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Article ; Online: Personalized therapy: prognostic factors in gastrointestinal stromal tumor (GIST).

Dematteo, Ronald P

Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract

2012 Volume 16, Issue 9, Page(s) 1645–1647

MeSH term(s)	Benzamides ; Gastrointestinal Stromal Tumors/drug therapy ; Gastrointestinal Stromal Tumors/genetics ; Gastrointestinal Stromal Tumors/secondary ; Humans ; Imatinib Mesylate ; Piperazines/therapeutic use ; Precision Medicine ; Prognosis ; Protein Kinase Inhibitors/therapeutic use ; Pyrimidines/therapeutic use
Chemical Substances	Benzamides ; Piperazines ; Protein Kinase Inhibitors ; Pyrimidines ; Imatinib Mesylate (8A1O1M485B)
Language	English
Publishing date	2012-07-03
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2012365-6
ISSN	1873-4626 ; 1934-3213 ; 1091-255X
ISSN (online)	1873-4626 ; 1934-3213
ISSN	1091-255X
DOI	10.1007/s11605-012-1944-0
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Article ; Online: Targeted therapy for cancer: the gastrointestinal stromal tumor model.

Balachandran, Vinod P / Dematteo, Ronald P

Surgical oncology clinics of North America

2013 Volume 22, Issue 4, Page(s) 805–821

Abstract: Gastrointestinal stromal tumors (GISTs) are unique tumors, arising largely due to oncogenic mutations in KIT or PDGFRA tyrosine kinases. Although surgery remains the most effective treatment, the remarkable clinical success achieved with kinase ... ...

Abstract	Gastrointestinal stromal tumors (GISTs) are unique tumors, arising largely due to oncogenic mutations in KIT or PDGFRA tyrosine kinases. Although surgery remains the most effective treatment, the remarkable clinical success achieved with kinase inhibition has made GIST one of the most successful examples of targeted therapy for the treatment of cancer. The insight gained from this approach has allowed a deeper understanding of the molecular biology driving kinase dependent cancers, and the adaptations to kinase inhibition, linking genotype to phenotype. Mutation tailored kinase inhibition with second generation TKI's, and combination immunotherapy to harness the effects of TKIs remain exciting areas of investigation.
MeSH term(s)	Animals ; Antineoplastic Agents/therapeutic use ; Gastrointestinal Stromal Tumors/drug therapy ; Humans ; Molecular Targeted Therapy ; Protein Kinase Inhibitors/therapeutic use ; Protein-Tyrosine Kinases/antagonists & inhibitors ; Signal Transduction/drug effects
Chemical Substances	Antineoplastic Agents ; Protein Kinase Inhibitors ; Protein-Tyrosine Kinases (EC 2.7.10.1)
Language	English
Publishing date	2013-07-24
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1196919-2
ISSN	1558-5042 ; 1055-3207
ISSN (online)	1558-5042
ISSN	1055-3207
DOI	10.1016/j.soc.2013.06.001
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Article ; Online: Updates on the management of gastrointestinal stromal tumors.

Bamboat, Zubin M / Dematteo, Ronald P

Surgical oncology clinics of North America

2012 Volume 21, Issue 2, Page(s) 301–316

Abstract: Despite being the most common sarcoma of the gastrointestinal tract, gastrointestinal stromal tumor (GIST) has been widely recognized as a unique entity for just over a decade. The advent of tyrosine kinase inhibitors has revolutionized the diagnosis and ...

Abstract	Despite being the most common sarcoma of the gastrointestinal tract, gastrointestinal stromal tumor (GIST) has been widely recognized as a unique entity for just over a decade. The advent of tyrosine kinase inhibitors has revolutionized the diagnosis and treatment of GIST. Although surgery remains the only chance for cure, multimodal treatment that includes molecular therapy continues to develop. Optimal management of GIST requires careful radiographic, pathologic, medical, and surgical care, emphasizing the need for a multidisciplinary approach. This review highlights recent developments in the management of GIST.
MeSH term(s)	Antineoplastic Agents/therapeutic use ; Benzamides ; Chemotherapy, Adjuvant ; Gastrointestinal Neoplasms/drug therapy ; Gastrointestinal Neoplasms/pathology ; Gastrointestinal Neoplasms/surgery ; Gastrointestinal Stromal Tumors/drug therapy ; Gastrointestinal Stromal Tumors/pathology ; Gastrointestinal Stromal Tumors/surgery ; Humans ; Imatinib Mesylate ; Mutation/genetics ; Neoplasm Metastasis ; Neoplasm Recurrence, Local/drug therapy ; Pedigree ; Piperazines/therapeutic use ; Pyrimidines/therapeutic use ; Radiotherapy, Adjuvant ; Receptor, Platelet-Derived Growth Factor alpha/genetics ; Risk Assessment
Chemical Substances	Antineoplastic Agents ; Benzamides ; Piperazines ; Pyrimidines ; Imatinib Mesylate (8A1O1M485B) ; Receptor, Platelet-Derived Growth Factor alpha (EC 2.7.10.1)
Language	English
Publishing date	2012-02-25
Publishing country	United States
Document type	Journal Article
ZDB-ID	1196919-2
ISSN	1558-5042 ; 1055-3207
ISSN (online)	1558-5042
ISSN	1055-3207
DOI	10.1016/j.soc.2011.12.004
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Article ; Online: Resection versus transplantation for early hepatocellular carcinoma: more art than science.

