PMID- 7539029
OWN - NLM
STAT- MEDLINE
DCOM- 19950628
LR  - 20220317
IS  - 0741-5400 (Print)
IS  - 0741-5400 (Linking)
VI  - 57
IP  - 5
DP  - 1995 May
TI  - Role of C-X-C chemokines as regulators of angiogenesis in lung cancer.
PG  - 752-62
AB  - Lung cancer is the leading cause of malignancy-related mortality in the U.S. and 
      is predicted to increase over the remainder of this decade. Despite attempts to 
      advance early diagnosis and use combination therapies, the clinical response of 
      this cancer yields an overall 5-year survival rate of less than 15%. Clearly, new 
      strategies for therapy are indicated. Although carcinogenesis is complex, tumor 
      growth beyond 1-2 mm3 is dependent on angiogenesis. One of the potential 
      mechanisms that allows for tumorigenesis is dysregulation of the balance of 
      angiogenic and angiostatic factors that favors net neovascularization within the 
      primary tumor. Numerous studies have investigated the role of a variety of 
      molecules in the regulation of angiogenesis. Recently, interleukin-8 (IL-8), a 
      member of the C-X-C chemokine family, has been found to be an angiogenic factor. 
      In contrast, platelet factor 4 (PF4), another C-X-C chemokine, has been shown to 
      have angiostatic properties. It is interesting that the major structural 
      difference between IL-8 and PF4 is the presence of the NH2-terminal ELR 
      (Glu-Leu-Arg) motif that precedes the first cysteine amino acid residue of IL-8 
      and is important in ligand/receptor interactions. We hypothesize that 
      angiogenesis associated with tumorigenesis is dependent on members of the C-X-C 
      chemokine family acting as either angiogenic or angiostatic factors. This 
      paradigm predicts that the biological balance in the expression of these C-X-C 
      chemokines dictates whether the neoplasm grows and develops metastatic potential 
      or regresses. In this review we discuss our recent laboratory findings that 
      support this contention and suggest that further elucidation of the biology of 
      C-X-C chemokines in the context of neovascularization of nonsmall cell lung 
      cancer will permit novel targeted therapy aimed specifically at attenuating tumor 
      growth and metastasis.
FAU - Strieter, R M
AU  - Strieter RM
AD  - University of Michigan Medical School, Department of Internal Medicine (Division 
      of Pulmonary and Critical Medicine), Ann Arbor 48109-0360, USA.
FAU - Polverini, P J
AU  - Polverini PJ
FAU - Arenberg, D A
AU  - Arenberg DA
FAU - Walz, A
AU  - Walz A
FAU - Opdenakker, G
AU  - Opdenakker G
FAU - Van Damme, J
AU  - Van Damme J
FAU - Kunkel, S L
AU  - Kunkel SL
LA  - eng
GR  - CA66180/CA/NCI NIH HHS/United States
GR  - HL02401/HL/NHLBI NIH HHS/United States
GR  - HL50057/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PT  - Review
PL  - England
TA  - J Leukoc Biol
JT  - Journal of leukocyte biology
JID - 8405628
RN  - 0 (Chemokine CXCL10)
RN  - 0 (Chemokines, CXC)
RN  - 0 (Cytokines)
RN  - 0 (Growth Inhibitors)
RN  - 0 (Interleukin-8)
RN  - 37270-94-3 (Platelet Factor 4)
SB  - IM
MH  - Amino Acid Sequence
MH  - Animals
MH  - Carcinoma, Non-Small-Cell Lung/blood supply
MH  - Chemokine CXCL10
MH  - *Chemokines, CXC
MH  - Cytokines/*physiology
MH  - Growth Inhibitors/physiology
MH  - Humans
MH  - Interleukin-8/*physiology
MH  - Lung Neoplasms/*blood supply
MH  - Mice
MH  - Mice, SCID
MH  - Molecular Sequence Data
MH  - *Neovascularization, Pathologic
MH  - Platelet Factor 4/physiology
MH  - Wound Healing
RF  - 138
EDAT- 1995/05/01 00:00
MHDA- 1995/05/01 00:01
CRDT- 1995/05/01 00:00
PHST- 1995/05/01 00:00 [pubmed]
PHST- 1995/05/01 00:01 [medline]
PHST- 1995/05/01 00:00 [entrez]
AID - 10.1002/jlb.57.5.752 [doi]
PST - ppublish
SO  - J Leukoc Biol. 1995 May;57(5):752-62. doi: 10.1002/jlb.57.5.752.