Linear model of colon cancer initiation

Franziska Michor, Yoh Iwasa, Harith Rajagopalan, Christoph Lengauer, Martin A. Nowak

研究成果: ジャーナルへの寄稿記事

67 引用 (Scopus)

抄録

Cancer results if regulatory mechanisms of cell birth and death are disrupted. Colorectal tumorigenesis is initiated by somatic or inherited mutations in the APC tumor suppressor gene pathway. Several additional genetic hits in other tumor suppressor genes and oncogenes drive the progression from polyps to malignant, invasive cancer. The majority of colorectal cancers present chromosomal instability, CIN, which is caused by mutations in genes that are required to maintain chromosomal stability. A major question in cancer genetics is whether CIN is an early event and thus a driving force of tumor progression. We present a new mathematical model of colon cancer initiation assuming a linear flow from stem cells to differentiated cells to apoptosis. We study the consequences of mutations in different cell types and calculate the conditions for CIN to precede APC inactivation. We find that early emergence of CIN is very likely in colorectal tumorigenesis.

元の言語英語
ページ(範囲)358-362
ページ数5
ジャーナルCell Cycle
3
発行部数3
出版物ステータス出版済み - 1 1 2004

Fingerprint

Colonic Neoplasms
Linear Models
Chromosomal Instability
Tumor Suppressor Genes
Mutation
Neoplasms
Carcinogenesis
Polyps
Oncogenes
Colorectal Neoplasms
Cell Death
Theoretical Models
Stem Cells
Parturition
Apoptosis
Genes

All Science Journal Classification (ASJC) codes

  • Molecular Biology
  • Developmental Biology
  • Cell Biology

これを引用

Michor, F., Iwasa, Y., Rajagopalan, H., Lengauer, C., & Nowak, M. A. (2004). Linear model of colon cancer initiation. Cell Cycle, 3(3), 358-362.

Linear model of colon cancer initiation. / Michor, Franziska; Iwasa, Yoh; Rajagopalan, Harith; Lengauer, Christoph; Nowak, Martin A.

:: Cell Cycle, 巻 3, 番号 3, 01.01.2004, p. 358-362.

研究成果: ジャーナルへの寄稿記事

Michor, F, Iwasa, Y, Rajagopalan, H, Lengauer, C & Nowak, MA 2004, 'Linear model of colon cancer initiation', Cell Cycle, 巻. 3, 番号 3, pp. 358-362.
Michor F, Iwasa Y, Rajagopalan H, Lengauer C, Nowak MA. Linear model of colon cancer initiation. Cell Cycle. 2004 1 1;3(3):358-362.
Michor, Franziska ; Iwasa, Yoh ; Rajagopalan, Harith ; Lengauer, Christoph ; Nowak, Martin A. / Linear model of colon cancer initiation. :: Cell Cycle. 2004 ; 巻 3, 番号 3. pp. 358-362.
@article{20bd5e5d6f36471eb7470c54cb051539,
title = "Linear model of colon cancer initiation",
abstract = "Cancer results if regulatory mechanisms of cell birth and death are disrupted. Colorectal tumorigenesis is initiated by somatic or inherited mutations in the APC tumor suppressor gene pathway. Several additional genetic hits in other tumor suppressor genes and oncogenes drive the progression from polyps to malignant, invasive cancer. The majority of colorectal cancers present chromosomal instability, CIN, which is caused by mutations in genes that are required to maintain chromosomal stability. A major question in cancer genetics is whether CIN is an early event and thus a driving force of tumor progression. We present a new mathematical model of colon cancer initiation assuming a linear flow from stem cells to differentiated cells to apoptosis. We study the consequences of mutations in different cell types and calculate the conditions for CIN to precede APC inactivation. We find that early emergence of CIN is very likely in colorectal tumorigenesis.",
author = "Franziska Michor and Yoh Iwasa and Harith Rajagopalan and Christoph Lengauer and Nowak, {Martin A.}",
year = "2004",
month = "1",
day = "1",
language = "English",
volume = "3",
pages = "358--362",
journal = "Cell Cycle",
issn = "1538-4101",
publisher = "Landes Bioscience",
number = "3",

}

TY - JOUR

T1 - Linear model of colon cancer initiation

AU - Michor, Franziska

AU - Iwasa, Yoh

AU - Rajagopalan, Harith

AU - Lengauer, Christoph

AU - Nowak, Martin A.

PY - 2004/1/1

Y1 - 2004/1/1

N2 - Cancer results if regulatory mechanisms of cell birth and death are disrupted. Colorectal tumorigenesis is initiated by somatic or inherited mutations in the APC tumor suppressor gene pathway. Several additional genetic hits in other tumor suppressor genes and oncogenes drive the progression from polyps to malignant, invasive cancer. The majority of colorectal cancers present chromosomal instability, CIN, which is caused by mutations in genes that are required to maintain chromosomal stability. A major question in cancer genetics is whether CIN is an early event and thus a driving force of tumor progression. We present a new mathematical model of colon cancer initiation assuming a linear flow from stem cells to differentiated cells to apoptosis. We study the consequences of mutations in different cell types and calculate the conditions for CIN to precede APC inactivation. We find that early emergence of CIN is very likely in colorectal tumorigenesis.

AB - Cancer results if regulatory mechanisms of cell birth and death are disrupted. Colorectal tumorigenesis is initiated by somatic or inherited mutations in the APC tumor suppressor gene pathway. Several additional genetic hits in other tumor suppressor genes and oncogenes drive the progression from polyps to malignant, invasive cancer. The majority of colorectal cancers present chromosomal instability, CIN, which is caused by mutations in genes that are required to maintain chromosomal stability. A major question in cancer genetics is whether CIN is an early event and thus a driving force of tumor progression. We present a new mathematical model of colon cancer initiation assuming a linear flow from stem cells to differentiated cells to apoptosis. We study the consequences of mutations in different cell types and calculate the conditions for CIN to precede APC inactivation. We find that early emergence of CIN is very likely in colorectal tumorigenesis.

UR - http://www.scopus.com/inward/record.url?scp=10944225680&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=10944225680&partnerID=8YFLogxK

M3 - Article

C2 - 14726709

AN - SCOPUS:10944225680

VL - 3

SP - 358

EP - 362

JO - Cell Cycle

JF - Cell Cycle

SN - 1538-4101

IS - 3

ER -