KIT (CD117)-positive breast cancers are infrequent and lack KIT gene mutations.
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KIT (CD117)-positive breast cancers are infrequent and lack KIT gene mutations. / Simon, Ronald; Panussis, Soti; Maurer, Robert; Spichtin, Hanspeter; Glatz, Kathrin; Tapia, Coya; Mirlacher, Martina; Rufle, Alex; Torhorst, Joachim; Sauter, Guido.
In: CLIN CANCER RES, Vol. 10(1 Pt 1), 2004, p. 178-183.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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TY - JOUR
T1 - KIT (CD117)-positive breast cancers are infrequent and lack KIT gene mutations.
AU - Simon, Ronald
AU - Panussis, Soti
AU - Maurer, Robert
AU - Spichtin, Hanspeter
AU - Glatz, Kathrin
AU - Tapia, Coya
AU - Mirlacher, Martina
AU - Rufle, Alex
AU - Torhorst, Joachim
AU - Sauter, Guido
PY - 2004
Y1 - 2004
N2 - PURPOSE: KIT (CD117) is a transmembrane tyrosine kinase representing a target for STI571 (Glivec) therapy. Some KIT-overexpressing solid tumors have responded favorably to STI571, potentially because of the presence of KIT-activating mutations. EXPERIMENTAL DESIGN: To investigate the epidemiology of KIT overexpression and mutations, we investigated a series of 1654 breast cancers. All tumors were analyzed by immunohistochemistry in a tissue microarray format. RESULTS: KIT expression was always present in normal breast epithelium. However, cancer analysis revealed the only 43 of 1654 (2.6%) tumors were KIT-positive. KIT expression was more frequent in medullary cancer (9 of 47 positive; 19.1%) than in any other histological tumor subtype (P <0.001). KIT expression was significantly associated with high tumor grade (P <0.0001) but unrelated to pT and pN categories or patient survival. Mutation analysis of exons 2, 8, 9, 11, 13, and 17 was negative in 10 KIT-positive tumors. CONCLUSIONS: Overall, our data show that a high level of KIT expression occurs infrequently in breast cancer. KIT-positive breast cancers may not reflect "KIT up-regulation" because KIT is also expressed in normal breast epithelium. The lack of KIT mutations also argues against the therapeutic efficacy of STI571 in breast cancer.
AB - PURPOSE: KIT (CD117) is a transmembrane tyrosine kinase representing a target for STI571 (Glivec) therapy. Some KIT-overexpressing solid tumors have responded favorably to STI571, potentially because of the presence of KIT-activating mutations. EXPERIMENTAL DESIGN: To investigate the epidemiology of KIT overexpression and mutations, we investigated a series of 1654 breast cancers. All tumors were analyzed by immunohistochemistry in a tissue microarray format. RESULTS: KIT expression was always present in normal breast epithelium. However, cancer analysis revealed the only 43 of 1654 (2.6%) tumors were KIT-positive. KIT expression was more frequent in medullary cancer (9 of 47 positive; 19.1%) than in any other histological tumor subtype (P <0.001). KIT expression was significantly associated with high tumor grade (P <0.0001) but unrelated to pT and pN categories or patient survival. Mutation analysis of exons 2, 8, 9, 11, 13, and 17 was negative in 10 KIT-positive tumors. CONCLUSIONS: Overall, our data show that a high level of KIT expression occurs infrequently in breast cancer. KIT-positive breast cancers may not reflect "KIT up-regulation" because KIT is also expressed in normal breast epithelium. The lack of KIT mutations also argues against the therapeutic efficacy of STI571 in breast cancer.
M3 - SCORING: Zeitschriftenaufsatz
VL - 10(1 Pt 1)
SP - 178
EP - 183
JO - CLIN CANCER RES
JF - CLIN CANCER RES
SN - 1078-0432
ER -
