Contents
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
Introduction Introduction
-
Oncogenes and tumour suppressor genes Oncogenes and tumour suppressor genes
-
The two-hit hypothesis The two-hit hypothesis
-
Characteristics of the malignant phenotype Characteristics of the malignant phenotype
-
-
Carcinogenesis Carcinogenesis
-
Initiators and promoters Initiators and promoters
-
Cellular transformation Cellular transformation
-
The origin of cancer cells The origin of cancer cells
-
Monoclonal theory Monoclonal theory
-
Cancer stem cell hypothesis Cancer stem cell hypothesis
-
-
-
Genetic alterations Genetic alterations
-
Types of mutation Types of mutation
-
Genetic instability Genetic instability
-
Repair of genetic damage Repair of genetic damage
-
Caretaker genes Caretaker genes
-
Gatekeeper genes Gatekeeper genes
-
-
-
Chromosomal instability Chromosomal instability
-
Nucleotide instability Nucleotide instability
-
Nucleotide excision repair Nucleotide excision repair
-
DNA mismatch repair DNA mismatch repair
-
-
Chromosomal translocations Chromosomal translocations
-
Complex translocations Complex translocations
-
Simple translocations Simple translocations
-
-
Gene amplification Gene amplification
-
-
Cell cycle checkpoints and cancer Cell cycle checkpoints and cancer
-
G1/S checkpoint G1/S checkpoint
-
G2/M checkpoint G2/M checkpoint
-
-
Oncogenes Oncogenes
-
Receptor protein tyrosine kinases as oncogenes Receptor protein tyrosine kinases as oncogenes
-
Cytoplasmic protein tyrosine kinases as oncogenes Cytoplasmic protein tyrosine kinases as oncogenes
-
Nuclear proteins as oncogenes Nuclear proteins as oncogenes
-
-
Tumour suppressor genes Tumour suppressor genes
-
Transcriptional factors as tumour suppressor genes Transcriptional factors as tumour suppressor genes
-
The retinoblastoma gene The retinoblastoma gene
-
TP53 gene and p53 gene product TP53 gene and p53 gene product
-
-
Cytoplasmic tumour suppressor genes Cytoplasmic tumour suppressor genes
-
Receptor tumour suppressor genes Receptor tumour suppressor genes
-
Transforming growth factor b (TGFb) Transforming growth factor b (TGFb)
-
Hedgehog Hedgehog
-
-
Transgenic studies Transgenic studies
-
Mutations in genes regulating apoptosis and cell death pathways Mutations in genes regulating apoptosis and cell death pathways
-
MicroRNA as oncogenes and tumour suppressors MicroRNA as oncogenes and tumour suppressors
-
-
Epigenetics Epigenetics
-
Cancer invasion and metastases Cancer invasion and metastases
-
Angiogenesis Angiogenesis
-
-
Viral causes of cancer Viral causes of cancer
-
Conclusions Conclusions
-
Further reading Further reading
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
Cite
Extract
Essentials
Introduction
Many biological processes including wound healing, development, and carcinogenesis involve well-defined patterns of cellular growth and differentiation. Rates of proliferation and differentiation are stringently regulated within normal tissues of a multicellular organism and ensure that organs do not exceed a specific size and that tissue renewal is proportionate and confined to replacement of damaged and/or effete cells only. Communication between cells is the essence of this ‘cellular society’ and may be based on several mechanisms. Direct cell-to-cell contact is restricted to cells in contiguous arrangement and involves specialized junctional elements permitting transfer of signals between cells. By contrast, indirect modes of communication allow interaction between neighbouring groups of cells which are not necessarily in direct contact. Thus cells may interact through the extracellular matrix which surrounds all cells in vivo and whose structure and composition is determined by tissue requirements. Alternatively, cells may communicate indirectly by means of soluble growth factors which are secreted by a particular cell type and diffuse through the extracellular matrix to reach target cells lying at variable distances from the source. An important mechanism for growth control in multicellular organisms is density-dependent growth inhibition which ensures that no single cell has unrestrained growth and competition for space and nutrients is ‘fair’. This may be mediated by an increase in cellular requirements for macromolecular growth factors. As confluency is reached, with crowding of cells, their innate sensitivity to these growth factors decreases, perhaps as a result of a reduction in the density of cell surface receptors.
Sign in
Get help with accessPersonal account
- Sign in with email/username & password
- Get email alerts
- Save searches
- Purchase content
- Activate your purchase/trial code
Institutional access
- Sign in through your institution
- Sign in with a library card Sign in with username/password Recommend to your librarian
Institutional account management
Sign in as administratorPurchase
Our books are available by subscription or purchase to libraries and institutions.
Purchasing informationMonth: | Total Views: |
---|---|
October 2022 | 10 |
November 2022 | 2 |
December 2022 | 2 |
January 2023 | 3 |
February 2023 | 4 |
March 2023 | 4 |
April 2023 | 1 |
May 2023 | 2 |
June 2023 | 4 |
July 2023 | 2 |
August 2023 | 4 |
September 2023 | 2 |
October 2023 | 2 |
November 2023 | 3 |
December 2023 | 2 |
January 2024 | 1 |
February 2024 | 5 |
March 2024 | 1 |
Get help with access
Institutional access
Access to content on Oxford Academic is often provided through institutional subscriptions and purchases. If you are a member of an institution with an active account, you may be able to access content in one of the following ways:
IP based access
Typically, access is provided across an institutional network to a range of IP addresses. This authentication occurs automatically, and it is not possible to sign out of an IP authenticated account.
Sign in through your institution
Choose this option to get remote access when outside your institution. Shibboleth/Open Athens technology is used to provide single sign-on between your institution’s website and Oxford Academic.
If your institution is not listed or you cannot sign in to your institution’s website, please contact your librarian or administrator.
Sign in with a library card
Enter your library card number to sign in. If you cannot sign in, please contact your librarian.
Society Members
Society member access to a journal is achieved in one of the following ways:
Sign in through society site
Many societies offer single sign-on between the society website and Oxford Academic. If you see ‘Sign in through society site’ in the sign in pane within a journal:
If you do not have a society account or have forgotten your username or password, please contact your society.
Sign in using a personal account
Some societies use Oxford Academic personal accounts to provide access to their members. See below.
Personal account
A personal account can be used to get email alerts, save searches, purchase content, and activate subscriptions.
Some societies use Oxford Academic personal accounts to provide access to their members.
Viewing your signed in accounts
Click the account icon in the top right to:
Signed in but can't access content
Oxford Academic is home to a wide variety of products. The institutional subscription may not cover the content that you are trying to access. If you believe you should have access to that content, please contact your librarian.
Institutional account management
For librarians and administrators, your personal account also provides access to institutional account management. Here you will find options to view and activate subscriptions, manage institutional settings and access options, access usage statistics, and more.