Genetic changes in ATM and ATR/CHEK1 as prognostic indicators in cancer
AssigneeUniversity of Pittsburgh—Of the Commonwealth System of Higher Education
InventorsSusanne M. Gollin, Rahul Atul Parikh, Xin Huang
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Abstract
The present invention relates to the discovery that, in human cancer, an 11q deletion of ATM together with an increase in ATR and CHEK1 expression correlates with resistance to ionizing radiation which could be overcome by inhibition of the ATR/CHEK1 pathway. It provides for methods of identifying patients unlikely to exhibit an adequate response to radiation therapy and/or chemotherapy who may benefit from ATR/CHEK1 pathway inhibition, as well as methods of treating said patients.
Claims12
A method of identifying a patient suffering from a head and neck squamous cell carcinoma which is likely to be refractory to radiation therapy comprising (i) identifying an 11q deletion in a patient sample considered to be representative of the head and neck squamous cell carcinoma and (ii) identifying, in the patient sample, overexpression of a gene selected from the group consisting of ATR, CHEK1, or both, wherein an 11q deletion and overexpression of ATR, CHEK1, or both, indicates that the head and neck squamous cell carcinoma is likely to be refractory to radiation therapy.
A method of identifying a patient suffering from a head and neck squamous cell carcinoma which is likely to be refractory to chemotherapy comprising (i) identifying an 11q deletion in a patient sample considered to be representative of the head and neck squamous cell carcinoma and (ii) identifying, in the patient sample, overexpression of a gene selected from the group consisting of ATR, CHEK1, or both, wherein an 11q deletion and overexpression of ATR, CHEK1, or both, indicates that the head and neck squamous cell carcinoma is likely to be refractory to chemotherapy.
Dependencies are inferred from the claim text.