R
Robert Karl Sto
Guest
How good is our genome?
Philosophical Transactions: Biological Sciences
fobike://rsl/rtb January 29, 2004, vol. 359, no. 1441,
pp. 95-98(4)
l/rtb/2004/00000359/00001441 Weill J-C.[1]; Radman M.[1]
[1] Faculte de Medecine Necker Enfants-Malades, Université
de Paris-V, Paris, France
Abstract: Our genome has evolved to perpetuate itself
through the maintenance of the species via an uninterrupted
chain of reproductive somas. Accordingly, evolution is not
concerned with diseases occurring after the soma's
reproductive stage. Following Richard Dawkins, we would like
to reassert that we indeed live as disposable somas, slaves
of our germline genome, but could soon start rebelling
against such slavery. Cancer and its relation to the TP53
gene may offer a paradigmatic example. The observation that
the latency period in cancer can be prolonged in mice by
increasing the number of TP53 genes in their genome,
suggests that sooner or later we will have to address the
question of heritable disease avoidance via the manipulation
of the human germline.
Keywords: evolution; germline modification; cancer;
latency; p53
Document Type: Research article ISSN: 0962-8436
DOI (article): 10.1098/rstb.2003.1369 SICI (online): 0962-8436(20040129)359:1441L.95;1-
Publisher: Royal Society
--
Posted by Robert Karl Stonjek.
Philosophical Transactions: Biological Sciences
fobike://rsl/rtb January 29, 2004, vol. 359, no. 1441,
pp. 95-98(4)
l/rtb/2004/00000359/00001441 Weill J-C.[1]; Radman M.[1]
[1] Faculte de Medecine Necker Enfants-Malades, Université
de Paris-V, Paris, France
Abstract: Our genome has evolved to perpetuate itself
through the maintenance of the species via an uninterrupted
chain of reproductive somas. Accordingly, evolution is not
concerned with diseases occurring after the soma's
reproductive stage. Following Richard Dawkins, we would like
to reassert that we indeed live as disposable somas, slaves
of our germline genome, but could soon start rebelling
against such slavery. Cancer and its relation to the TP53
gene may offer a paradigmatic example. The observation that
the latency period in cancer can be prolonged in mice by
increasing the number of TP53 genes in their genome,
suggests that sooner or later we will have to address the
question of heritable disease avoidance via the manipulation
of the human germline.
Keywords: evolution; germline modification; cancer;
latency; p53
Document Type: Research article ISSN: 0962-8436
DOI (article): 10.1098/rstb.2003.1369 SICI (online): 0962-8436(20040129)359:1441L.95;1-
Publisher: Royal Society
--
Posted by Robert Karl Stonjek.