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Titolo:
Molecular clonality of in-transit melanoma metastasis
Autore:
Nakayama, T; Taback, B; Turner, R; Morton, DL; Hoon, DSB;
Indirizzi:
John Wayne Canc Inst, Dept Mol Oncol, Santa Monica, CA 90404 USA John Wayne Canc Inst Santa Monica CA USA 90404 Santa Monica, CA 90404 USA St Johns Hlth Ctr, Dept Pathol, Santa Monica, CA USA St Johns Hlth Ctr Santa Monica CA USA Dept Pathol, Santa Monica, CA USA
Titolo Testata:
AMERICAN JOURNAL OF PATHOLOGY
fascicolo: 4, volume: 158, anno: 2001,
pagine: 1371 - 1378
SICI:
0002-9440(200104)158:4<1371:MCOIMM>2.0.ZU;2-W
Fonte:
ISI
Lingua:
ENG
Soggetto:
CUTANEOUS MALIGNANT-MELANOMA; HOMOZYGOUS DELETIONS; TUMOR PROGRESSION; MAJOR AMPUTATION; 1ST RECURRENCE; STAGE-I; HETEROZYGOSITY; REGION; PERFUSION; GENETICS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
30
Recensione:
Indirizzi per estratti:
Indirizzo: Hoon, DSB John Wayne Canc Inst, Dept Mol Oncol, 2200 Santa Monica Blvd, Santa Monica, CA 90404 USA John Wayne Canc Inst 2200 Santa Monica Blvd Santa Monica CA USA 90404
Citazione:
T. Nakayama et al., "Molecular clonality of in-transit melanoma metastasis", AM J PATH, 158(4), 2001, pp. 1371-1378

Abstract

In-transit melanoma is characterized by an aggressive pattern of recurrence that is associated with a poorer prognosis. Because in-transit melanoma is considered to result from the intralymphatic trapping of melanoma cells between the primary tumor and regional lymph nodes, it provides an excellentmodel to assess genetic events associated with early metastasis, The hypothesis of this study was to determine whether in-transit metastases are clonal in origin and therefore, may have specific genetic alterations uniquely associated with this disease and the development of early metastasis, This was assessed using loss of heterozygosity (LOH) analysis for specific DNA microsatellite loci. Seventy-nine paraffin-embedded in-transit melanoma lesions from 25 patients (range, 2 to 9 lesions per patient; average, 3.4 lesions per patient) were assessed for LOH using eight microsatellite DNA markers on six chromosomes. In 19 of 25 patients (76%) LOH was demonstrated for at least one marker. The most frequent microsatellite marker demonstrating IX)H was D9S157 (56%). Using LOH microsatellite markers to assess intertumorheterogeneity, six of 79 tumors (7.6%) demonstrated different profiles when compared to other lesions from the same patient, In-transit metastases from those patients demonstrating intertumor heterogeneity were further assessed using Laser capture microdissection and DNA analysis, and revealed no significant intratumor heterogeneity, In conclusion, LOH was frequently observed in in-transit melanoma metastasis, Based on LOH analysis, in-transit metastases are clonal in origin The establishment of clinically successful in-transit melanoma metastasis requires specific genetic events that seem tobe unique and homogeneous for each patient.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 01/12/20 alle ore 00:27:52