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STRUCTURE OF KIT RECEPTOR (STEM CELL FACTOR, SCF, RECEPTOR) * receptor tyrosine kinase; * extracellular domain binds ligand = stem cell factor (SCF); * intracellular domain: - 2 tyrosine kinase domains; - multiple auto - phosphorylation sites Taylor and Metcalfe, Hematol Oncol Clin North Am 2000; 14: 517 − SCF binding site − 5 IgG domains cell membrane tyrosine kinase domains
* KIT kinase intracellular domain activates substrate proteins by phosphorylation; - activated substrates initiate a signaling cascade culminating in cell proliferation and survival → downstream effects of SCF binding to KIT = proliferative and antiapoptotic KIT SIGNALING kinase domains ADP P P P P ATP substrate P P effector P SIGNALING Savage and Antman NEJM 2002; 346: 683 Scheijen and Griffin Oncogene 2002; 21: 3314
Page 1 and 2: GASTROINTESTINAL STROMAL TUMORS * m
Page 3: ORIGIN OF GASTROINTESTINAL STROMAL
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 and 70:
IMATINIB TARGETS IN SOLID TUMORS. I
Page 71 and 72:
IMATINIB TARGETS IN SOLID TUMORS. I
Page 73 and 74:
IMATINIB TARGETS IN SOLID TUMORS. V
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IMATINIB TARGETS IN SOLID TUMORS. V
Page 77 and 78:
IMATINIB TARGETS IN SOLID TUMORS. X
Page 79 and 80:
Page 81 and 82:
Page 83 and 84:
% of total IMATINIB TARGETS IN SOLI
Page 85 and 86:
Page 87 and 88:
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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