Turcotte, Simon / Dematteo, Ronald P

Annals of surgery

2012 Volume 256, Issue 6, Page(s) 892–893

MeSH term(s)	Carcinoma, Hepatocellular/surgery ; Early Medical Intervention ; Hepatectomy ; Humans ; Liver Neoplasms/surgery ; Liver Transplantation
Language	English
Publishing date	2012-12
Publishing country	United States
Document type	Editorial
ZDB-ID	340-2
ISSN	1528-1140 ; 0003-4932
ISSN (online)	1528-1140
ISSN	0003-4932
DOI	10.1097/SLA.0b013e318275a183
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Article ; Online: The GIST of targeted therapy for malignant melanoma.

Bello, Danielle M / Dematteo, Ronald P / Ariyan, Charlotte E

Annals of surgical oncology

2014 Volume 21, Issue 6, Page(s) 2059–2067

Abstract: The high response rates to the tyrosine kinase inhibitor imatinib in KIT-mutated gastrointestinal stromal tumors (GIST) has led to a paradigm shift in cancer treatment. In a parallel fashion, the field of melanoma is shifting with the utilization of ... ...

Abstract	The high response rates to the tyrosine kinase inhibitor imatinib in KIT-mutated gastrointestinal stromal tumors (GIST) has led to a paradigm shift in cancer treatment. In a parallel fashion, the field of melanoma is shifting with the utilization of targeted therapy to treat BRAF-mutated melanoma. We reviewed published literature in PubMed on GIST and melanoma, with a focus on both past and current clinical trials. The data presented centers on imatinib, vemurafenib, and most recently dabrafenib, targeting KIT and BRAF mutations and their outcomes in GIST and melanoma. The BRAF(V600E) melanoma mutation, like the KIT exon 11 mutation in GIST, has the highest response to therapy. High response rates with inhibition of KIT in GIST have not been recapitulated in KIT-mutated melanoma. Median time to resistance to targeted agents occurs in ~7 months with BRAF inhibitors and 2 years for imatinib in GIST. In GIST, the development of secondary mutations leads to resistance; however, there have been no similar gatekeeper mutations found in melanoma. Although surgery remains an important component of the treatment of early GIST and melanoma, surgeons will need to continue to define the thresholds and timing for operation in the setting of metastatic disease with improved targeted therapies. Combination treatment strategies may result in more successful clinical outcomes in the management of melanoma in the future.
MeSH term(s)	Antineoplastic Agents/therapeutic use ; Benzamides/adverse effects ; Benzamides/therapeutic use ; Drug Resistance, Neoplasm ; Gastrointestinal Stromal Tumors/drug therapy ; Gastrointestinal Stromal Tumors/genetics ; Humans ; Imatinib Mesylate ; Indoles/adverse effects ; Indoles/therapeutic use ; Melanoma/drug therapy ; Melanoma/genetics ; Melanoma/secondary ; Molecular Targeted Therapy ; Mutation ; Piperazines/adverse effects ; Piperazines/therapeutic use ; Proto-Oncogene Proteins B-raf/genetics ; Proto-Oncogene Proteins c-kit/genetics ; Pyrimidines/adverse effects ; Pyrimidines/therapeutic use ; Sulfonamides/adverse effects ; Sulfonamides/therapeutic use ; Vemurafenib
Chemical Substances	Antineoplastic Agents ; Benzamides ; Indoles ; Piperazines ; Pyrimidines ; Sulfonamides ; Vemurafenib (207SMY3FQT) ; Imatinib Mesylate (8A1O1M485B) ; Proto-Oncogene Proteins c-kit (EC 2.7.10.1) ; BRAF protein, human (EC 2.7.11.1) ; Proto-Oncogene Proteins B-raf (EC 2.7.11.1)
Language	English
Publishing date	2014-02-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	1200469-8
ISSN	1534-4681 ; 1068-9265
ISSN (online)	1534-4681
ISSN	1068-9265
DOI	10.1245/s10434-013-3373-z
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Article: Neoadjuvant therapy for gastrointestinal stromal tumor (GIST): racing against resistance.

