A phase I dose escalation study of oral c-MET inhibitor tivantinib (ARQ 197) in combination with gemcitabine in patients with solid tumors

Pant, Shubham; Saleh, Mansoor N.; Bendell, Johanna C.; Infante, Jeffrey R.; Jones, Suzanne F.; Kurkjian, Carla; Moore, Kathleen; Kazakin, Julia; Abbadessa, Giovanni; Wang, Y; Chen, Y; Schwartz, Brian; Camacho, Luis H.

doi:10.1093/annonc/mdu157

Cited by 78 publications

(51 citation statements)

References 16 publications

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“…Interestingly, a number of phase I trials of HGF/cMET targeting agents have included patients with ovarian cancer, [82,97,88,54,98,61] …”

Section: Hgf/cmet Inhibitors Trials In Ovarian Cancermentioning

confidence: 99%

The Therapeutic Potential of Targeting the HGF/cMET Axis in Ovarian Cancer

Moran-Jones

2016

Mol Diagn Ther

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Survival rates for ovarian cancer have remained relatively stable for the past two decades, despite advances in surgical techniques and cytotoxic chemotherapeutics, indicating a requirement for better therapies. One pathway currently proposed for targeting is the HGF/cMET pathway. Up-regulated in a number of tumour types, cMET is a tyrosine kinase receptor expressed on epithelial cells. In ovarian cancer, it has been identified as highly expressed in the four major subtypes, with expression estimates ranging from 11-68% of cases. HGF, the only known ligand for cMET, is found at high levels in both serum and ascites in women with ovarian cancer, and proposed to induce both migration and metastasis. However, clinically validated biomarkers are not yet available for either HGF or cMET, preventing a clear understanding of the true rate of over-expression, or its correlation with prognosis.

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“…Interestingly, a number of phase I trials of HGF/cMET targeting agents have included patients with ovarian cancer, [82,97,88,54,98,61] …”

Section: Hgf/cmet Inhibitors Trials In Ovarian Cancermentioning

confidence: 99%

The Therapeutic Potential of Targeting the HGF/cMET Axis in Ovarian Cancer

Moran-Jones

2016

Mol Diagn Ther

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“…Further, there is some suggestion that overexpression of c-MET can lead to EGFR resistance; thus leading to the use of c-MET inhibitors in cholangiocarcinoma (69). A recent study evaluated the combination of tivantinib (ARQ 197) with gemcitabine in patients with solid tumors (70). In this study, 20% of the patients achieved a partial response including one patient with cholangiocarcinoma.…”

Section: Met Inhibitorsmentioning

confidence: 82%

Therapeutic options for intrahepatic cholangiocarcinoma

Bupathi

Ahn

Bekaii‐Saab

2017

Hepatobiliary Surg. Nutr.

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Biliary tract cancer (BTC) is a heterogeneous group of cancers, which is composed of intrahepatic cholangiocarcinoma (ICCA), extrahepatic cholangiocarcinoma (ECCA), gallbladder cancers and ampullary carcinomas. While all anatomic subgroups are treated uniformly, our understanding about the pathogenesis has allowed us to reason that each group represents a clinically and genetically diverse disease.The majority of patients present with locally advanced or metastatic disease, where the standard treatment is combination systemic cytotoxic chemotherapy with gemcitabine and cisplatin. While most receive a clinical benefit from chemotherapy, patients eventually progress where no standardized therapies are available in the refractory setting. With the use of next generation sequencing, we have come to understand that ICCA is a diverse genomic disease with many actionable alterations that may serve as potential therapeutic targets. Further studies investigating the role of novel targeted agents (as a single agent or with combination chemotherapy) will hopefully provide additional treatment options for this highly lethal disease.

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“…Although the mechanism remains unclear, SU11274 may exert (17). Combined treatment with tivantinib and gemcitabine is safe and tolerable (17). Although these are preliminary results, the antitumor effect of this combination appears promising.…”

Section: Su11274 Suppresses Pancreatic Cell Motilitymentioning

confidence: 98%

“…However, SU11274 nevertheless suppressed proliferation in this cell line. Although the mechanism remains unclear, SU11274 may exert (17). Combined treatment with tivantinib and gemcitabine is safe and tolerable (17).…”

Section: Su11274 Suppresses Pancreatic Cell Motilitymentioning

confidence: 99%