Linked Life Data

16507405

Source:http://linkedlifedata.com/resource/pubmed/id/16507405

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2006-3-1
pubmed:abstractText
Mutations of oncogenes and tumor suppressor genes often lead to transformation of a normal cell to become a malignant cell. However, most malignant cells cannot grow to a clinically detectable tumor mass in the absence of blood vessels. Thus, a clinically manifested large tumor has to switch on an angiogenic phenotype to support their growth. The switch of an angiogenic phenotype may represent an imbalanced expression of angiogenic factors and antiogenesis inhibitors. Overexpression of angiogenic factors and down-regulation of angiogenesis inhibitors are both necessary and sufficient to induce new blood vessels growth, and these two processes usually occur simultaneously to switch on tumor angiogenesis. The growth of blood vessels in a malignant tumor also provides structural basis for cancer metastasis. In addition to blood vessels, many tumors have the ability to induce lymphangiogenesis, which is essential for lymphatic metastasis. In this review, I will discuss current development of antiangiogenic therapy in the treatment of cancer. I present data obtained from our own research laboratory to demonstrate antiangiogenic cancer therapy.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0753-3322
pubmed:author
pubmed:issnType
Print
pubmed:volume
59 Suppl 2
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
S340-3
pubmed:meshHeading
pubmed:year
2005
pubmed:articleTitle
Tumor angiogenesis and therapy.
pubmed:affiliation
Laboratory of Angiogenesis Research, Microbiology and Tumor Biology Center, Karolinska Institutet, Stockholm, Sweden. yihai.cao@mtc.ki.se
pubmed:publicationType
Journal Article, Review