F-18 FDG PET/CT Assessment of Gastrointestinal Stromal Tumor Response to Sunitinib Malate Therapy

Banzo, Ignacio; Quirce, R.; Martínez-Rodríguez, I.; Jiménez-Bonilla, J.; Sainz-Esteban, Aurora; Barragán, Jorge; Portilla-Quattrociocchi, H.; Carril, J.M.

doi:10.1097/rlu.0b013e318162dddb

Cited by 8 publications

(3 citation statements)

References 7 publications

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“…PET/CT is an emerging tool for treatment response evaluation, as well as diagnosis, in various tumors and has been used in estimating treatment response in GIST patients [10, 11]. In addition, PET/CT is known to be able to predict the malignant potential of a GIST [12].…”

Section: Discussionmentioning

confidence: 99%

An Extragastrointestinal Stromal Tumor in the Omentum With Peritoneal Seeding Mimicking an Appendiceal Mucinous Cancer With Carcinomatosis

et al. 2014

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Gastrointestinal stromal tumors (GISTs) are the most common mesenchymal tumors of the gastrointestinal tract. These tumors tend to present most frequently in the stomach, followed by the small intestine. GISTs can also arise from the omentum, retroperitoneum, mesentery, or pleura and are termed extragastrointestinal stromal tumors (EGISTs) when they do so. EGISTs arising from the omentum are very rare. Due to the limited incidence of EGISTs in the omentum, the diagnostic criteria are not well established, and making a correct diagnosis may be difficult. In this report, we present a case of an EGIST of the omentum with peritoneal metastasis that was initially suspected to be an appendiceal mucinous carcinoma with carcinomatosis on positron emission tomography/computed tomography imaging.

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Section: Discussionmentioning

confidence: 99%

An Extragastrointestinal Stromal Tumor in the Omentum With Peritoneal Seeding Mimicking an Appendiceal Mucinous Cancer With Carcinomatosis

et al. 2014

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“…These mechanisms may be responsible for tumor blood vessel resistance to sunitinib inhibition of VEGFRs and platelet-derived growth factor receptors. At the tumor epithelial cell level, sunitinib inhibition of receptor tyrosine kinase phosphorylation decreases survival signaling through AKT and extracellular signal-regulated kinase and decreases glucose uptake (20)(21)(22)(23). However, inhibition of tumor cell growth is not long-lasting as shown by clinical trials using fluorodeoxyglucose positron emission tomography imaging.…”

Section: Introductionmentioning

confidence: 99%

“…However, inhibition of tumor cell growth is not long-lasting as shown by clinical trials using fluorodeoxyglucose positron emission tomography imaging. In these studies, sunitinib treatment incompletely inhibited fluorodeoxyglucose uptake or induced rebound fluorodeoxyglucose uptake during the initial post-treatment rest period (22,23).…”

Section: Introductionmentioning

confidence: 99%

Targeting both HIF-1 and HIF-2 in human colon cancer cells improves tumor response to sunitinib treatment

Burkitt

Chun

Dang

et al. 2009

Molecular Cancer Therapeutics

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Sunitinib is an oral small-molecule multitargeted receptor tyrosine kinase inhibitor that has recently been shown to have clinical benefit as a single agent in renal cell cancer and gastrointestinal stromal tumors, leading to its Food and Drug Administration approval for treatment of these cancers. However, the benefit is short-lived; and for the majority of cancers, sunitinib single-agent clinical activity is low. Therefore, combination strategies with sunitinib are currently in clinical development. The hypoxia-inducible transcription factors, HIF-1 and HIF-2, induce gene programs important for cancer cell growth and angiogenesis. We hypothesized that inhibiting HIF-1 and HIF-2 would further improve tumor response to sunitinib therapy. To test this hypothesis, HIF-1α and HIF-2α genes were disrupted in colon cancer cells. We found that disruption of HIF-1α, HIF-2α, or both HIF-1α and HIF-2α genes led to improved tumor response to sunitinib. For xenografts in which both HIF-1α and HIF-2α genes were disrupted, there was prolonged complete remission with sunitinib treatment in 50% of mice. This enhanced response was mediated by two potential mechanisms. First, tumor angiogenesis and perfusion were almost completely inhibited by sunitinib when both HIF-1α and HIF-2α genes were disrupted. The enhanced inhibitory effect on tumor angiogenesis was mediated by the inhibition of multiple proangiogenic factors, including vascular endothelial growth factor and angiopoietin-like protein 4, and the induction of the antiangiogenic factor, thrombospondin 1. Second, disruption of HIF-1α, HIF-2α, or both HIF-1α and HIF-2α genes directly inhibited tumor cell proliferation. These preclinical findings have clinical implications and suggest novel clinical trials.

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Imaging Studies in Anticancer Drug Development

Mankoff

2010

Principles of Anticancer Drug Development

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F-18 FDG PET/CT Assessment of Gastrointestinal Stromal Tumor Response to Sunitinib Malate Therapy

Cited by 8 publications

References 7 publications

An Extragastrointestinal Stromal Tumor in the Omentum With Peritoneal Seeding Mimicking an Appendiceal Mucinous Cancer With Carcinomatosis

An Extragastrointestinal Stromal Tumor in the Omentum With Peritoneal Seeding Mimicking an Appendiceal Mucinous Cancer With Carcinomatosis

Targeting both HIF-1 and HIF-2 in human colon cancer cells improves tumor response to sunitinib treatment

Imaging Studies in Anticancer Drug Development

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