A Non-T, Non-B Human Leukemia Cell Line (NALM-1): Establishment of the Cell Line and Presence of Leukemia-Associated Antigens2

Minowada, Jun; Tsubota, Teruhiko; Greaves, MF; Walters, Thomas R.

doi:10.1093/jnci/59.1.83

Cited by 129 publications

(15 citation statements)

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“…Therefore, we examined the response to 2-DOG and imatinb in p53 wild type (Nalm-1)(33) and null (K562)(34) human CML cell lines (Figure 6E, Supplemental Figure 9). Consistent with findings from BCR-Abl-expressing murine cells, Nalm-1 cells underwent apoptosis in response to imatinib that was enhanced by addition of a sub-lethal dose of 2-DOG.…”

Section: Resultsmentioning

confidence: 99%

Aerobic Glycolysis Suppresses p53 Activity to Provide Selective Protection from Apoptosis upon Loss of Growth Signals or Inhibition of BCR-Abl

et al. 2010

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Unlike the growth factor dependence of normal cells, cancer cells can maintain growth factor-independent glycolysis and survival through expression of oncogenic kinases, such as BCR-Abl. Although targeted kinase inhibition can promote cancer cell death, therapeutic resistance develops frequently, and further mechanistic understanding is needed. Cell metabolism may be central to this cell death pathway, as we have shown that growth factor deprivation leads to decreased glycolysis that promotes apoptosis via p53 activation and induction of the proapoptotic protein Puma. Here, we extend these findings to show that elevated glucose metabolism, characteristic of cancer cells, can suppress protein kinase Cδ (PKCδ)-dependent p53 activation to maintain cell survival after growth factor withdrawal. In contrast, DNA damage-induced p53 activation was PKCδ independent and was not metabolically sensitive. Both stresses required p53 Ser 18 phosphorylation for maximal activity but led to unique patterns of p53 target gene expression, showing distinct activation and response pathways for p53 that were differentially regulated by metabolism. Consistent with oncogenic kinases acting to replace growth factors, treatment of BCR-Abl-expressing cells with the kinase inhibitor imatinib led to reduced metabolism and p53-and Puma-dependent cell death. Accordingly, maintenance of glucose uptake inhibited p53 activation and promoted imatinib resistance. Furthermore, inhibition of glycolysis enhanced imatinib sensitivity in BCR-Abl-expressing cells with wild-type p53 but had little effect on p53-null cells. These data show that distinct pathways regulate p53 after DNA damage and metabolic stress and that inhibiting glucose metabolism may enhance the efficacy of and overcome resistance to targeted molecular cancer therapies. Cancer Res; 70(20); 8066-76. ©2010 AACR.

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Section: Resultsmentioning

confidence: 99%

Aerobic Glycolysis Suppresses p53 Activity to Provide Selective Protection from Apoptosis upon Loss of Growth Signals or Inhibition of BCR-Abl

et al. 2010

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“…Cell lines Laz 221 (15), 2072, and 6972 were derived from patients with non-T cell ALL. The NALM-1 cell line was derived from a patient with lymphoid blast crisis of chronic myelocytic leukemias (16). The HL-60 cell line was developed from a patient with promyelocytic leukemia (17) and the CEM cell line was developed from a patient with a T cell lymphoblastic lymphoma (18).…”

Section: Methodsmentioning

confidence: 99%

Induction of human B cell antigens in non-T cell acute lymphoblastic leukemia.

Nadler¹,

Ritz²,

Bates³

et al. 1982

J. Clin. Invest.

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“…However, controls with pepsin-digested normal rabbit IgG were high (9%) with this line. No significant increment in staining was noted with either Ia+ B-cell lines or the lines REH and NALM-6-1 originally obtained from patients with non-T and non-B ALL (27).…”

Section: Resultsmentioning

confidence: 81%

Lymphocyte antigens in systemic lupus erythematosus: studies with heterologous antisera.

Williams¹,

Hughes²,

Snaith³

et al. 1980

J. Clin. Invest.

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A Non-T, Non-B Human Leukemia Cell Line (NALM-1): Establishment of the Cell Line and Presence of Leukemia-Associated Antigens2

Cited by 129 publications

References 0 publications

Aerobic Glycolysis Suppresses p53 Activity to Provide Selective Protection from Apoptosis upon Loss of Growth Signals or Inhibition of BCR-Abl

Aerobic Glycolysis Suppresses p53 Activity to Provide Selective Protection from Apoptosis upon Loss of Growth Signals or Inhibition of BCR-Abl

Induction of human B cell antigens in non-T cell acute lymphoblastic leukemia.

Lymphocyte antigens in systemic lupus erythematosus: studies with heterologous antisera.

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