Genomic Profiling Shows Increased Glucose Metabolism in Luminal B Breast Cancer.
10.4048/jbc.2013.16.3.342
- Author:
Shigeto UEDA
1
;
Toshiaki SAEKI
;
Hideki TAKEUCHI
;
Takashi SHIGEKAWA
;
Kazuo MATSUURA
;
Noriko NAKAMIYA
;
Hiroshi SANO
;
Hiroko SHIMADA
;
Eiko HIROKAWA
;
Akihiko OSAKI
Author Information
1. Department of Breast Oncology, International Medical Center, Saitama Medical School, Saitama, Japan. syueda@saitama-med.ac.jp
- Publication Type:Brief Communication
- Keywords:
Breast neoplasms;
Estrogen receptor;
Fluorodeoxyglucose positron emission tomography;
Glucose metabolism
- MeSH:
Breast;
Breast Neoplasms;
Estrogens;
Glucose;
Humans;
Phenobarbital;
Positron-Emission Tomography;
Receptors, Progesterone
- From:Journal of Breast Cancer
2013;16(3):342-344
- CountryRepublic of Korea
- Language:English
-
Abstract:
We had previously reported a close association between pathological response and the maximum tumor standardized uptake value (SUVmax) measured by 18F-fluorodeoxyglucose positron emission tomography prior to chemotherapy in estrogen receptor (ER)-positive breast cancer. We hypothesized that glucose hypermetabolism by luminal B tumors may result in chemotherapy responsiveness. Using a single-gene expression assay, TargetPrint(R) (Agendia) and a 70-gene expression classifier, MammaPrint(R) (Agendia), we divided 20 patients with ER-positive primary breast cancer into luminal A and luminal B subtypes and compared the tumor SUVmax value between the two groups. A significantly higher SUVmax was measured for luminal B tumors (n=10; mean+/-SD, 7.6+/-5.6) than for luminal A tumors (n=10; mean+/-SD, 2.6+/-1.2; p=0.01). Glucose hypermetabolism could help predict intrinsic subtyping and chemotherapy responsiveness as a supplement to ER, progesterone receptor, HER2, and Ki-67 histochemical scores.
