The Role of Cell Proliferation in the Etiology of Neoplasia

Research output: Chapter in Book/Report/Conference proceedingChapter

1 Citation (Scopus)

Abstract

Cancer is due to multiple genetic errors in a single stem cell fixed permanently during replication, produced either by directly damaging DNA or by increasing DNA replications. Synergies occur when both processes are produced. Cell proliferation can be increased by increasing cell births (direct mitogenicity or cytotoxicity and regeneration) or decreasing cell deaths (inhibit apoptosis or differentiation). Screening for these effects provides a rational basis for mode of action analysis and relevance of model findings to human cancer risk.

Original languageEnglish (US)
Title of host publicationCarcinogenesis
PublisherElsevier Inc.
Pages229-253
Number of pages25
Volume14
ISBN (Print)9780080468686
DOIs
StatePublished - Aug 12 2010

Fingerprint

Cell Proliferation
DNA Replication
Regeneration
Neoplasms
Cell Death
Stem Cells
Parturition
Apoptosis
DNA

Keywords

  • 2-acetylaminoflourene
  • Breast
  • Calculi
  • Cell proliferation
  • Chemoprevention
  • Cytotoxicity
  • DNA reactivity
  • Forestomach
  • Hormones
  • Immunosuppression
  • Initiation
  • Kidney
  • Liver
  • Mitogenesis
  • Progression
  • Promotion
  • Regeneration
  • Stomach
  • Thyroid
  • Urinary bladder

ASJC Scopus subject areas

  • Medicine(all)

Cite this

The Role of Cell Proliferation in the Etiology of Neoplasia. / Cohen, Samuel Monroe.

Carcinogenesis. Vol. 14 Elsevier Inc., 2010. p. 229-253.

Research output: Chapter in Book/Report/Conference proceedingChapter

Cohen, Samuel Monroe. / The Role of Cell Proliferation in the Etiology of Neoplasia. Carcinogenesis. Vol. 14 Elsevier Inc., 2010. pp. 229-253
@inbook{78466174c8eb452aa48477db10f0d5df,
title = "The Role of Cell Proliferation in the Etiology of Neoplasia",
abstract = "Cancer is due to multiple genetic errors in a single stem cell fixed permanently during replication, produced either by directly damaging DNA or by increasing DNA replications. Synergies occur when both processes are produced. Cell proliferation can be increased by increasing cell births (direct mitogenicity or cytotoxicity and regeneration) or decreasing cell deaths (inhibit apoptosis or differentiation). Screening for these effects provides a rational basis for mode of action analysis and relevance of model findings to human cancer risk.",
keywords = "2-acetylaminoflourene, Breast, Calculi, Cell proliferation, Chemoprevention, Cytotoxicity, DNA reactivity, Forestomach, Hormones, Immunosuppression, Initiation, Kidney, Liver, Mitogenesis, Progression, Promotion, Regeneration, Stomach, Thyroid, Urinary bladder",
author = "Cohen, {Samuel Monroe}",
year = "2010",
month = "8",
day = "12",
doi = "10.1016/B978-0-08-046884-6.01412-3",
language = "English (US)",
isbn = "9780080468686",
volume = "14",
pages = "229--253",
booktitle = "Carcinogenesis",
publisher = "Elsevier Inc.",

}

TY - CHAP

T1 - The Role of Cell Proliferation in the Etiology of Neoplasia

AU - Cohen, Samuel Monroe

PY - 2010/8/12

Y1 - 2010/8/12

N2 - Cancer is due to multiple genetic errors in a single stem cell fixed permanently during replication, produced either by directly damaging DNA or by increasing DNA replications. Synergies occur when both processes are produced. Cell proliferation can be increased by increasing cell births (direct mitogenicity or cytotoxicity and regeneration) or decreasing cell deaths (inhibit apoptosis or differentiation). Screening for these effects provides a rational basis for mode of action analysis and relevance of model findings to human cancer risk.

AB - Cancer is due to multiple genetic errors in a single stem cell fixed permanently during replication, produced either by directly damaging DNA or by increasing DNA replications. Synergies occur when both processes are produced. Cell proliferation can be increased by increasing cell births (direct mitogenicity or cytotoxicity and regeneration) or decreasing cell deaths (inhibit apoptosis or differentiation). Screening for these effects provides a rational basis for mode of action analysis and relevance of model findings to human cancer risk.

KW - 2-acetylaminoflourene

KW - Breast

KW - Calculi

KW - Cell proliferation

KW - Chemoprevention

KW - Cytotoxicity

KW - DNA reactivity

KW - Forestomach

KW - Hormones

KW - Immunosuppression

KW - Initiation

KW - Kidney

KW - Liver

KW - Mitogenesis

KW - Progression

KW - Promotion

KW - Regeneration

KW - Stomach

KW - Thyroid

KW - Urinary bladder

UR - http://www.scopus.com/inward/record.url?scp=85012842398&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85012842398&partnerID=8YFLogxK

U2 - 10.1016/B978-0-08-046884-6.01412-3

DO - 10.1016/B978-0-08-046884-6.01412-3

M3 - Chapter

AN - SCOPUS:85012842398

SN - 9780080468686

VL - 14

SP - 229

EP - 253

BT - Carcinogenesis

PB - Elsevier Inc.

ER -