K562 cells

K562 cells were the first human immortalised myelogenous leukemia cell line to be established. K562 cells are of the erythroleukemia type, and the cell line is derived from a 53-year-old female chronic myelogenous leukemia patient in blast crisis.[1][2] The cells are non-adherent and rounded, are positive for the bcr:abl fusion gene, and bear some proteomic resemblance to both undifferentiated granulocytes[3] and erythrocytes.[4]

In culture they exhibit much less clumping than many other suspension lines, presumably due to the downregulation of surface adhesion molecules by bcr:abl.[5] However, another study suggests that bcr:abl over-expression may actually increase cell adherence to cell culture plastic.[6] K562 cells can spontaneously develop characteristics similar to early-stage erythrocytes, granulocytes and monocytes[7] and are easily killed by natural killer cells[8] as they lack the MHC complex required to inhibit NK activity.[2] They also lack any trace of Epstein-Barr virus and other herpesviruses. In addition to the Philadelphia chromosome they also exhibit a second reciprocal translocation between the long arm of chromosome 15 with chromosome 17.[1]

Two sub-lines are available which express MHC class-I A2[9] and A3.[10]

K562 cells are part of the NCI-60 cancer cell line panel used by the National Cancer Institute.[11]

  1. ^ a b Lozzio CB, Lozzio BB (March 1975). "Human chronic myelogenous leukemia cell-line with positive Philadelphia chromosome". Blood. 45 (3): 321–334. doi:10.1182/blood.V45.3.321.321. PMID 163658.
  2. ^ a b Drexler HG (2000). The Leukemia-Lymphoma Cell Line Factsbook. San Diego: Academic Press.
  3. ^ Klein E, Ben-Bassat H, Neumann H, Ralph P, Zeuthen J, Polliack A, Vánky F (October 1976). "Properties of the K562 cell line, derived from a patient with chronic myeloid leukemia". International Journal of Cancer. 18 (4): 421–431. doi:10.1002/ijc.2910180405. PMID 789258. S2CID 36818335.
  4. ^ Andersson LC, Nilsson K, Gahmberg CG (February 1979). "K562--a human erythroleukemic cell line". International Journal of Cancer. 23 (2): 143–147. doi:10.1002/ijc.2910230202. PMID 367973. S2CID 24886439.
  5. ^ Jongen-Lavrencic M, Salesse S, Delwel R, Verfaillie CM (March 2005). "BCR/ABL-mediated downregulation of genes implicated in cell adhesion and motility leads to impaired migration toward CCR7 ligands CCL19 and CCL21 in primary BCR/ABL-positive cells". Leukemia. 19 (3): 373–380. doi:10.1038/sj.leu.2403626. PMID 15674360.
  6. ^ Karimiani EG, Marriage F, Merritt AJ, Burthem J, Byers RJ, Day PJ (March 2014). "Single-cell analysis of K562 cells: an imatinib-resistant subpopulation is adherent and has upregulated expression of BCR-ABL mRNA and protein". Experimental Hematology. 42 (3): 183–191.e5. doi:10.1016/j.exphem.2013.11.006. PMID 24269846.
  7. ^ Lozzio BB, Lozzio CB, Bamberger EG, Feliu AS (April 1981). "A multipotential leukemia cell line (K-562) of human origin". Proceedings of the Society for Experimental Biology and Medicine. 166 (4): 546–550. doi:10.3181/00379727-166-41106. PMID 7194480. S2CID 7571401.
  8. ^ Lozzio BB, Lozzio CB (1979). "Properties and usefulness of the original K-562 human myelogenous leukemia cell line". Leukemia Research. 3 (6): 363–370. doi:10.1016/0145-2126(79)90033-X. PMID 95026.
  9. ^ Britten CM, Meyer RG, Kreer T, Drexler I, Wölfel T, Herr W (January 2002). "The use of HLA-A*0201-transfected K562 as standard antigen-presenting cells for CD8(+) T lymphocytes in IFN-gamma ELISPOT assays". Journal of Immunological Methods. 259 (1–2): 95–110. doi:10.1016/S0022-1759(01)00499-9. PMID 11730845.
  10. ^ Clark RE, Dodi IA, Hill SC, Lill JR, Aubert G, Macintyre AR, et al. (November 2001). "Direct evidence that leukemic cells present HLA-associated immunogenic peptides derived from the BCR-ABL b3a2 fusion protein" (PDF). Blood. 98 (10): 2887–2893. doi:10.1182/blood.V98.10.2887. PMID 11698267. S2CID 8529369.
  11. ^ "Cellosaurus K-562 (CVCL_0004)". Cellosaurus. SIB Swiss Institute of Bioinformatics. Retrieved 7 January 2018. Part of: NCI60 cancer cell line panel.