CEM/C2 (ATCC® CRL-2264)

Organism: Homo sapiens, human  /  Cell Type: T lymphoblast  /  Disease: acute lymphoblastic leukemia

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Organism Homo sapiens, human
Cell Type T lymphoblast
Product Format frozen
Morphology lymphoblast
Culture Properties suspension
Biosafety Level 1

Biosafety classification is based on U.S. Public Health Service Guidelines, it is the responsibility of the customer to ensure that their facilities comply with biosafety regulations for their own country.

Disease acute lymphoblastic leukemia
Age 4 years
Gender female
Ethnicity Caucasian
Applications
The cells are approximately 970-fold less sensitive to CPT than the parental CEM cells.
CEM/C2 cells exhibit cross resistance to both the water soluble (topotecan) and water insoluble (9-amino-CPT and 10,11-methylenedioxy-CPT) analogs of CPT.
CEM/C2 cells are also cross resistant to etoposide, dactinomycin, bleomycin, mitoxantrone, 4'-(9-acridinylamino)methanesulfon-m-anisidide, and the anthracyclines daunorubicin and doxorubicin but retain sensitivity to the Vinca alkaloid vincristine.
Storage Conditions liquid nitrogen vapor temperature
Derivation
CEM/C2 is a camptothecin (CPT) resistant derivative of the human T cell leukemia cell line CCRF-CEM (see ATCC CCL-119).
Clinical Data
female
Caucasian
4 years
Comments
CEM/C2 is a camptothecin (CPT) resistant derivative of the human T cell leukemia cell line CCRF-CEM (see ATCC CCL-119).
The cell line was selected and subcloned in 1991 for resistance to CPT.
The cells are approximately 970-fold less sensitive to CPT than the parental CEM cells.
CEM/C2 cells exhibit cross resistance to both the water soluble (topotecan) and water insoluble (9-amino-CPT and 10,11-methylenedioxy-CPT) analogs of CPT.
CEM/C2 cells are also cross resistant to etoposide, dactinomycin, bleomycin, mitoxantrone, 4'-(9-acridinylamino)methanesulfon-m-anisidide, and the anthracyclines daunorubicin and doxorubicin but retain sensitivity to the Vinca alkaloid vincristine.
CEM/C2 cells display atypical multidrug resistance (MDR), altered topoisomerase I catalytic activity and a unique topoisomerase I mutation (Asn722Ser).
Resistance to CPT is stable for up to six months.
Complete Growth Medium The base medium for this cell line is ATCC-formulated RPMI-1640 Medium, ATCC 30-2001. To make the complete growth medium, add the following components to the base medium: fetal bovine serum (ATCC 30-2020) to a final concentration of 10%.
Subculturing
Protocol: Cultures can be maintained by addition or replacement of medium. Establish new cultures at 2 X 10 exp5 viable cells/ml and maintain between 1 X 10 exp5 and 2 X 10 exp6.
Medium Renewal: Every 2 to 3 days
Cryopreservation
Freeze medium: Complete growth medium 95%; DMSO, 5%
Storage temperature: liquid nitrogen vapor temperature
Culture Conditions
Temperature: 37.0°C
STR Profile
Amelogenin: X
CSF1PO: 11
D13S317: 11,12
D16S539: 10,13
D5S818: 13
D7S820: 9,8.3
THO1: 6,7
TPOX: 8
vWA: 17,19
Population Doubling Time 30 hrs
Name of Depositor WG Harker
References

Kapoor R, et al. Altered topoisomerase I expression in two subclones of human CEM leukemia selected for resistance to camptothecin. Oncol. Res. 7: 83-95, 1995. PubMed: 7579731

Fujimori A, et al. Mutation at the catalytic site of topoisomerase I in CEM/C2, a human leukemia cell line resistant to camptothecin. Cancer Res. 55: 1339-1346, 1995. PubMed: 7882333

Notice: Necessary PermitsPermits

These permits may be required for shipping this product:

  • Customers located in the state of Hawaii will need to contact the Hawaii Department of Agriculture to determine if an Import Permit is required. A copy of the permit or documentation that a permit is not required must be sent to ATCC in advance of shipment.
Basic Documentation
References

Kapoor R, et al. Altered topoisomerase I expression in two subclones of human CEM leukemia selected for resistance to camptothecin. Oncol. Res. 7: 83-95, 1995. PubMed: 7579731

Fujimori A, et al. Mutation at the catalytic site of topoisomerase I in CEM/C2, a human leukemia cell line resistant to camptothecin. Cancer Res. 55: 1339-1346, 1995. PubMed: 7882333