PMID- 25593940
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20150116
LR  - 20220317
IS  - 2296-875X (Print)
IS  - 2296-875X (Electronic)
IS  - 2296-875X (Linking)
VI  - 1
DP  - 2014
TI  - Endometriosis: a new cellular and molecular genetic approach for understanding 
      the pathogenesis and evolutivity.
PG  - 16
LID - 10.3389/fsurg.2014.00016 [doi]
LID - 16
AB  - Endometriosis is a benign disease with high prevalence in women of reproductive 
      age estimated between 10 and 15% and is associated with considerable morbidity. 
      Its etiology and pathogenesis are controversial but it is believed to involve 
      multiple genetic, environmental, immunological, angiogenic, and endocrine 
      processes. Altered expressions of growth factors, cytokines, adhesion molecules, 
      matrix metalloproteinases, and enzymes for estrogen synthesis and metabolism have 
      been frequently observed in this condition. The possibility of genetic basis of 
      endometriosis is demonstrated in studies of familial disease, in which the 
      incidence of endometriosis is higher for first-degree relatives of probands as 
      compared to controls. This review describes mainly the cellular, cytochemical, 
      cytogenetic, and molecular genetic features of endometriotic lesions and cultured 
      endometriotic cells. In attempts to identify candidate gene (s) involved in the 
      pathogenesis of endometriosis, a tissue-based approaches including conventional 
      cytogenetics (RHG-banding), loss of heterozygosity (LOH), and comparative genomic 
      hybridization (CGH) were employed. In addition to the karyotypic anomalies, 
      consistent chromosome instability was confirmed by CGH and fluorescence in situ 
      hybridization (FISH). The nature and significance of the molecular genetic 
      aberrations in relation to the locations and function of oncogenes and tumor 
      suppressor genes will be discussed. At last, a possible pathogenic role of 
      embryonic duct remnants was observed in seven female fetal reproductive tract in 
      endometriosis and may induce a discussion about the beginning of ovarian tumors 
      and malignant proliferations.
FAU - Bouquet De Joliniere, Jean
AU  - Bouquet De Joliniere J
AD  - Maternity and Surgical Department of Gynecology, HFR Hopital Cantonal Fribourg , 
      Fribourg , Switzerland ; Endodiag Research Laboratory Genopole , Evry , France.
FAU - Ayoubi, Jean Marc Bernard
AU  - Ayoubi JM
AD  - Endodiag Research Laboratory Genopole , Evry , France ; Department of Gynecologic 
      Surgery, Foch Hospital , Suresnes , France.
FAU - Gianaroli, Luca
AU  - Gianaroli L
AD  - S.I.S.Me.R. Reproductive Medicine Unit , Bologna , Italy.
FAU - Dubuisson, Jean Bernard
AU  - Dubuisson JB
AD  - Maternity and Surgical Department of Gynecology, HFR Hopital Cantonal Fribourg , 
      Fribourg , Switzerland.
FAU - Gogusev, Jean
AU  - Gogusev J
AD  - Endodiag Research Laboratory Genopole , Evry , France ; INSERM U507, Hospital 
      Necker, Universite Paris Descartes , Paris , France.
FAU - Feki, Anis
AU  - Feki A
AD  - Maternity and Surgical Department of Gynecology, HFR Hopital Cantonal Fribourg , 
      Fribourg , Switzerland.
LA  - eng
PT  - Journal Article
DEP - 20140527
PL  - Switzerland
TA  - Front Surg
JT  - Frontiers in surgery
JID - 101645127
PMC - PMC4286973
OTO - NOTNLM
OT  - chromosome
OT  - comparative genomic hybridization
OT  - embryonic duct remnants
OT  - endometriosis
OT  - fluorescence in situ hybridization
OT  - permanent cell line
EDAT- 2015/01/17 06:00
MHDA- 2015/01/17 06:01
PMCR- 2014/05/27
CRDT- 2015/01/17 06:00
PHST- 2013/11/22 00:00 [received]
PHST- 2014/05/02 00:00 [accepted]
PHST- 2015/01/17 06:00 [entrez]
PHST- 2015/01/17 06:00 [pubmed]
PHST- 2015/01/17 06:01 [medline]
PHST- 2014/05/27 00:00 [pmc-release]
AID - 10.3389/fsurg.2014.00016 [doi]
PST - epublish
SO  - Front Surg. 2014 May 27;1:16. doi: 10.3389/fsurg.2014.00016. eCollection 2014.