Language:
English
繁體中文
Help
回圖書館首頁
手機版館藏查詢
Login
Back
Switch To:
Labeled
|
MARC Mode
|
ISBD
Evolutionary dynamics of cancer.
~
Michor, Franziska.
Linked to FindBook
Google Book
Amazon
博客來
Evolutionary dynamics of cancer.
Record Type:
Electronic resources : Monograph/item
Title/Author:
Evolutionary dynamics of cancer./
Author:
Michor, Franziska.
Description:
163 p.
Notes:
Source: Dissertation Abstracts International, Volume: 66-05, Section: B, page: 2395.
Contained By:
Dissertation Abstracts International66-05B.
Subject:
Biology, Genetics. -
Online resource:
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3173982
ISBN:
0542114399
Evolutionary dynamics of cancer.
Michor, Franziska.
Evolutionary dynamics of cancer.
- 163 p.
Source: Dissertation Abstracts International, Volume: 66-05, Section: B, page: 2395.
Thesis (Ph.D.)--Harvard University, 2005.
Evolutionary dynamics of mutation and selection can be formulated by mathematical equations. Cancer arises as a consequence of somatic evolution. Therefore, a mathematical approach can be used to understand cancer initiation and progression. Tumorigenesis is driven by genetic alterations of oncogenes, tumor suppressor genes and genetic instability genes. First, I discuss the fundamental principles that govern the dynamics of activating oncogenes and inactivating tumor suppressor genes in populations of reproducing cells. A quantitative theory of mutation and selection provides insights into the role of genetic instability in cancer initiation. Second, I analyze the dynamics of cancer progression via inactivation of one or two tumor suppressor genes. Third, I derive a mathematical framework for the complete mutational sequence of colorectal tumorigenesis (as known today) and the effect of chromosomal instability therein. Fourth, I present a new mathematical model of colon cancer initiation that assumes a linear flow from stem cells to differentiated cells to apoptosis. Finally, a mathematical model of chronic myeloid leukemia (CML) and the molecular response to imatinib therapy suggests that leukemic stein cells are spared by therapy. The model provides quantitative insights into the in vivo kinetics of this cancer and determines the probability of disease relapse due to resistance mutations.
ISBN: 0542114399Subjects--Topical Terms:
1017730
Biology, Genetics.
Evolutionary dynamics of cancer.
LDR
:02252nmm 2200277 4500
001
1812914
005
20060427132643.5
008
130610s2005 eng d
020
$a
0542114399
035
$a
(UnM)AAI3173982
035
$a
AAI3173982
040
$a
UnM
$c
UnM
100
1
$a
Michor, Franziska.
$3
1902447
245
1 0
$a
Evolutionary dynamics of cancer.
300
$a
163 p.
500
$a
Source: Dissertation Abstracts International, Volume: 66-05, Section: B, page: 2395.
500
$a
Adviser: Martin A. Nowak.
502
$a
Thesis (Ph.D.)--Harvard University, 2005.
520
$a
Evolutionary dynamics of mutation and selection can be formulated by mathematical equations. Cancer arises as a consequence of somatic evolution. Therefore, a mathematical approach can be used to understand cancer initiation and progression. Tumorigenesis is driven by genetic alterations of oncogenes, tumor suppressor genes and genetic instability genes. First, I discuss the fundamental principles that govern the dynamics of activating oncogenes and inactivating tumor suppressor genes in populations of reproducing cells. A quantitative theory of mutation and selection provides insights into the role of genetic instability in cancer initiation. Second, I analyze the dynamics of cancer progression via inactivation of one or two tumor suppressor genes. Third, I derive a mathematical framework for the complete mutational sequence of colorectal tumorigenesis (as known today) and the effect of chromosomal instability therein. Fourth, I present a new mathematical model of colon cancer initiation that assumes a linear flow from stem cells to differentiated cells to apoptosis. Finally, a mathematical model of chronic myeloid leukemia (CML) and the molecular response to imatinib therapy suggests that leukemic stein cells are spared by therapy. The model provides quantitative insights into the in vivo kinetics of this cancer and determines the probability of disease relapse due to resistance mutations.
590
$a
School code: 0084.
650
4
$a
Biology, Genetics.
$3
1017730
650
4
$a
Health Sciences, Oncology.
$3
1018566
690
$a
0369
690
$a
0992
710
2 0
$a
Harvard University.
$3
528741
773
0
$t
Dissertation Abstracts International
$g
66-05B.
790
1 0
$a
Nowak, Martin A.,
$e
advisor
790
$a
0084
791
$a
Ph.D.
792
$a
2005
856
4 0
$u
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3173982
based on 0 review(s)
Location:
ALL
電子資源
Year:
Volume Number:
Items
1 records • Pages 1 •
1
Inventory Number
Location Name
Item Class
Material type
Call number
Usage Class
Loan Status
No. of reservations
Opac note
Attachments
W9203785
電子資源
11.線上閱覽_V
電子書
EB
一般使用(Normal)
On shelf
0
1 records • Pages 1 •
1
Multimedia
Reviews
Add a review
and share your thoughts with other readers
Export
pickup library
Processing
...
Change password
Login