiology, Valencia University, Valencia, Spain.
    Malorni, W.
    Italian Natl. Inst. of Hlth. (ISS), Rome, Italy.
    Manini, P.
    Department of Organic Chemistry, Federico II Naples University, Naples, Italy, Department of Physiology, Valencia University, Valencia, Spain.
    Masella, R.
    Italian Natl. Inst. of Hlth. (ISS), Rome, Italy.
    Nobili, B.
    Department of Paediatrics, 2nd Naples University, Naples, Italy.
    Pallardo, F.V.
    Pallardó, F.V., Department of Organic Chemistry, Federico II Naples University, Naples, Italy, Department of Physiology, Valencia University, Valencia, Spain.
    Schweiger, M.
    Department of Biochemistry, Free University Berlin, Berlin, Germany.
    Vuttariello, E.
    Italian National Cancer Institute, Genoa, Italy.
    Youssoufian, G.
    John Whiterspoon Middle School, Princeton, NJ, United States.
    Zatterale, A.
    Department of Genetics, Elena d'Aosta Hospital, Naples, Italy.
    Fanconi anaemia proteins: Major roles in cell protection against oxidative damage2003In: Bioessays, ISSN 0265-9247, E-ISSN 1521-1878, Vol. 25, no 6, p. 589-595Article, review/survey (Refereed)
    Abstract [en]

    Fanconi anaemia (FA) is a cancer-prone genetic disorder that is characterised by cytogenetic instability and redox abnormalities. Although rare subtypes of FA (B, D1 and D2) have been implicated in DNA repair through links with BRCA1 and BRCA2, such a role has yet to be demonstrated for gene products of the common subtypes. Instead, these products have been strongly implicated in xenobiotic metabolism and redox homeostasis through interactions of FANCC with cytochrome P-450 reductase and with glutathione S-transferase, and of FANCG with cytochrome P-450 2E1, as well as redox-dependent signalling through an interaction between FANCA and Akt kinase. We hypothesise that FA proteins act directly (via FANCC and FANCG) and indirectly (via FANCA, BRCA2 and FANCD2) with the machinery of cellular defence to modulate oxidative stress. The latter interactions may co-ordinate the link between the response to DNA damage and oxidative stress parameters (3, 6-12). © 2003 Wiley Periodicals, Inc.

  • 5.
    Rice, William R.
    et al.
    Department of Ecology, Evolution & Marine Biology, University of California, Santa Barbara, CA, USA.
    Friberg, Urban
    Department of Evolutionary Biology, Uppsala University, Uppsala, Sweden.
    Gavrilets, Sergey
    Department of Ecology and Evolutionary Biology, Department of Mathematics, National Institute for Mathematical and Biological Synthesis (NIMBioS), University of Tennessee, Knoxville, TN, USA.
    Homosexuality via canalized sexual development: A testing protocol for a new epigenetic model2013In: Bioessays, ISSN 0265-9247, E-ISSN 1521-1878, Vol. 35, no 9, p. 764-770Article in journal (Refereed)
    Abstract [en]

    We recently synthesized and reinterpreted published studies to advance an epigenetic model for the development of homosexuality (HS). The model is based on epigenetic marks laid down in response to the XX vs. XY karyotype in embryonic stem cells. These marks boost sensitivity to testosterone in XY fetuses and lower it in XX fetuses, thereby canalizing sexual development. Our model predicts that a subset of these canalizing epigenetic marks stochastically carry over across generations and lead to mosaicism for sexual development in opposite-sex offspring - the homosexual phenotype being one such outcome. Here, we begin by outlining why HS has been under-appreciated as a commonplace phenomenon in nature, and how this trend is currently being reversed in the field of neurobiology. We next briefly describe our epigenetic model of HS, develop a set of predictions, and describe how epigenetic profiles of human stem cells can provide for a strong test of the model.

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