PMID- 19475528
OWN - NLM
STAT- MEDLINE
DCOM- 20090819
LR  - 20221207
IS  - 1699-5848 (Electronic)
IS  - 0213-3911 (Linking)
VI  - 24
IP  - 7
DP  - 2009 Jul
TI  - Analysis of gene status in cervical dysplastic lesions and squamous cell 
      carcinoma using tissue microarrays.
PG  - 821-9
LID - 10.14670/HH-24.821 [doi]
AB  - Cervical displasia are classified as CIN-I, CIN-II and CIN-III. It has been 
      observed that in at least 60% of CIN-I and CIN-II, the pathology disappears 
      spontaneously, while around 30% persist at 24 months, 10% progress to CIN-III and 
      1% develops as a SCC. The factors involved in the evolution of the pathology are 
      not defined, although infection of HPV is a necessary condition, but not the only 
      one. For this reason, the identification of genetic changes is an essential 
      element for understanding the carcinogenic process. It can also serve as a 
      helpful tool for identifying patients who may be susceptible to its evolution and 
      treatment, from patients whose lesions could regress spontaneous and for whom 
      periodic follow-ups would be enough. Fifty three cervical biopsies from patients 
      with dysplasia and ISCC were included in the study. These biopsies were set into 
      nine macroarrays. Eight genes and five proteins were examined in each samples 
      (hTERT, PIK3CA, hTERC, MYC, CCND1, BCL2, ZNF217 and p16) by fluorescence in situ 
      hybridization (FISH) and/or immunohistochemistry (IHC). The results reflected 
      that the genetic alterations of PIK3CA, ZNF217 and CCND1 were associated with the 
      evolution of normal tissue to CIN I, those of hTERC and ERBB with the evolution 
      of LSIL to HSIL, those of hTERT and MYC with the evolution of CIN-II/CIN-III to 
      ISCC, and those of BCL-2 with the inception of ISCC. With regards to proteins, 
      the expression of MYC and CCND1 in the initial stages of the illness would help 
      in the acquisition of the altered cellular phenotype.
FAU - Costa, Carlota
AU  - Costa C
AD  - Pathology Department, Cytogenetic and Molecular Biology Laboratory, Citology 
      Section, Mar Hospital, IMAS, Barcelona, Spain. 93710@imas.imim.es
FAU - Espinet, Blanca
AU  - Espinet B
FAU - Molina, Miguel A
AU  - Molina MA
FAU - Salgado, Rocio
AU  - Salgado R
FAU - Salido, Marta
AU  - Salido M
FAU - Baro, Teresa
AU  - Baro T
FAU - Fuste, Pere
AU  - Fuste P
FAU - Mancebo, Gemma
AU  - Mancebo G
FAU - Carreras, Ramon
AU  - Carreras R
FAU - Sole, Francesc
AU  - Sole F
FAU - Serrano, Sergi
AU  - Serrano S
FAU - Alameda, Francesc
AU  - Alameda F
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Spain
TA  - Histol Histopathol
JT  - Histology and histopathology
JID - 8609357
RN  - 0 (CCND1 protein, human)
RN  - 0 (Trans-Activators)
RN  - 0 (ZNF217 protein, human)
RN  - 0 (telomerase RNA)
RN  - 136601-57-5 (Cyclin D1)
RN  - 63231-63-0 (RNA)
RN  - EC 2.7.1.- (Phosphatidylinositol 3-Kinases)
RN  - EC 2.7.1.137 (Class I Phosphatidylinositol 3-Kinases)
RN  - EC 2.7.1.137 (PIK3CA protein, human)
RN  - EC 2.7.7.49 (TERT protein, human)
RN  - EC 2.7.7.49 (Telomerase)
SB  - IM
MH  - Biopsy
MH  - Carcinoma, Squamous Cell/*genetics
MH  - Case-Control Studies
MH  - Class I Phosphatidylinositol 3-Kinases
MH  - Cyclin D1/genetics
MH  - Disease Progression
MH  - Female
MH  - *Genes
MH  - Genes, bcl-2
MH  - Genes, erbB-2
MH  - Genes, myc
MH  - Humans
MH  - Immunohistochemistry
MH  - In Situ Hybridization, Fluorescence
MH  - Oligonucleotide Array Sequence Analysis/*methods
MH  - Phosphatidylinositol 3-Kinases/genetics
MH  - RNA/genetics
MH  - Telomerase/genetics
MH  - Trans-Activators/genetics
MH  - Uterine Cervical Dysplasia/*genetics
EDAT- 2009/05/29 09:00
MHDA- 2009/08/20 09:00
CRDT- 2009/05/29 09:00
PHST- 2009/05/29 09:00 [entrez]
PHST- 2009/05/29 09:00 [pubmed]
PHST- 2009/08/20 09:00 [medline]
AID - 10.14670/HH-24.821 [doi]
PST - ppublish
SO  - Histol Histopathol. 2009 Jul;24(7):821-9. doi: 10.14670/HH-24.821.