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INTERSTITIAL CELLS OF CAJAL (ICC) * originally depicted by Cajal; * pacemaker (regulatory) cells of gut (intercalated between intramural neurons and smooth muscle cells); - generate electrical slow waves; * loss of ICC function implicated in diabetic gastroenteropathy, gastroenteric arrhythmia and Hirschsprung’s disease confocal micrographs showing c - Kit immunoreactivity Takayama et al Arch Histol Cytol 2002; 65: 1
ORIGIN OF GASTROINTESTINAL STROMAL TUMORS * GIST cells share several characteristics with interstitial cells of Cajal (ICC: ICC hyperplasia evident in GI tract of pts with familial GIST); - mixture of neural and myogenous features by electron microscopy; - expression of KIT (CD117) in ~ 95% of cases; → GIST and ICC arise from a common mesenchymal stem cell associated with enteric neural plexus?
Page 1: GASTROINTESTINAL STROMAL TUMORS * m
Page 5 and 6: * 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
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IMATINIB MESYLATE: BACKGROUND * sel
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IMATINIB MESYLATE MECHANISM OF ACTI
Page 63 and 64:
IMATINIB MESYLATE SPECTRUM OF ACTIV
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IMATINIB AND BCR - ABL TK IN CHRONI
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TRANSLOCATION LEADING TO PHILADELPH
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IMATINIB TARGETS IN SOLID TUMORS. I
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IMATINIB TARGETS IN SOLID TUMORS. I
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IMATINIB TARGETS IN SOLID TUMORS. V
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IMATINIB TARGETS IN SOLID TUMORS. V
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IMATINIB TARGETS IN SOLID TUMORS. X
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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
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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
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Structures of some representative s
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Imatinib blocks KIT cancer cell KIT
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SUNITINIB (SUTENT@ ): ORAL MULTI -
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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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