Cell lines by genetic mutation

Tumor cell lines become more powerful research models and drug discovery tools when the genetic abnormalities that drive their phenotype are known. ATCC has created a list of ATCC tumor cell lines based on the gene mutation information maintained in the Sanger Institute COSMIC database.
Lung endothelia carvalho


APC mutations lead to loss of β-catenin regulation, altered cell migration and chromosome instability. They have been implicated in colon, lung and esophageal cancers.


BRAF mutations lead to excessive cell proliferation and survival, independent of growth factors, and are commonly found in birth defects and thyroid and skin cancers.
Prostate cancer cells.jpg


CDKN2A encodes for three splice variants, two of which serve as inhibitors of CDK4-kinase. Mutations of CDKN2A are present in a wide variety of tumors.


CTNNB1 can function as an oncogene and mutations of CTNNB1 play a role in a host of cancers.
Skin cancer cells.jpg


The identification of EGFR as an oncogene has made it a direct target for the development of anticancer therapeutics.
Human colon cancer cells


Mutations in phosphatidylinositol 3-kinase (PIK3CA), encoding the p110α catalytic subunit of the class I PI3K, have been implicated in colon, lung, ovarian and breast cancer.
Human Breast Cancer cell dividing


Mutations in phosphatidylinositol 3-kinase (PIK3R1), encoding the regulatory subunit of p85, have been implicated in colon, lung, ovarian and breast cancer.
Prostate cancer cells


Mutations of PTEN gene are associated with a variety of cancers including prostate, brain, skin and breast.
Human colon cancer cells


Mutant RAS has been identified in pancreas, colon, thyroid, bladder and ovarian cancers and is predictive of a very poor response to EGFR-inhibiting drugs.
Lung cancer cell 4.jpg


The retinoblastoma (RB1) tumor suppressor gene encodes a protein that regulates cell proliferation by controlling progression through the cell cycle, specifically through the G1 checkpoint.
Pancreatic cancer cells


SMAD4, frequently inactivated in pancreas and colon cancers, is activated by serine-threonine kinases, forms DNA binding complexes and activates the transcription of DPP target genes.
Lung cancer cells 2.jpg


TP53 encodes a major tumor suppressor transcription factor, p53, which plays a significant role in regulating cellular responses to DNA damage and other genomic anomalies.