Gold, Jason S / Dematteo, Ronald P

Annals of surgical oncology

2007 Volume 14, Issue 4, Page(s) 1247–1248

MeSH term(s)	Antineoplastic Agents/therapeutic use ; Benzamides ; Drug Resistance, Neoplasm ; Gastrointestinal Stromal Tumors/drug therapy ; Humans ; Imatinib Mesylate ; Neoadjuvant Therapy ; Piperazines/therapeutic use ; Pyrimidines/therapeutic use ; Stomach Neoplasms/drug therapy
Chemical Substances	Antineoplastic Agents ; Benzamides ; Piperazines ; Pyrimidines ; Imatinib Mesylate (8A1O1M485B)
Language	English
Publishing date	2007-04
Publishing country	United States
Document type	Comment ; Editorial
ZDB-ID	1200469-8
ISSN	1534-4681 ; 1068-9265
ISSN (online)	1534-4681
ISSN	1068-9265
DOI	10.1245/s10434-006-9291-6
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Article: Combined surgical and molecular therapy: the gastrointestinal stromal tumor model.

Gold, Jason S / Dematteo, Ronald P

Annals of surgery

2006 Volume 244, Issue 2, Page(s) 176–184

Abstract: Objective: This review describes the pathologic and epidemiologic features of gastrointestinal stromal tumor (GIST) as well as the contemporary management of this tumor. The integration of surgery and treatment with targeted molecular agents in the ... ...

Abstract	Objective: This review describes the pathologic and epidemiologic features of gastrointestinal stromal tumor (GIST) as well as the contemporary management of this tumor. The integration of surgery and treatment with targeted molecular agents in the treatment of GIST is highlighted. Summary background data: GIST is the most common mesenchymal tumor of the gastrointestinal tract. Its cellular origin from the interstitial cell of Cajal and distinctness from smooth muscles tumors were only recently appreciated. The discovery of the centrality of KIT proto-oncogene mutations in the pathogenesis of this tumor, and the development of imatinib mesylate, a specific inhibitor of KIT tyrosine kinase function have revolutionized the treatment of GIST. Methods: We conducted a review of the English literature on GIST. The pathology, epidemiology, diagnosis, and treatment of this tumor are summarized with particular emphasis on recent developments in the field. Results: GIST is a rare tumor that usually arises from the stomach or small intestine. It is characterized by immunohistochemical staining for KIT. Treatment of primary localized tumors is surgical. The benefit of adjuvant treatment with the KIT tyrosine kinase inhibitor imatinib is the subject of investigation. The treatment of unresectable, recurrent, or metastatic GIST is primarily imatinib treatment. The integration of surgery or ablative modalities is often employed, particularly when all disease is amenable to gross resection or destruction, or when GIST becomes resistant to imatinib. Newer tyrosine kinase inhibitors, such as sunitinib are the subject of ongoing investigation. Conclusions: The treatment paradigm for GIST has required the integration of surgery and molecular therapy and this will likely serve as a paradigm for the treatment of other solid tumors as targeted agents are developed.
MeSH term(s)	Antineoplastic Agents/therapeutic use ; Benzamides ; Gastrointestinal Neoplasms/drug therapy ; Gastrointestinal Neoplasms/surgery ; Gastrointestinal Stromal Tumors/drug therapy ; Gastrointestinal Stromal Tumors/surgery ; Humans ; Imatinib Mesylate ; Neoadjuvant Therapy ; Piperazines/therapeutic use ; Protein Kinase Inhibitors/therapeutic use ; Protein-Tyrosine Kinases/antagonists & inhibitors ; Proto-Oncogene Proteins c-kit/analysis ; Pyrimidines/therapeutic use
Chemical Substances	Antineoplastic Agents ; Benzamides ; Piperazines ; Protein Kinase Inhibitors ; Pyrimidines ; Imatinib Mesylate (8A1O1M485B) ; Protein-Tyrosine Kinases (EC 2.7.10.1) ; Proto-Oncogene Proteins c-kit (EC 2.7.10.1)
Language	English
Publishing date	2006-08
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	340-2
ISSN	1528-1140 ; 0003-4932
ISSN (online)	1528-1140
ISSN	0003-4932
DOI	10.1097/01.sla.0000218080.94145.cf
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Article: Molecular mechanisms in hepatocellular carcinoma development.

