CEM/C1 Human Acute Lymphoblastic Leukemia Cells

CEM/C1 is a derivative of human T-cell leukemia cell line CCRF-CEM (see ATCCCCL-119) with camptothecin resistance. In 1991, the cell line selected and subcloned the resistance to CPT. The cells showed cross resistance to the water-soluble Topotecan and the insoluble 9-amino-CPT and 10,11-methylenedioxy-CPT of CPT analogues. The sensitivity of CEM/C1 cells to CPT was 31 times lower than that of maternal CEM cells. CEM/C1 cells showed atypical multidrug resistance and conversion complement isomerase I catalytic activity. The resistance to CPT was maintained for more than 6 months. It was identified as free of mycoplasma/STR and put into storage.

Animal species/Organism human

Tissue and Cell Type Peripheral blood

Morphology:Lymphocyte like, suspended growth

Culture media and additives/Complete Growth Medium and Culture Conditions:

90% 1640 (MD0200)+10% fetal bovine serum (SD0200)+G/A (SD0038)

Complete medium: 1640 complete medium (article number: MD0201)

Gas phase: air, 95%; Carbon dioxide, 5%. Temperature: 37 ℃.

Freezing conditions: basic medium+5% DMSO+20% FBS (SD0200)

Complete cryopreservation solution: non-programmed cooling cell cryopreservation solution (low serum) (SD0001)

Note: This product is for scientific research only

PubMed=7579731

Kapoor R., Slade D.L., Fujimori A., Pommier Y., Harker W.G.

Altered topoisomerase I expression in two subclones of human CEM leukemia selected for resistance to camptothecin.

Oncol. Res. 7:83-95(1995)

PubMed=8895760

Geley S., Hartmann B.L., Hala M., Strasser-Wozak E.M.C., Kapelari K., Kofler R.

Resistance to glucocorticoid-induced apoptosis in human T-cell acute lymphoblastic leukemia CEM-C1 cells is due to insufficient glucocorticoid receptor expression.

Cancer Res. 56:5033-5038(1996)

PubMed=12068308; DOI=10.1038/nature00766

Davies H., Bignell G.R., Cox C., Stephens P., Edkins S., Clegg S., Teague J.W., Woffendin H., Garnett M.J., Bottomley W., Davis N., Dicks E., Ewing R., Floyd Y., Gray K., Hall S., Hawes R., Hughes J., Kosmidou V., Menzies A., Mould C., Parker A., Stevens C., Watt S., Hooper S., Wilson R., Jayatilake H., Gusterson B.A., Cooper C., Shipley J.M., Hargrave D., Pritchard-Jones K., Maitland N.J., Chenevix-Trench G., Riggins G.J., Bigner D.D., Palmieri G., Cossu A., Flanagan A.M., Nicholson A., Ho J.W.C., Leung S.Y., Yuen S.T., Weber B.L., Seigler H.F., Darrow T.L., Paterson H., Marais R., Marshall C.J., Wooster R., Stratton M.R., Futreal P.A.

Mutations of the BRAF gene in human cancer.

Nature 417:949-954(2002)

PubMed=20215515; DOI=10.1158/0008-5472.CAN-09-3458

Rothenberg S.M., Mohapatra G., Rivera M.N., Winokur D., Greninger P., Nitta M., Sadow P.M., Sooriyakumar G., Brannigan B.W., Ulman M.J., Perera R.M., Wang R., Tam A., Ma X.-J., Erlander M., Sgroi D.C., Rocco J.W., Lingen M.W., Cohen E.E.W., Louis D.N., Settleman J., Haber D.A.

A genome-wide screen for microdeletions reveals disruption of polarity complex genes in diverse human cancers.

Cancer Res. 70:2158-2164(2010)