KIT (CD117)-Positive Breast Cancers Are Infrequent and Lack KIT Gene Mutations

Simon, Ronald; Panussis, S.; Maurer, Robert; Spichtin, Hanspeter; Glatz, Kathrin; Tapia, Coya; Mirlacher, Martina; Rufle, Alex; Torhorst, J.; Sauter, Guido

doi:10.1158/1078-0432.ccr-0597-3

Cited by 96 publications

(56 citation statements)

References 53 publications

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“…The striking link of high Cdc7 expression rate with medullary or medullary-like breast carcinomas constitutes another argument in favor of a biologic uniqueness of this rare subtype of breast cancer. Expression of other relevant proteins like KIT, cytokeratin 5/6, p63, or EGFR has been associated with the medullary phenotype of breast cancer before [21,22].…”

Section: Discussionmentioning

confidence: 99%

Overexpression of cell division cycle 7 homolog is associated with gene amplification frequency in breast cancer

et al. 2010

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Section: Discussionmentioning

confidence: 99%

Overexpression of cell division cycle 7 homolog is associated with gene amplification frequency in breast cancer

et al. 2010

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“…Soft tissue tumours other than GIST and germinal cell tumours are rarely KIT-positive [16]. KIT expression has also been reported in melanocytic tumours [17] and carcinomas of the lung [18], ovarium [19], breast [20], colon [21], prostate [22] and kidney [23].…”

Section: Introductionmentioning

confidence: 99%

KIT protein expression and mutational status of KIT gene in pituitary adenomas

et al. 2012

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KIT protein expression and mutational status of KIT gene in different types of tumours have been intensively studied since Imatinib Mesylate, KIT/PDGFRA tyrosine kinase inhibitor became available. However, only one immunohistochemical study on KIT expression in pituitary adenomas has been published. There are currently no reports on mutational status of KIT gene in pituitary adenomas. We have immunohistochemically investigated KIT expression in 252 pituitary adenomas and found cytoplasmic reactivity in 52.4% and membranous reactivity in 8.3% of all adenomas. There was statistically significant difference in KIT expression between clinically non-functioning, growth hormone- and adrenocorticotroph hormone-producing adenomas. The group with membranous expression was dominated by somatotropinomas and clinically non-functioning adenomas. KIT expression in a subset of adenomas was also confirmed by western blot analysis of 48 adenomas. Immunohistochemical KIT expression was correlated with basic clinical data and in a cohort of acromegalic patients with additional data (somatostatin receptor type 2A expression, response to somatostatin analogue treatment and mutational status of gsp oncogene). Exons 9, 11, 13 and 17 of KIT gene were searched for mutations in the tumours with membranous KIT expression and in a minority of tumours with cytoplasmic KIT expression using denaturing high-performance liquid chromatography and in suspected cases sequencing of one or more exons. No mutations in the examined exons were found. Our results may suggest a role of KIT in the pathogenesis of a subset of pituitary adenomas and point out the need for further research to find out if KIT-reactive adenomas could be sensitive to Imatinib Mesylate.

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“…In fact, the presence of activating mutations in specific exons of c-kit are associated with a greater response to imatinib therapy in KIT-positive GISTs [22]. Most recently, the results of a large retrospective study have shown that of 1654 cases of breast cancer tested for KIT expression by IHC on archived tissues, only 43 cases (2.6%) had detectable protein; 10 of 10 KIT-positive cases also tested negative for known activating gene mutations [23]. Hence, it seems unlikely that drugs targeting this pathway would be of major clinical importance in breast cancer.…”

Section: Discussionmentioning

confidence: 99%