Cha, Charles / Dematteo, Ronald P

Best practice & research. Clinical gastroenterology

2005 Volume 19, Issue 1, Page(s) 25–37

Abstract: Hepatocellular carcinoma (HCC) is one of the most common cancers in the world. It usually develops in patients with chronic viral hepatitis, aflatoxin exposure, or excessive alcohol use. Most patients with HCC present with advanced disease and have a ... ...

Abstract	Hepatocellular carcinoma (HCC) is one of the most common cancers in the world. It usually develops in patients with chronic viral hepatitis, aflatoxin exposure, or excessive alcohol use. Most patients with HCC present with advanced disease and have a poor prognosis. The implementation of antiviral drugs and the availability of a vaccine for hepatitis B should help reduce the incidence of HCC. Considerable effort has now focused on unraveling the molecular pathogenesis of HCC in order to design better treatments, or to prevent the disease altogether. However, so far, the pathogenesis of HCC appears to be quite heterogeneous among patients. In particular, several mechanisms of tumorigenesis seem to be involved, including loss of tumor suppressor gene function, oncogene activation, direct viral effects, DNA methylation, and angiogenesis. It is not clear which events are critical in tumor initiation versus tumor progression. RNA expression arrays and proteomics hold promise to provide further clues about this common and complex cancer.
MeSH term(s)	Carcinoma, Hepatocellular/genetics ; DNA Methylation ; DNA Mutational Analysis ; DNA, Viral/physiology ; Gene Expression Regulation ; Genes, Tumor Suppressor/physiology ; Hepatitis B virus/pathogenicity ; Hepatitis B virus/physiology ; Humans ; Liver Neoplasms/genetics ; Loss of Heterozygosity
Chemical Substances	DNA, Viral
Language	English
Publishing date	2005-02
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	2048181-0
ISSN	1521-6918
ISSN	1521-6918
DOI	10.1016/j.bpg.2004.11.005
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Article ; Online: Invasive central venous monitoring during hepatic resection: unnecessary for most patients.

O'Connor, David C / Seier, Kenneth / Gonen, Mithat / McCormick, Patrick J / Correa-Gallego, Camilo / Parker, Benjamin / Weiser, Emily / Balachandran, Vinod P / Dematteo, Ronald P / D'Angelica, Michael / Kingham, Peter T / Allen, Peter J / Drebin, Jeffrey A / Jarnagin, William R / Fischer, Mary E

HPB : the official journal of the International Hepato Pancreato Biliary Association

2020 Volume 22, Issue 12, Page(s) 1732–1737

Abstract: Background: Low central venous pressure (LCVP) anesthesia reduces blood loss during hepatic resection and historically has required a central venous catheter (CVC) for intra-operative monitoring. The aim of this study was to assess the effect of an ... ...

Abstract	Background: Low central venous pressure (LCVP) anesthesia reduces blood loss during hepatic resection and historically has required a central venous catheter (CVC) for intra-operative monitoring. The aim of this study was to assess the effect of an evolution of practice to CVP monitoring without CVC on the perioperative outcomes after liver resection. Methods: A retrospective study of partial hepatectomy patients from 2007 to 2016 who were over 18 years of age was performed. Results: Of 3903 patients having partial hepatectomy, 2445 (62%) met inclusion criteria, and 404 (16%) had a CVC. Overall morbidity (33% non-CVC vs 38% CVC P = 0.076), major morbidity (16% vs 20% P = 0.067), and infective complications (superficial wound infection) 3% vs 4% P = 0.429; deep wound infection (5% vs 6% P = 0.720) did not differ between the two groups. In multivariate analysis, superficial wound infection, deep wound infection, and major complications were not associated with the presence of a CVC. All-cause mortality at 90 days was associated with CVC presence (OR 3.45, CI 1.74-6.85, P = 0.001) and age (OR 1.05, CI 1.02-1.08, P < 0.001). Conclusion: Since the adoption of non-invasive CVP monitoring, there has been no increase in adverse peri-operative outcomes.
MeSH term(s)	Adolescent ; Adult ; Blood Loss, Surgical ; Central Venous Pressure ; Hepatectomy/adverse effects ; Humans ; Liver ; Prospective Studies ; Retrospective Studies
Language	English
Publishing date	2020-04-23
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2131251-5
ISSN	1477-2574 ; 1365-182X
ISSN (online)	1477-2574
ISSN	1365-182X
DOI	10.1016/j.hpb.2020.03.020
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Article ; Online: Sustained inhibition of receptor tyrosine kinases and macrophage depletion by PLX3397 and rapamycin as a potential new approach for the treatment of MPNSTs.

