title: Gene expression in primary, metastatic and recurrent lesions of endometrial cancer.
abstract: Seventeen patients with endometrial cancer were studied. Tissues of primary (P) and metastatic (M) lesions were obtained from 8 patients and complete sets of P, M and Recurrent (R) lesions were obtained from 9 patients during a follow-up period of 1-10 years. Expressions of estrogen receptors, progesterone receptors, multidrug resistance protein-1, multidrug resistance-related protein, c-erbB-2, membrane-type metalloproteinase, human telomerase RNA, human telomerase reverse transcriptase RNA, E-cadherin and autocrine motility factor receptor were studied by RT-PCR. Also, telomeric restriction fragment length (TRFL) and microsatellite instability were determined between P, M and R. The results indicate that there are significant differences in the gene expression frequency during tumor progression. The mismatch rate ranged from 0 to 47.1% between P and M and from 14.3% to 66.7% between P and R, respectively. The TRFL analysis showed a marked reduction in P and M (P vs. M: 8.2 +/- 0.9 vs. 5.6 +/- 0.4 kb, mean +/-SEM, n = 9, p = 0.002 by paired Student's t test). The length further decreased in R (P vs. R: 8.2 +/- 0.9 vs. 3.2 +/- 0.7, p = 0.01, M vs. R: 5.6 +/- 0.4 vs. 3.2 +/- 0.7, p = 0.005). The genomic instability/replication error was tested by AluI arbitrary primed polymerase chain reaction (AP-PCR). Five out of 17 patients showed an altered replication error pattern (29.4%). The mean number of abnormal AluI AP-PCR patterns in M and R compared to the P was 1.5 (M) and 4 (R). The difference between the P and R was statistically significant (p < 0.04). The present data indicate that biological behavior of cancer cells in P, M and R may differ significantly.
authors.affiliation: Department of Obstetrics and Gynecology, Nihon University School of Medicine, Tokyo, Japan. sakamoto@med.nihon-u.ac.jp
authors.forename: H
authors.initials: H
authors.lastname: Sakamoto
authors.forename: K
authors.initials: K
authors.lastname: Kinoshita
authors.forename: Y
authors.initials: Y
authors.lastname: Nakayama
authors.forename: T
authors.initials: T
authors.lastname: Takami
authors.forename: K
authors.initials: K
authors.lastname: Ohtani
authors.forename: S
authors.initials: S
authors.lastname: Izuka
authors.forename: K
authors.initials: K
authors.lastname: Satoh
mesh_terms: D020168:ATP Binding Cassette Transporter, Subfamily B, Member 1 / Q000235:genetics; D000328:Adult; D000368:Aged; D015820:Cadherins / Q000235:genetics; D004261:DNA Replication; D016889:Endometrial Neoplasms / Q000378:metabolism*; D005260:Female; D015870:Gene Expression; D006801:Humans; D020782:Matrix Metalloproteinases / Q000235:genetics; D053504:Matrix Metalloproteinases, Membrane-Associated; D008666:Metalloendopeptidases; D008875:Middle Aged; D009362:Neoplasm Metastasis; D009364:Neoplasm Recurrence, Local; D016133:Polymerase Chain Reaction; D018719:Erb-b2 Receptor Tyrosine Kinases / Q000235:genetics; D060285:Receptors, Autocrine Motility Factor; D018121:Receptors, Cytokine / Q000235:genetics; D011960:Receptors, Estrogen / Q000235:genetics; D011980:Receptors, Progesterone / Q000235:genetics; D019098:Telomerase / Q000235:genetics; D044767:Ubiquitin-Protein Ligases
chemical_list: D020168:ATP Binding Cassette Transporter, Subfamily B, Member 1; D015820:Cadherins; D020782:Matrix Metalloproteinases; D053504:Matrix Metalloproteinases, Membrane-Associated; D008666:Metalloendopeptidases; D018719:Erb-b2 Receptor Tyrosine Kinases; D060285:Receptors, Autocrine Motility Factor; D018121:Receptors, Cytokine; D011960:Receptors, Estrogen; D011980:Receptors, Progesterone; D019098:Telomerase; D044767:Ubiquitin-Protein Ligases; C555000:AMFR protein, human