PIK3CA wild type and AKT1 E17K and PIK3CA H1047R knock-in MCF-7 cells

Case ID:
C12186

C12186: PIK3CA Wild Type and AKT1 E17K and PIK3CA H1047R Knock-in MCF-7 Cells

Novelty:

MCF-7 derivatives with different mutations in the phosphatidylinositol-3-kinase (PI3-kinase) pathway gene PIK3CA and AKT1.

Value Proposition:

MCF-7 is the most widely used human breast cancer cell line, and it serves as a valuable model for preclinical investigations of breast cancer biology and therapy. The most commonly used techniques to study gene function in human cell lines include transgene expression or gene knockdown using short interfering RNA technology. These methods do not allow physiologic expression of different genotypes in their normal genomic context and are subject to off-target biological effects. The MCF-7 derivatives have phosphatidylinositol-3-kinase (PI3-kinase) pathway gene PIK3CA and AKT1 in their natural genomic context. The advantages of these modified cell lines are:

• Activating mutations in PIC3CA occur in over 25% of breast cancers
• Direct comparisons of the effects of these mutations in their physiologic context on phenotypes such as tumor growth and drug sensitivity

Technical Details:

Johns Hopkins researchers have developed MCF-7 derivatives with different mutations in the phosphatidylinositol-3-kinase (PI3-kinase) pathway gene PIK3CA and AKT1. These MCF-7 derivatives were created using somatic gene targeting to replace existing E545K mutations in the oncogene PIK3CA in the MCF-7 human breast cancer cell line with the wild type PIK3CA sequence. In addition, we have used gene targeting to introduce AKT1 E17K and PIK3CA H1047R mutations in situ on an otherwise wild type background.

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Data Availability:

Under CDA/NDA

Publications/Associated Cases:

Not available at this time

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For Information, Contact:
Christine Joseph
cjoseph6@jhmi.edu
410-614-0300
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