Patwardhan, Parag P / Surriga, Oliver / Beckman, Michael J / de Stanchina, Elisa / Dematteo, Ronald P / Tap, William D / Schwartz, Gary K

Clinical cancer research : an official journal of the American Association for Cancer Research

2014 Volume 20, Issue 12, Page(s) 3146–3158

Abstract: Purpose: Malignant peripheral nerve sheath tumor (MPNST) is a highly aggressive tumor type that is resistant to chemotherapy and there are no effective therapies. MPNSTs have been shown to have gene amplification for receptor tyrosine kinases (RTK), ... ...

Abstract	Purpose: Malignant peripheral nerve sheath tumor (MPNST) is a highly aggressive tumor type that is resistant to chemotherapy and there are no effective therapies. MPNSTs have been shown to have gene amplification for receptor tyrosine kinases (RTK), PDGFR and c-Kit. We tested the c-Kit inhibitor, imatinib, and PLX3397, a selective c-Fms and c-Kit inhibitor, to evaluate their efficacy against MPNST cells in vitro and in vivo. Experimental design: We tested the efficacy of imatinib or PLX3397 either alone or in combination with TORC1 inhibitor rapamycin in a cell proliferation assay in vitro and by immunoblotting to determine target inhibition. Immunoblotting and immunohistochemical analysis was further carried out using xenograft samples in vivo. Results: Our in vitro studies show that imatinib and PLX3397 similarly inhibit cell growth and this can be enhanced with rapamycin with comparable target specificity. However, in vivo studies clearly demonstrate that compared with imatinib, PLX3397 results in sustained blockade of c-Kit, c-Fms, and PDGFRβ, resulting in significant suppression of tumor growth. Moreover, staining for Iba-1, a marker for macrophages, indicates that PLX3397 results in significant depletion of macrophages in the growing tumors. The combination of PLX3397 and rapamycin results in even greater macrophage depletion with continued growth suppression, even when the drug treatment is discontinued. Conclusions: Taken together, our data strongly suggest that PLX3397 is superior to imatinib in the treatment of MPNSTs, and the combination of PLX3397 with a TORC1 inhibitor could provide a new therapeutic approach for the treatment of this disease.
MeSH term(s)	Aminopyridines/pharmacology ; Animals ; Antineoplastic Combined Chemotherapy Protocols/pharmacology ; Apoptosis/drug effects ; Benzamides/administration & dosage ; Blotting, Western ; Cell Proliferation/drug effects ; Humans ; Imatinib Mesylate ; Macrophages/drug effects ; Macrophages/metabolism ; Macrophages/pathology ; Mice ; Mice, Inbred ICR ; Mice, SCID ; Neurilemmoma/drug therapy ; Neurilemmoma/metabolism ; Neurilemmoma/pathology ; Piperazines/administration & dosage ; Proto-Oncogene Proteins c-kit/antagonists & inhibitors ; Pyrimidines/administration & dosage ; Pyrroles/pharmacology ; Receptor, Platelet-Derived Growth Factor beta/antagonists & inhibitors ; Sirolimus/administration & dosage ; Tumor Cells, Cultured ; Xenograft Model Antitumor Assays
Chemical Substances	Aminopyridines ; Benzamides ; Piperazines ; Pyrimidines ; Pyrroles ; pexidartinib (6783M2LV5X) ; Imatinib Mesylate (8A1O1M485B) ; Proto-Oncogene Proteins c-kit (EC 2.7.10.1) ; Receptor, Platelet-Derived Growth Factor beta (EC 2.7.10.1) ; Sirolimus (W36ZG6FT64)
Language	English
Publishing date	2014-04-09
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1225457-5
ISSN	1557-3265 ; 1078-0432
ISSN (online)	1557-3265
ISSN	1078-0432
DOI	10.1158/1078-0432.CCR-13-2576
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