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P21/WAF1 mutation and drug resistance to paclitaxel in locally advanced breast cancer

✍ Scribed by Ranjan Chrisanthar; Stian Knappskog; Vidar Staalesen; Johan Richard Lillehaug; Per Eystein Lønning

Publisher
John Wiley and Sons
Year
2007
Tongue
French
Weight
40 KB
Volume
120
Category
Article
ISSN
0020-7136

No coin nor oath required. For personal study only.

✦ Synopsis

We read with great interest the recent article by Galmarini and colleagues in the journal. 1 The authors reported a point mutation in exon 2 of the p21 gene (WAF1, CIP1, CDKN1A), leading to a premature STOP in codon 127 and paclitaxel resistance in noncancerous epithelial breast cells. The cyclin-dependent kinase inhibitor p21 is a main effector of growth arrest induced by p53. The role of p21 in breast cancer is still unclear, particularly with respect to drug resistance. Thus, if corroborated by clinical findings, identification of p21 as a key element for response to paclitaxel would be a major breakthrough to our understanding of drug resistance.

Several groups have addressed the potential role of p21 polymorphisms as a risk factor for cancer development. 2-5 However, we are not aware of any study exploring p21 polymorphism or mutation status in relation to response to paclitaxel or other chemotherapy treatment in breast or other type of cancers in vivo.

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