(GISTs), in

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IMATINIB TARGETS IN SOLID TUMORS. III. ABNORMAL C - KIT IN GIST * point mutations in c - kit → ligand - independent constitutive activation of c - kit in gastro - intestinal stromal tumors (GIST) and other tumors; - in GIST, mutations of c - kit in juxta - membrane domain (exon 11) in ~ 60% of cases [mutations also occur in extracellular domain (exon 9) and in more distal phosphokinase domain (exon 13)]
IMATINIB TARGETS IN SOLID TUMORS. IV. ABNORMAL C - KIT IN GIST AND OTHER TUMORS * sites of activating mutations of KIT associated with human cancers (arrows); - mutations of either extracellular or intracellular (kinase and non - kinase domains) can result in ligand - independent activation of KIT kinase activity
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GASTROINTESTINAL STROMAL TUMORS * m
Page 3 and 4:
ORIGIN OF GASTROINTESTINAL STROMAL
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* KIT kinase intracellular domain a
Page 7 and 8:
CLINICAL PRESENTATION. I. * anywher
Page 9 and 10:
PATHOLOGY
Page 11 and 12:
PATHOLOGY. II. spindle cell epithel
Page 13 and 14:
PATHOLOGY. IV. Historical classific
Page 15 and 16:
Courtesy of Dr C Corless PATHOLOGY.
Page 17 and 18:
PATHOLOGY. VIII. Assessing malignan
Page 19 and 20: Estimated proportion surviving 1.0
Page 21 and 22: DIAGNOSIS
Page 23 and 24: Initial workup for suspected or est
Page 25 and 26: ENDOSCOPY. II. Courtesy of Dr R De
Page 27 and 28: irregular submucosal mass in fundus
Page 29 and 30: COMPUTED TOMOGRAPHY. I. * diagnosis
Page 31 and 32: hepatic metastasis (hyperdense enha
Page 33 and 34: 18 FDG - PET IMAGING. II. large hep
Page 35 and 36: GIST: CT and 18 FDG - PET compariso
Page 37 and 38: TRADITIONAL TREATMENT OPTIONS
Page 39 and 40: TRADITIONAL TREATMENT. II SURGERY F
Page 41 and 42: TREATMENT. III. SURGERY OF PRIMARY
Page 43 and 44: TREATMENT. V. HEPATIC ARTERY EMBOLI
Page 45 and 46: SURGERY. VII. SURVIVAL FOLLOWING TR
Page 47 and 48: SURGERY. IX. TUMOR RESECTION AS A P
Page 49 and 50: RECEPTOR TYROSINE KINASE MUTATIONS
Page 51 and 52: TYROSINE KINASES IN CANCER. II. * 2
Page 53 and 54: NORMAL KIT RECEPTOR (STEM CELL FACT
Page 55 and 56: Signalling mechanisms controlling p
Page 57 and 58: NORMAL BIOLOGIC FUNCTION OF KIT REC
Page 59 and 60: IMATINIB MESYLATE: BACKGROUND * sel
Page 61 and 62: IMATINIB MESYLATE MECHANISM OF ACTI
Page 63 and 64: IMATINIB MESYLATE SPECTRUM OF ACTIV
Page 65 and 66: IMATINIB AND BCR - ABL TK IN CHRONI
Page 67 and 68: TRANSLOCATION LEADING TO PHILADELPH
Page 69: IMATINIB TARGETS IN SOLID TUMORS. I
Page 73 and 74: IMATINIB TARGETS IN SOLID TUMORS. V
Page 75 and 76: IMATINIB TARGETS IN SOLID TUMORS. V
Page 77 and 78: IMATINIB TARGETS IN SOLID TUMORS. X
Page 83 and 84: % of total IMATINIB TARGETS IN SOLI
Page 89 and 90: SECONDARY CYTOGENETIC CHANGES * con
Page 91 and 92: IMATINIB TARGETS IN SOLID TUMORS GI
Page 93 and 94: IMATINIB TARGETS IN SOLID TUMORS: G
Page 95 and 96: IMATINIB TARGETS IN SOLID TUMORS GI
Page 97 and 98: Structures of some representative s
Page 99 and 100: Imatinib blocks KIT cancer cell KIT
Page 101 and 102: SUNITINIB (SUTENT@ ): ORAL MULTI -
Page 103 and 104: EFFICACY AND SAFETY OF SUNITINIB IN
Page 105 and 106: Kaplan - Meier estimates of time to
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(GISTs), in

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