Kit expression in spindle cell rhabdomyosarcoma can possibly create a different approach for its tumorigenesis and therapy

Diniz G., Aktas S., Ortac R., Tunakan M., Unlu I., Vergin C.

PATHOLOGY RESEARCH AND PRACTICE, cilt.202, sa.9, ss.671-677, 2006 (SCI-Expanded) identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 202 Sayı: 9
  • Basım Tarihi: 2006
  • Doi Numarası: 10.1016/j.prp.2006.04.007
  • Dergi Adı: PATHOLOGY RESEARCH AND PRACTICE
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.671-677
  • Anahtar Kelimeler: KIT expression, STI-571, spindle cell rhabdomyosarcoma, tumorigenesis, SOFT-TISSUE SARCOMAS, OF-THE-LITERATURE, C-KIT, INHIBITS PROLIFERATION, IMATINIB MESYLATE, INDUCED APOPTOSIS, IN-VITRO, TUMORS, RECEPTOR, LUNG
  • Dokuz Eylül Üniversitesi Adresli: Hayır

Özet

The use of a relatively nontoxic tyrosine kinase receptor inhibitor, imatimb mesylate (IM) (STI-571), has increasingly become a valuable therapeutic alternative in some KIT (CD117)-overexpressing neoplasms potentially because of the presence of KIT-activating mutations. As the treatment eligibility for this drug hinges on CD117 expression. KIT immunostaining has recently been widely examined in various different tumors.