PMID- 16931767
OWN - NLM
STAT- MEDLINE
DCOM- 20070409
LR  - 20221109
IS  - 0163-769X (Print)
IS  - 0163-769X (Linking)
VI  - 28
IP  - 1
DP  - 2007 Feb
TI  - The role of the IGF system in cancer growth and metastasis: overview and recent 
      insights.
PG  - 20-47
AB  - IGF-I receptor (IGF-IR) signaling and functions are mediated through the 
      activities of a complex molecular network of positive (e.g., type I IGF) and 
      negative (e.g., the type II IGF receptor, IGF-IIR) effectors. Under normal 
      physiological conditions, the balance between the expression and activities of 
      these molecules is tightly controlled. Changes in this delicate balance (e.g., 
      overexpression of one effector) may trigger a cascade of molecular events that 
      can ultimately lead to malignancy. In recent years, evidence has been mounting 
      that the IGF axis may be involved in human cancer progression and can be targeted 
      for therapeutic intervention. Here we review old and more recent evidence on the 
      role the IGF system in malignancy and highlight experimental and clinical studies 
      that provide novel insights into the complex mechanisms that contribute to its 
      oncogenic potential. Controversies arising from conflicting evidence on the 
      relevance of IGF-IR and its ligands to human cancer are discussed. Our review 
      highlights the importance of viewing the IGF axis as a complex multifactorial 
      system and shows that changes in the expression levels of any one component of 
      the axis, in a given malignancy, should be interpreted with caution and viewed in 
      a wider context that takes into account the expression levels, state of 
      activation, accessibility, and functionality of other interacting components. 
      Because IGF targeting for anticancer therapy is rapidly becoming a clinical 
      reality, an understanding of this complexity is timely because it is likely to 
      have an impact on the design, mode of action, and clinical outcomes of newly 
      developed drugs.
FAU - Samani, Amir Abbas
AU  - Samani AA
AD  - Department of Medicine, McGill University Health Center, Royal Victoria Hospital, 
      Room H6.25687, Pine Avenue West, Montreal, Quebec, Canada H3A 1A1.
FAU - Yakar, Shoshana
AU  - Yakar S
FAU - LeRoith, Derek
AU  - LeRoith D
FAU - Brodt, Pnina
AU  - Brodt P
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20060824
PL  - United States
TA  - Endocr Rev
JT  - Endocrine reviews
JID - 8006258
RN  - 0 (Somatomedins)
RN  - EC 2.7.10.1 (Receptor, IGF Type 1)
SB  - IM
MH  - Animals
MH  - Cell Cycle
MH  - Cell Transformation, Neoplastic
MH  - Disease Progression
MH  - Drug Resistance, Neoplasm
MH  - Humans
MH  - Models, Biological
MH  - *Neoplasm Metastasis
MH  - Neoplasms/*pathology
MH  - Protein Processing, Post-Translational
MH  - Radiation Tolerance
MH  - Receptor, IGF Type 1/physiology
MH  - Signal Transduction
MH  - Somatomedins/*physiology
RF  - 340
EDAT- 2006/08/26 09:00
MHDA- 2007/04/10 09:00
CRDT- 2006/08/26 09:00
PHST- 2006/08/26 09:00 [pubmed]
PHST- 2007/04/10 09:00 [medline]
PHST- 2006/08/26 09:00 [entrez]
AID - er.2006-0001 [pii]
AID - 10.1210/er.2006-0001 [doi]
PST - ppublish
SO  - Endocr Rev. 2007 Feb;28(1):20-47. doi: 10.1210/er.2006-0001. Epub 2006 Aug 24.