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Responses with Crizotinib in MET-Amplified Lung Cancer Show New Targetable Form of Disease

Responses with Crizotinib in MET-Amplified Lung Cancer Show New Targetable Form of Disease | Lung Cancer Dispatch | Scoop.it

"In 2011, the drug crizotinib earned accelerated approval by the US FDA to target the subset of advanced non-small cell lung cancers caused by rearrangements of the anaplastic lymphoma kinase (ALK) gene, and subsequently was granted regular approval in 2013. The drug also has shown dramatic responses in patients whose lung cancers harbored a different molecular abnormality, namely ROS1 gene rearrangements. Previously unreported phase 1 clinical trial results now show that crizotinib may have a third important molecular target. In advanced non-small cell lung cancer patients with intermediate and high amplifications of the MET gene, crizotinib produced either disease stabilization or tumor response. Sixty-seven percent of patients with high MET amplification showed prolonged response to the drug, which lasted from approximately 6 months to nearly 2.5 years."


Editor's note: Crizotinib (aka Xalkori) is a targeted therapy drug that kills cancer cells by targeting certain molecules found in the cells. It was already known that crizotinib works well for some patients with advanced non-small cell lung cancer (NSCLC) whose cancer cells have mutations in the ALK gene and in the ROS1 gene; such mutations, or "molecular biomarkers," are detected by a medical procedure known as "molecular testing," or "genetic testing." Now, scientists say that crizotinib may also be effective for patients with advanced NSCLC whose tumors have abnormally high activity of a protein called MET, which can also be detected via molecular testing.

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ScienceDaily  |  May 31, 2014

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Effect of New Lung Cancer Drug Depends on MET Protein Expression Levels

Effect of New Lung Cancer Drug Depends on MET Protein Expression Levels | Lung Cancer Dispatch | Scoop.it

The cell protein MET is overexpressed in more than half of non-small cell lung cancer (NSCLC) tumors. MET overexpression is associated with worse prognoses and plays a role in drug resistance to EGFR inhibitors like erlotinib (Tarceva). A recent clinical trial examined the effects of onartuzumab, which inhibits MET function, on recurrent NSCLC. Patients received either onartuzumab and Tarceva or Tarceva only. In patients who overexpressed MET, adding onartuzumab increased the time until cancer progression and prolonged overall survival. In contrast, in patients without MET overexpression, adding onartuzumab worsened outcomes. This finding highlights the importance of diagnostic testing in choosing the best cancer treatment. A clinical trial investigating the onartuzumab-Tarceva combination in MET-overexpressing patients only is currently enrolling participants.

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ASCO Post | Oct 10, 2013

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Improved MET Inhibitors May Have Potential as Lung Cancer Treatments

Improved MET Inhibitors May Have Potential as Lung Cancer Treatments | Lung Cancer Dispatch | Scoop.it

MET, also known as c-Met, is a protein that normally occurs only at low levels in healthy tissues, but is overabundant and often mutated in many tumors, including non-small cell lung cancer (NSCLC). It is therefore a promising target for cancer treatments called MET inhibitors. However, currently available MET inhibitors also interfere with other proteins, leading to serious side effects and limiting their usefulness. In a recent study, researchers showed that the new MET inhibitors EMD 1214063 and EMD 1204831 are highly selective for MET only. The two drugs also shrank NSCLC tumors implanted into mice, suggesting that they may be promising treatments for NSCLC.

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Clinical Cancer Research | Apr 3, 2013

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Committee: NSCLC Study Should be Halted Due to Lack of Efficacy

Committee: NSCLC Study Should be Halted Due to Lack of Efficacy | Lung Cancer Dispatch | Scoop.it

"An independent data monitoring committee recommended that a phase 3 study designed to evaluate the combination of onartuzumab and erlotinib in a subset of patients with non–small cell lung cancer be stopped due to lack of clinically meaningful efficacy, according to a press release issued by the drugs’ manufacturer.


"The randomized, multicenter, double-blind, placebo-controlled MetLung study compared the humanized monoclonal antibody onartuzumab (MetMab, Genentech) plus the protein kinase inhibitor erlotinib(Tarceva, Genentech) vs. erlotinib alone in patients with previously treated advanced NSCLC whose tumors were MET-positive."

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Healio  |  Mar 3, 2014

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MET Inhibitor Fails to Prolong Life in NSCLC Trial

MET Inhibitor Fails to Prolong Life in NSCLC Trial | Lung Cancer Dispatch | Scoop.it

A clinical trial of a MET inhibitor has been stopped because the drug doesn't keep people with non-small cell lung cancer (NSCLC) alive longer, researchers reported at the 2013 European Cancer Congress in Amsterdam, Netherlands. The phase III trial included 1,048 people with NSCLC, where half were given the MET inhibitor tivantinib, in combination with erlotinib, which inhibits a protein linked to abnormal cell division. Although tivantinib did not extend life, it did keep tumors from growing for awhile (3.6 mo with this drug vs 1.9 mo without it). Now, the researchers are analyzing the results to see if tivantinib benefitted people with tumors that make too much of the MET protein.

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European Society For Medical Oncology│Sep 29, 2013

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Raja Mudad's curator insight, October 3, 2013 7:27 AM

A new oral drug may help a subset of patients with NS|CL|C who have over expression of cmet

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Inhibition of MET May Help Overcome TKI Drug Resistance in Lung Cancer

Inhibition of MET May Help Overcome TKI Drug Resistance in Lung Cancer | Lung Cancer Dispatch | Scoop.it

Tyrosine kinase inhibitors (TKIs) that block EGFR are effective treatments for many cases of advanced non-small cell lung cancer (NSCLC), but are limited by the fact that patients will eventually develop resistance against them. Overexpression of the MET gene may contribute to EGFR-TKI resistance, suggesting that combined inhibition of both EGFR and MET may prevent or overcome this drug resistance. Several MET inhibitors have been developed, including cabozantinib (Cometriq), tivantinib, onartuzumab, and ficlatuzumab, and ongoing trials are investigating the safety and effectiveness of combining them with an EGFR-TKI like erlotinib (Tarceva) or gefitinib (Iressa).


Research paper: http://theoncologist.alphamedpress.org/content/early/2013/01/25/theoncologist.2012-0262.full.pdf

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The Oncologist | Jan 28, 2013

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