title: Acute myeloid leukemia cell lines MOLM-17 and MOLM-18 derived from patient with advanced myelodysplastic syndromes.
abstract: The two acute myelomonocytic leukemia sister cell lines MOLM-17 and MOLM-18 and the Epstein-Barr-virus positive non-malignant B-lymphoblastoid cell lines (B-LCLs) B422 and B423 were established from the bone marrow sample of a 60-year-old Japanese male in the advanced leukemic phase of refractory anemia with excess of blasts, a subtype of myelodysplastic syndromes (MDS). MOLM-17/-18 are proliferatively responsive to the growth factors present in the culture supernatant of the 5637 cell line. The B-LCLs are constitutively growth factor-independent. MOLM-17 and B422 were established at eight months after the initial diagnosis, while MOLM-18 and B423 were derived from a sample one month later. Immunophenotyping of the first leukemia sample revealed a mixed lineage leukemia immunophenotype with positivity for terminal deoxynucleotidyl transferase (TdT), CD13 and CD19; the second sample revealed solely myeloid characteristics with positivity for CD13, CD41 and CD61, whereas TdT was negative. MOLM-17/-18 showed immunomarker profiles typical of the myelomonocytic lineage. The karyotype analysis of MOLM-17/-18 revealed various non-random numerical and structural abnormalities including del(5)(q?), -7, der(11)add(11)(p11.2)add(11)(q23), add(17)(p11.2), add(18)(p11.2), -20, -22 as common aberrations. Treatment with tumor necrosis factor-alpha induced pronounced cellular differentiation of both cell lines into macrophage-like cells. The overall profile of MOLM-17/-18 based on their extensive immunological, cytogenetic and functional characterization suggests that these cell lines together with the paired B-LCLs B422 and B423 may represent scientifically significant in vitro models which could facilitate investigations into the pathobiology of MDS.
authors.affiliation: Fujisaki Cell Center, Hayashibara Biochemical Labs. Inc., 675-1 Fujisaki, Okayama 702-8006, Japan. yomatsuo@hayashibara.co.jp
authors.forename: Yoshinobu
authors.initials: Y
authors.lastname: Matsuo
authors.forename: Hans G
authors.initials: HG
authors.lastname: Drexler
authors.forename: Akira
authors.initials: A
authors.lastname: Harashima
authors.forename: Ayumi
authors.initials: A
authors.lastname: Okochi
authors.forename: Kensuke
authors.initials: K
authors.lastname: Kojima
authors.forename: Shoji
authors.initials: S
authors.lastname: Asakura
authors.forename: Mitsune
authors.initials: M
authors.lastname: Tanimoto
authors.forename: Kunzo
authors.initials: K
authors.lastname: Orita
mesh_terms: D045744:Cell Line, Tumor / Q000473:pathology*; D020732:Cytogenetic Analysis; D016172:DNA Fingerprinting / Q000379:methods; D005838:Genotype; D006801:Humans; D016130:Immunophenotyping; D015470:Leukemia, Myeloid, Acute / Q000235:genetics / Q000473:pathology*; D008297:Male; D008875:Middle Aged; D009190:Myelodysplastic Syndromes / Q000150:complications* / Q000473:pathology*; D012333:RNA, Messenger / Q000187:drug effects / Q000235:genetics / Q000378:metabolism; D014157:Transcription Factors / Q000187:drug effects / Q000235:genetics / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology
chemical_list: D012333:RNA, Messenger; D014157:Transcription Factors; D014409:Tumor Necrosis Factor-alpha