Association of a murine chromosome 9 locus (Psl1) with susceptibility to mouse skin tumor promotion by 12-O-tetradecanoylphorbol-13-acetate

Angel, Joe M.; Beltrán, Linda; Minda, Karolina; Rupp, Tim; DiGiovanni, John

doi:10.1002/(sici)1098-2744(199710)20:2<162::aid-mc2>3.0.co;2-p

Cited by 39 publications

(43 citation statements)

References 18 publications

(19 reference statements)

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“…These studies identified a ''promotion-susceptibility'' locus on chromosome 9 (D9Mit271; 48 cM; ref. 19) close to the Skts6 locus (D9Mit76; 49 cM) and a locus designated Skts4 on chromosome 5 (20). Although direct comparisons are complicated by differences in the methodologies used, these results involving intraspecific crosses contrast with the relatively large number of strong modifier loci detected in the Mus spretus͞Mus musculus backcross described in this report.…”

Section: Discussionmentioning

confidence: 55%

A subset of skin tumor modifier loci determines survival time of tumor-bearing mice

Nagase

Mao

Balmain

1999

Proc. Natl. Acad. Sci. U.S.A.

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Studies of mouse models of human cancer have established the existence of multiple tumor modifiers that influence parameters of cancer susceptibility such as tumor multiplicity, tumor size, or the probability of malignant progression. We have carried out an analysis of skin tumor susceptibility in interspecific Mus musculus͞ Mus spretus hybrid mice and have identified another seven loci showing either significant (six loci) or suggestive (one locus) linkage to tumor susceptibility or resistance. A specific search was carried out for skin tumor modifier loci associated with time of survival after development of a malignant tumor. A combination of resistance alleles at three markers [D6Mit15 (Skts12), D7Mit12 (Skts2), and D17Mit7 (Skts10)], all of which are close to or the same as loci associated with carcinoma incidence and͞or papilloma multiplicity, is significantly associated with increased survival of mice with carcinomas, whereas the reverse combination of susceptibility alleles is significantly linked to early mortality caused by rapid carcinoma growth ( 2 ‫؍‬ 25.22; P ‫؍‬ 5.1 ؋ 10 ؊8 ). These data indicate that host genetic factors may be used to predict carcinoma growth rate and͞or survival of individual backcross mice exposed to the same carcinogenic stimulus and suggest that mouse models may provide an approach to the identification of genetic modifiers of cancer survival in humans.

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Section: Discussionmentioning

confidence: 55%

A subset of skin tumor modifier loci determines survival time of tumor-bearing mice

Nagase

Mao

Balmain

1999

Proc. Natl. Acad. Sci. U.S.A.

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“…d The combined LOD equivalent score, is the sum of the individual LOD equivalent scores, was calculating using the program Qlink. overlap between a locus involved in skin tumor promotion, Psl1, previously mapped to a region of Chromosome 9 (Angel et al, 1997), and the Ksc1 locus (Popova et al, 2003). Moreover, Mock et al (1998) reported a higher than expected linkage score for the marker D9Mit271 (48 cM) in association with skin tumor susceptibility.…”

Section: Discussionmentioning

confidence: 85%

Independent Inheritance of Genes Regulating Two Subpopulations of Mouse Clonogenic Keratinocyte Stem Cells

Попова

Suleimanian

Stepanova

et al. 2004

Journal of Investigative Dermatology Symposium Proceedings

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Mouse keratinocyte stem cells originate from the bulge of hair follicle, and, according to definition, possess a clonogenic activity in vitro. We have investigated seven inbred (C57BL/6, C3H, DBA/2, BALB/c, FVB) and outbred (SENCAR, CD-1) mouse strains and found that three genetically distinct subsets of mouse strains differ significantly in the frequency of clonogenic activity in vitro. The analysis of keratinocyte colonies in two reciprocal backcross [C57BL/6 x (BALB/c x C57BL/6); BALB/c x (BALB/c x C57BL/6)] and intercross [(BALB/c x C57BL/ 6)F2] of BALB/c and C57BL/6 mice allowed us to identify two subpopulations of clonogenic keratinocytes able to produce small (less than 2 mm2) and large (more than 2 mm2) colonies. We conducted linkage analysis and found that small colonies associated with mouse chromosomes 1, 6, 7, 8, and 9; but large colonies--with the chromosome 4. We defined locus on the chromosome 9 that associated with small colonies as keratinocyte stem cell locus 1 (Ksc1), and locus on the mouse chromosome 4 associated with large colonies-keratinocyte stem cell locus 2 (Ksc2). Ksc1 and loci on chromosomes 6 and 7 are close if not equal to loci associated with sensitivity to skin carcinogenesis. We conclude that two subpopulations of stem cells able to produce small and large colonies regulated by different genes and genes regulating small colonies might be responsible for sensitivity to skin carcinogenesis.

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“…Moreover, two genetic linkage studies performed in genetic crosses in which both parental strains carried the same Tyr allele, either functional (Angel et al, 1997) or albino (Mock et al, 1998), did not detect any skin tumor-modifier locus in the Tyr region; a test locus cannot exert allele-specific phenotypic effects in a cross originating from two strains carrying the same allele (Manenti et al, 1997).…”

Section: Discussionmentioning

confidence: 96%

Loss of tyrosinase activity confers increased skin tumor susceptibility in mice

et al. 2004

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The tyrosinase (Tyr) gene encodes the enzyme tyrosinase that catalyses the conversion of L-tyrosine into DOPA (3,4-dihydroxyphenylalanine)-quinone. The albino mutation abrogates functional activity of tyrosinase resulting in deficiency of melanin pigment production in skin and retina. Tyr maps to a region in the central position of Chromosome 7 that contains a skin tumor-modifier locus. We rescued the albino mutation in transgenic mice to assess a possible role of Tyr gene in two-stage skin carcinogenesis. Transgenic expression of the functional Tyr Cys allele in albino mice (Tyr Ser ) caused a reduction in skin papilloma multiplicity, in four independent experiments and at three dose levels of DMBA (9,10-dimethyl-1,2-benzanthracene). In vitro mechanistic studies demonstrated that transfection of the Tyr Cys allele in a human squamous cell carcinoma cell line (NCI-H520) increases tyrosinase enzyme activity and confers resistance to hydrogen peroxide-induced oxidative DNA damage. These results provide direct evidence that the Tyr gene can act as a skin cancer-modifier gene, whose mechanism of action may involve modulation of oxidative DNA damage.

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Association of a murine chromosome 9 locus (Psl1) with susceptibility to mouse skin tumor promotion by 12-O-tetradecanoylphorbol-13-acetate

Cited by 39 publications

References 18 publications

A subset of skin tumor modifier loci determines survival time of tumor-bearing mice

A subset of skin tumor modifier loci determines survival time of tumor-bearing mice

Independent Inheritance of Genes Regulating Two Subpopulations of Mouse Clonogenic Keratinocyte Stem Cells

Loss of tyrosinase activity confers increased skin tumor susceptibility in mice

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