PMID- 11166915
OWN - NLM
STAT- MEDLINE
DCOM- 20010329
LR  - 20190720
IS  - 0304-3835 (Print)
IS  - 0304-3835 (Linking)
VI  - 164
IP  - 1
DP  - 2001 Mar 10
TI  - Human neuroblastomas with unfavorable biologies express high levels of 
      brain-derived neurotrophic factor mRNA and a variety of its variants.
PG  - 51-60
AB  - The expression of human brain-derived neurotrophic factor (BDNF) was investigated 
      in 16 primary human neuroblastomas with favorable biologies, 15 with unfavorable 
      biologies, and in human neuroblastoma cell lines. We demonstrated higher 
      expressions of human BDNF mRNA in neuroblastomas with unfavorable biologies and 
      with N-myc amplification than in those with favorable biologies. For the first 
      time we revealed the composition of splice variants of human BDNF mRNA and 
      analyzed their expression in neuroblastomas by reverse transcription polymerase 
      chain reaction (RT-PCR). Interestingly, human BDNF mRNA consisted of at least six 
      isoforms, four isoforms resembling those of rat BDNF mRNA, a human-specific 
      isoform and a new isoform. The expression of four isoforms were more prominent in 
      tumors with unfavorable biologies than in those with favorable biologies 
      (P<0.05). As previously we had reported, over 80% of the primary tumors expressed 
      either the full-length form of BDNF receptor, TRKB, or a truncated form of TRKB 
      lacking the tyrosine kinase domain. The full-length TRKB was predominantly 
      detected in tumors with unfavorable biologies, and the truncated one in those 
      with favorable biologies. These results suggest that an autocrine and/or 
      paracrine mechanism involving BDNF may stimulate signal transduction via TRKB 
      receptors rich in neuroblastomas with unfavorable biologies, resulting in an 
      aberrant survival of tumor cells.
FAU - Aoyama, M
AU  - Aoyama M
AD  - Department of Pediatrics, Nagoya City University Medical School, Mizuho-ku, 
      467-8601, Nagoya, Japan. ao.mine@med.nagoya-cu.ac.jp
FAU - Asai, K
AU  - Asai K
FAU - Shishikura, T
AU  - Shishikura T
FAU - Kawamoto, T
AU  - Kawamoto T
FAU - Miyachi, T
AU  - Miyachi T
FAU - Yokoi, T
AU  - Yokoi T
FAU - Togari, H
AU  - Togari H
FAU - Wada, Y
AU  - Wada Y
FAU - Kato, T
AU  - Kato T
FAU - Nakagawara, A
AU  - Nakagawara A
LA  - eng
SI  - GENBANK/E05935
SI  - GENBANK/X67106
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Ireland
TA  - Cancer Lett
JT  - Cancer letters
JID - 7600053
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (DNA, Complementary)
RN  - 0 (Protein Isoforms)
RN  - 0 (Proto-Oncogene Proteins c-myc)
RN  - 0 (RNA, Messenger)
SB  - IM
MH  - Age Factors
MH  - Alternative Splicing
MH  - Amino Acid Sequence
MH  - Animals
MH  - Base Sequence
MH  - Brain-Derived Neurotrophic Factor/*biosynthesis
MH  - DNA, Complementary/metabolism
MH  - Exons
MH  - Humans
MH  - Infant
MH  - Infant, Newborn
MH  - Molecular Sequence Data
MH  - Neuroblastoma/*metabolism
MH  - Protein Isoforms
MH  - Proto-Oncogene Proteins c-myc/biosynthesis
MH  - RNA, Messenger/*metabolism
MH  - Rats
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Sequence Homology, Amino Acid
MH  - Signal Transduction
MH  - Tumor Cells, Cultured
EDAT- 2001/02/13 11:00
MHDA- 2001/04/03 10:01
CRDT- 2001/02/13 11:00
PHST- 2001/02/13 11:00 [pubmed]
PHST- 2001/04/03 10:01 [medline]
PHST- 2001/02/13 11:00 [entrez]
AID - S0304383500007151 [pii]
AID - 10.1016/s0304-3835(00)00715-1 [doi]
PST - ppublish
SO  - Cancer Lett. 2001 Mar 10;164(1):51-60. doi: 10.1016/s0304-3835(00)00715-1.