PMID- 12812651
OWN - NLM
STAT- MEDLINE
DCOM- 20040909
LR  - 20211203
IS  - 0376-2491 (Print)
IS  - 0376-2491 (Linking)
VI  - 83
IP  - 4
DP  - 2003 Feb 25
TI  - [Deletion of p15 and p16 genes and overexpression of STK15 gene in human 
      laryngeal squamous cell carcinoma].
PG  - 316-9
AB  - OBJECTIVE: To investigate the association of p15 and p16 genes deletion, and 
      STK15 gene overexpression with laryngeal squamous cell carcinoma (LSCC). METHODS: 
      The cancer tissue and surrounding normal tissue were taken during operation from 
      50 cases of LSCC who had undergone neither chemotherapy nor radiotherapy 
      preoperatively. DNA was extracted and PCR was used to test the homozygous 
      deletion of p15 exon 2 (p15E2) and p16 exon 2 (p16E2). RNA was extracted, cDNA 
      was synthesized by reverse transcription, and the expression of STK15 gene was 
      tested by PCR with beta-actin as inner control. At the same time the expression 
      of STK15 in human LSCC Hep-2 cell line was tested. The ratio of ADV (average 
      density value) of STK15 gene to the ADV of beta-actin gene was calculated. 
      RESULTS: The rate of p15E2 deletion was 12% (6/50) and that of p16E2 was 14% 
      (7/50). The p15E2 and p16E2 codeletion rate was 6% (3/50). In 34 of the 50 cases 
      (68%) the expression of STK15 gene in tumor tissue was higher than that of the 
      paired surrounding normal tissue with a significant difference. The ratio of ADV 
      of STK15 gene to ADV of beta-actin gene was 1.03 +/- 0.30 in the cancer tissue, 
      and 0.89 +/- 0.22 in the paired normal tissue with a significant difference (t = 
      4.333, P < 0.01). The expression of STK15 gene was higher than that of beta-actin 
      in Hep-2 cell line. CONCLUSION: The homozygous deletion of p15E2 and p16E2 and 
      overexpression of STK15 gene may play a role in the oncogenesis and malignant 
      progression of laryngeal squamous cell carcinoma.
FAU - Li, Fu-cai
AU  - Li FC
AD  - Department of Medical Genetics, China Medical University, Shenyang 110001, China. 
      fucaili@msn.com
FAU - Li, Ying-hui
AU  - Li YH
FAU - Zhao, Xu
AU  - Zhao X
FAU - Kang, Ning
AU  - Kang N
FAU - Fu, Wei-neng
AU  - Fu WN
FAU - Xu, Zhen-ming
AU  - Xu ZM
FAU - Li, Zeng-gang
AU  - Li ZG
FAU - Sun, Kai-lai
AU  - Sun KL
LA  - chi
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - China
TA  - Zhonghua Yi Xue Za Zhi
JT  - Zhonghua yi xue za zhi
JID - 7511141
RN  - 0 (CDKN2B protein, human)
RN  - 0 (Cell Cycle Proteins)
RN  - 0 (Cyclin-Dependent Kinase Inhibitor p15)
RN  - 0 (Tumor Suppressor Proteins)
RN  - EC 2.7.11.1 (AURKA protein, human)
RN  - EC 2.7.11.1 (Aurora Kinase A)
RN  - EC 2.7.11.1 (Aurora Kinases)
RN  - EC 2.7.11.1 (Protein Serine-Threonine Kinases)
SB  - IM
MH  - Aurora Kinase A
MH  - Aurora Kinases
MH  - Carcinoma, Squamous Cell
MH  - Cell Cycle Proteins/*genetics
MH  - Cyclin-Dependent Kinase Inhibitor p15
MH  - *Gene Deletion
MH  - *Genes, p16
MH  - Humans
MH  - Laryngeal Neoplasms/*genetics
MH  - Protein Serine-Threonine Kinases/*genetics
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Tumor Suppressor Proteins/*genetics
EDAT- 2003/06/19 05:00
MHDA- 2004/09/10 05:00
CRDT- 2003/06/19 05:00
PHST- 2003/06/19 05:00 [pubmed]
PHST- 2004/09/10 05:00 [medline]
PHST- 2003/06/19 05:00 [entrez]
PST - ppublish
SO  - Zhonghua Yi Xue Za Zhi. 2003 Feb 25;83(4):316-9.