Reference Detail

Ref Type

Journal Article

PMID

(17314276)

Authors

Hollestelle A, Elstrodt F, Nagel JH, Kallemeijn WW, Schutte M

Title

Phosphatidylinositol-3-OH kinase or RAS pathway mutations in human breast cancer cell lines.

Journal	Vol	Issue	Date	Pages	Journal Short Title
Molecular cancer research : MCR	5	2	2007 Feb	195-201	Mol Cancer Res

URL

Abstract Text

Constitutive activation of the phosphatidylinositol-3-OH kinase (PI3K) and RAS signaling pathways are important events in tumor formation. This is illustrated by the frequent genetic alteration of several key players from these pathways in a wide variety of human cancers. Here, we report a detailed sequence analysis of the PTEN, PIK3CA, KRAS, HRAS, NRAS, and BRAF genes in a collection of 40 human breast cancer cell lines. We identified a surprisingly large proportion of cell lines with mutations in the PI3K or RAS pathways (54% and 25%, respectively), with mutants for each of the six genes. The PIK3CA, KRAS, and BRAF mutation spectra of the breast cancer cell lines were similar to those of colorectal cancers. Unlike in colorectal cancers, however, mutational activation of the PI3K pathway was mutually exclusive with mutational activation of the RAS pathway in all but 1 of 30 mutant breast cancer cell lines (P = 0.001). These results suggest that there is a fine distinction between the signaling activators and downstream effectors of the oncogenic PI3K and RAS pathways in breast epithelium and those in other tissues.

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Molecular Profile	Treatment Approach

Gene Name	Source	Synonyms	Protein Domains	Gene Description	Gene Role

Therapy Name	Drugs	Efficacy Evidence	Clinical Trials

Drug Name	Trade Name	Synonyms	Drug Classes	Drug Description

Gene	Variant	Impact	Protein Effect	Variant Description	Associated with drug Resistance
PIK3CA	K567R	missense	unknown	PIK3CA K567R lies within the PIK helical domain of the Pik3ca protein (UniProt.org). K567R has been identified in the scientific literature (PMID: 17314276), but has not been biochemically characterized and therefore, its effect on Pik3ca protein function is unknown (PubMed, Mar 2024).

Molecular Profile	Indication/Tumor Type	Response Type	Therapy Name	Approval Status	Evidence Type	Efficacy Evidence	References
PTEN A72fs	breast cancer	sensitive	Gedatolisib	Preclinical	Actionable	In a preclinical study, Gedatolisib (PKI-587) inhibited growth of human breast cancer cells harboring PTEN A72fs*5 in culture (PMID: 21325073, PMID: 17314276).	17314276 21325073
PIK3CA E545K	breast cancer	sensitive	Gedatolisib	Preclinical	Actionable	In a preclinical study, Gedatolisib (PKI-587) inhibited growth of human breast cancer cells harboring PIK3CA E545K in culture (PMID: 21325073, PMID: 17314276).	17314276 21325073
PIK3CA H1047R	breast cancer	sensitive	Gedatolisib	Preclinical	Actionable	In a preclinical study, Gedatolisib (PKI-587) inhibited growth of human breast cancer cells harboring PIK3CA H1047R in culture (PMID: 21325073, PMID: 17314276).	17314276 21325073