Muir-Torre-like syndrome in Fhit-deficient mice

Louise Y.Y. Fong; Vincenzo Fidanza; Nicola Zanesi; Leslie F. Lock; Linda D. Siracusa; Rita Mancini; Zurab Siprashvili; Michelle Ottey; S. Eric Martin; Teresa Druck; Peter A. McCue; Carlo M. Croce; Kay Huebner

doi:10.1073/pnas.080063497

Muir-Torre-like syndrome in Fhit-deficient mice

Louise Y.Y. Fong
, Vincenzo Fidanza
, Nicola Zanesi
, Leslie F. Lock
, Linda D. Siracusa
, Rita Mancini
, Zurab Siprashvili
, Michelle Ottey
, S. Eric Martin
, Teresa Druck
, Peter A. McCue
, Carlo M. Croce
, Kay Huebner

Pathology

Thomas Jefferson University

Research output: Contribution to journal › Article › peer-review

191 Scopus citations

Abstract

To investigate the role of the Fhit gene in carcinogen induction of neoplasia, we have inactivated one Fhit allele in mouse embryonic stem cells and produced (129/SvJ x C57BL/6J) F₁ mice with a Fhit allele inactivated (+/-). Fhit +/+ and +/- mice were treated intragastrically with nitrosomethylbenzylamine and observed for 10 wk posttreatment. A total of 25% of the +/+ mice developed adenoma or papilloma of the forestomach, whereas 100% of the +/- mice developed multiple tumors that were a mixture of adenomas, squamous papillomas, invasive carcinomas of the forestomach, as well as tumors of sebaceous glands. The visceral and sebaceous tumors, which lacked Fhit protein, were similar to those characteristic of Muir-Torre familial cancer syndrome.

Original language	English
Pages (from-to)	4742-4747
Number of pages	6
Journal	Proceedings of the National Academy of Sciences of the United States of America
Volume	97
Issue number	9
DOIs	https://doi.org/10.1073/pnas.080063497
State	Published - Apr 25 2000

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

SDG 3 Good Health and Well-being

Keywords

Acid Anhydride Hydrolases
Adenoma/genetics
Animals
Carcinogens
Dimethylnitrosamine/analogs & derivatives
Female
Humans
Male
Mice
Mice, Inbred C57BL
Mice, Inbred Strains
Mice, Knockout
Neoplasm Proteins/deficiency
Neoplasms, Multiple Primary/chemically induced
Papilloma/genetics
Proteins/genetics
Restriction Mapping
Sebaceous Gland Neoplasms/genetics
Stomach Neoplasms/chemically induced
Syndrome

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10.1073/pnas.080063497

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Fong, L. Y. Y., Fidanza, V., Zanesi, N., Lock, L. F., Siracusa, L. D., Mancini, R., Siprashvili, Z., Ottey, M., Martin, S. E., Druck, T., McCue, P. A., Croce, C. M., & Huebner, K. (2000). Muir-Torre-like syndrome in Fhit-deficient mice. Proceedings of the National Academy of Sciences of the United States of America, 97(9), 4742-4747. https://doi.org/10.1073/pnas.080063497

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title = "Muir-Torre-like syndrome in Fhit-deficient mice",

abstract = "To investigate the role of the Fhit gene in carcinogen induction of neoplasia, we have inactivated one Fhit allele in mouse embryonic stem cells and produced (129/SvJ x C57BL/6J) F1 mice with a Fhit allele inactivated (+/-). Fhit +/+ and +/- mice were treated intragastrically with nitrosomethylbenzylamine and observed for 10 wk posttreatment. A total of 25\% of the +/+ mice developed adenoma or papilloma of the forestomach, whereas 100\% of the +/- mice developed multiple tumors that were a mixture of adenomas, squamous papillomas, invasive carcinomas of the forestomach, as well as tumors of sebaceous glands. The visceral and sebaceous tumors, which lacked Fhit protein, were similar to those characteristic of Muir-Torre familial cancer syndrome.",

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doi = "10.1073/pnas.080063497",

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AU - Fong, Louise Y.Y.

AU - Fidanza, Vincenzo

AU - Zanesi, Nicola

AU - Lock, Leslie F.

AU - Siracusa, Linda D.

AU - Mancini, Rita

AU - Siprashvili, Zurab

AU - Ottey, Michelle

AU - Martin, S. Eric

AU - Druck, Teresa

AU - McCue, Peter A.

AU - Croce, Carlo M.

AU - Huebner, Kay

PY - 2000/4/25

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N2 - To investigate the role of the Fhit gene in carcinogen induction of neoplasia, we have inactivated one Fhit allele in mouse embryonic stem cells and produced (129/SvJ x C57BL/6J) F1 mice with a Fhit allele inactivated (+/-). Fhit +/+ and +/- mice were treated intragastrically with nitrosomethylbenzylamine and observed for 10 wk posttreatment. A total of 25% of the +/+ mice developed adenoma or papilloma of the forestomach, whereas 100% of the +/- mice developed multiple tumors that were a mixture of adenomas, squamous papillomas, invasive carcinomas of the forestomach, as well as tumors of sebaceous glands. The visceral and sebaceous tumors, which lacked Fhit protein, were similar to those characteristic of Muir-Torre familial cancer syndrome.

AB - To investigate the role of the Fhit gene in carcinogen induction of neoplasia, we have inactivated one Fhit allele in mouse embryonic stem cells and produced (129/SvJ x C57BL/6J) F1 mice with a Fhit allele inactivated (+/-). Fhit +/+ and +/- mice were treated intragastrically with nitrosomethylbenzylamine and observed for 10 wk posttreatment. A total of 25% of the +/+ mice developed adenoma or papilloma of the forestomach, whereas 100% of the +/- mice developed multiple tumors that were a mixture of adenomas, squamous papillomas, invasive carcinomas of the forestomach, as well as tumors of sebaceous glands. The visceral and sebaceous tumors, which lacked Fhit protein, were similar to those characteristic of Muir-Torre familial cancer syndrome.

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KW - Animals

KW - Carcinogens

KW - Dimethylnitrosamine/analogs & derivatives

KW - Female

KW - Humans

KW - Male

KW - Mice

KW - Mice, Inbred C57BL

KW - Mice, Inbred Strains

KW - Mice, Knockout

KW - Neoplasm Proteins/deficiency

KW - Neoplasms, Multiple Primary/chemically induced

KW - Papilloma/genetics

KW - Proteins/genetics

KW - Restriction Mapping

KW - Sebaceous Gland Neoplasms/genetics

KW - Stomach Neoplasms/chemically induced

KW - Syndrome

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SP - 4742

EP - 4747

JO - Proceedings of the National Academy of Sciences of the United States of America

JF - Proceedings of the National Academy of Sciences of the United States of America

IS - 9

ER -

Muir-Torre-like syndrome in Fhit-deficient mice

Abstract

UN SDGs

Keywords

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