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Cancer turnover at old age.

Pompei, Francesco.

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Cancer turnover at old age.

Record Type:	Language materials, printed : Monograph/item
Title/Author:	Cancer turnover at old age./
Author:	Pompei, Francesco.
Description:	131 p.
Notes:	Adviser: Richard Wilson.
Contained By:	Dissertation Abstracts International63-04B.
Subject:	Biophysics, Medical. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3051260
ISBN:	0493658343

Cancer turnover at old age.
Pompei, Francesco.

Cancer turnover at old age. - 131 p.

Adviser: Richard Wilson.

Thesis (Ph.D.)--Harvard University, 2002.

It has been commonly assumed for a half century that if a person lives long enough, he or she will eventually develop cancer. Cancer age-specific incidence data does not support that assumption, showing instead that incidence flattens at about age 80 and declines thereafter, approaching zero where there is data at about age 100. Previous cancer models of long standing have been unable to explain the turnover in incidence beyond age 80, and investigators have tended to ascribe under-reporting of cancers, or that the oldest persons are somehow not susceptible, as explanations for the data. This work presents the first model of cancer incidence incorporating the biological process of cellular replicative senescence. The model provides good fits to human cancer age distribution data for 40 organ sites from databases from the U.S., Holland, and Hong Kong. Newly developed mice data from a 24,000 mice study has also been found to be well fit by the model, confirming that cancers peak at about 80% of lifespan and actually reach zero for the oldest mice. The model, mathematically a form of Beta function, is derived by adding to standard multi-stage or clonal expansion models the observation that <italic>in vitro</italic> data show aging cells lose their proliferative ability with age. Since senescent cells cannot produce cancer, the pool of cells available to produce cancer declines, thus lowering the incidence, reaching zero when all cells are senescent. Further tests of the model performed against data on interventions that might alter senescence shows agreement in cancer rate and longevity changes, and also suggests that longevity might be increased when cancers can be treated. The results also suggest that studies of cancer associations with various dietary or environmental factors should include the effect on longevity, since both results depend on senescence.

ISBN: 0493658343Subjects--Topical Terms:

1017681
Biophysics, Medical.

Cancer turnover at old age.
LDR:03077nam 2200301 a 45 001 934092
005 20110509
008 110509s2002 eng d
020 $a 0493658343
035 $a (UnM)AAI3051260
035 $a AAI3051260
040 $a UnM $c UnM
100 1 $a Pompei, Francesco. $3 1257816
245 1 0 $a Cancer turnover at old age.
300 $a 131 p.
500 $a Adviser: Richard Wilson.
500 $a Source: Dissertation Abstracts International, Volume: 63-04, Section: B, page: 1747.
502 $a Thesis (Ph.D.)--Harvard University, 2002.
520 $a It has been commonly assumed for a half century that if a person lives long enough, he or she will eventually develop cancer. Cancer age-specific incidence data does not support that assumption, showing instead that incidence flattens at about age 80 and declines thereafter, approaching zero where there is data at about age 100. Previous cancer models of long standing have been unable to explain the turnover in incidence beyond age 80, and investigators have tended to ascribe under-reporting of cancers, or that the oldest persons are somehow not susceptible, as explanations for the data. This work presents the first model of cancer incidence incorporating the biological process of cellular replicative senescence. The model provides good fits to human cancer age distribution data for 40 organ sites from databases from the U.S., Holland, and Hong Kong. Newly developed mice data from a 24,000 mice study has also been found to be well fit by the model, confirming that cancers peak at about 80% of lifespan and actually reach zero for the oldest mice. The model, mathematically a form of Beta function, is derived by adding to standard multi-stage or clonal expansion models the observation that <italic>in vitro</italic> data show aging cells lose their proliferative ability with age. Since senescent cells cannot produce cancer, the pool of cells available to produce cancer declines, thus lowering the incidence, reaching zero when all cells are senescent. Further tests of the model performed against data on interventions that might alter senescence shows agreement in cancer rate and longevity changes, and also suggests that longevity might be increased when cancers can be treated. The results also suggest that studies of cancer associations with various dietary or environmental factors should include the effect on longevity, since both results depend on senescence.
520 $a The most desirable intervention both reduces cancer by reducing cellular damage causes of carcinogenesis, and reduces cellular damage causes of senescence, thus achieving both cancer reduction and longer life. This combination is thus far known only for dietary restriction, but others might be discovered from further research.
590 $a School code: 0084.
650 4 $a Biophysics, Medical. $3 1017681
650 4 $a Health Sciences, Human Development. $3 1019218
650 4 $a Health Sciences, Oncology. $3 1018566
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690 $a 0760
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710 2 0 $a Harvard University. $3 528741
773 0 $t Dissertation Abstracts International $g 63-04B.
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790 1 0 $a Wilson, Richard, $e advisor
791 $a Ph.D.
792 $a 2002
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3051260