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Trabectedin expands treatment options for some forms of advanced soft tissue sarcoma

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Trabectedin expands treatment options for some forms of advanced soft tissue sarcoma
In the fall of 2015, the United States joined the growing list of countries in which trabectedin, a novel form of chemotherapy, is approved for the treatment of certain types of advanced soft tissue sarcoma. The drug, a synthetic derivative of a compound originally isolated from a sea squirt, has a complex mechanism of action that distinguishes it from other cytotoxic drugs, allowing it to target both the tumor and its microenvironment. Based on the results of a randomized, open-label, multicenter phase 3 clinical trial, trabectedin received regulatory approval for the treatment of unresectable or metastatic liposarcoma or leiomyosarcoma.

 

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The Journal of Community and Supportive Oncology - 14(5)
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189-191
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trabectedin, soft tissue sarcoma, ET743-SAR-3007, liposarcoma, leiomyosarcoma, dacarbazine
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In the fall of 2015, the United States joined the growing list of countries in which trabectedin, a novel form of chemotherapy, is approved for the treatment of certain types of advanced soft tissue sarcoma. The drug, a synthetic derivative of a compound originally isolated from a sea squirt, has a complex mechanism of action that distinguishes it from other cytotoxic drugs, allowing it to target both the tumor and its microenvironment. Based on the results of a randomized, open-label, multicenter phase 3 clinical trial, trabectedin received regulatory approval for the treatment of unresectable or metastatic liposarcoma or leiomyosarcoma.

 

Click on the PDF icon at the top of this introduction to read the full article. 

 

In the fall of 2015, the United States joined the growing list of countries in which trabectedin, a novel form of chemotherapy, is approved for the treatment of certain types of advanced soft tissue sarcoma. The drug, a synthetic derivative of a compound originally isolated from a sea squirt, has a complex mechanism of action that distinguishes it from other cytotoxic drugs, allowing it to target both the tumor and its microenvironment. Based on the results of a randomized, open-label, multicenter phase 3 clinical trial, trabectedin received regulatory approval for the treatment of unresectable or metastatic liposarcoma or leiomyosarcoma.

 

Click on the PDF icon at the top of this introduction to read the full article. 

 

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The Journal of Community and Supportive Oncology - 14(5)
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The Journal of Community and Supportive Oncology - 14(5)
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189-191
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189-191
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Trabectedin expands treatment options for some forms of advanced soft tissue sarcoma
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Trabectedin expands treatment options for some forms of advanced soft tissue sarcoma
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trabectedin, soft tissue sarcoma, ET743-SAR-3007, liposarcoma, leiomyosarcoma, dacarbazine
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More success for immunotherapy with nivolumab approval for metastatic RCC

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More success for immunotherapy with nivolumab approval for metastatic RCC
Following its recent success in non–small-cell lung cancer (NSCLC), the immunotherapeutic agent nivolumab received approval from the US Food and Drug Administration last fall for the treatment of advanced clear-cell renal-cell carcinoma (RCC) after prior antiangiogenic therapy. Nivolumab, an immune checkpoint inhibitor, is a fully human immunoglobulin G4 monoclonal antibody that binds to the programmed cell death 1 (PD-1) receptor on the surface of T cells, prevents their inactivation by tumor cells overexpressing PD-1 ligands, and helps to reinstate the anti-tumor immune response.
 
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The Journal of Community and Supportive Oncology - 14(4)
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Page Number
138-140
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renal cell carcinoma, RCC, immunotherapy, nivolumab, CheckMate-025, programmed death cell

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Following its recent success in non–small-cell lung cancer (NSCLC), the immunotherapeutic agent nivolumab received approval from the US Food and Drug Administration last fall for the treatment of advanced clear-cell renal-cell carcinoma (RCC) after prior antiangiogenic therapy. Nivolumab, an immune checkpoint inhibitor, is a fully human immunoglobulin G4 monoclonal antibody that binds to the programmed cell death 1 (PD-1) receptor on the surface of T cells, prevents their inactivation by tumor cells overexpressing PD-1 ligands, and helps to reinstate the anti-tumor immune response.
 
Click on the PDF icon at the top of this introduction to read the full article.  
 
Following its recent success in non–small-cell lung cancer (NSCLC), the immunotherapeutic agent nivolumab received approval from the US Food and Drug Administration last fall for the treatment of advanced clear-cell renal-cell carcinoma (RCC) after prior antiangiogenic therapy. Nivolumab, an immune checkpoint inhibitor, is a fully human immunoglobulin G4 monoclonal antibody that binds to the programmed cell death 1 (PD-1) receptor on the surface of T cells, prevents their inactivation by tumor cells overexpressing PD-1 ligands, and helps to reinstate the anti-tumor immune response.
 
Click on the PDF icon at the top of this introduction to read the full article.  
 
Issue
The Journal of Community and Supportive Oncology - 14(4)
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The Journal of Community and Supportive Oncology - 14(4)
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138-140
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138-140
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More success for immunotherapy with nivolumab approval for metastatic RCC
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More success for immunotherapy with nivolumab approval for metastatic RCC
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renal cell carcinoma, RCC, immunotherapy, nivolumab, CheckMate-025, programmed death cell

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renal cell carcinoma, RCC, immunotherapy, nivolumab, CheckMate-025, programmed death cell

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Encapsulated irinotecan provides novel option for hard-to-treat pancreatic cancer

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In the fall of 2015, the US Food and Drug Administration approved the addition of a novel, much-needed treatment option for patients with metastatic pancreatic cancer, a particularly hard-to-treat form of the disease, in the second-line setting following progression on gemcitabine- based chemotherapy.1 MM-398 is a modified version of the chemotherapeutic agent irinotecan, in which the drug is encapsulated in a nanoliposomal construct that is designed to improve delivery to the tumor and enhance anti-tumor efficacy while minimizing side effects in the rest of the body.

 

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The Journal of Community and Supportive Oncology - 14(3)
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91-93
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irinotecan, pancreatic cancer, NAPOLI-1 trial, fluorouracil, leucovorin
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Edited by Jame Abraham, MD; report prepared by Jane de Lartigue, PhD

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In the fall of 2015, the US Food and Drug Administration approved the addition of a novel, much-needed treatment option for patients with metastatic pancreatic cancer, a particularly hard-to-treat form of the disease, in the second-line setting following progression on gemcitabine- based chemotherapy.1 MM-398 is a modified version of the chemotherapeutic agent irinotecan, in which the drug is encapsulated in a nanoliposomal construct that is designed to improve delivery to the tumor and enhance anti-tumor efficacy while minimizing side effects in the rest of the body.

 

Click on the PDF icon at the top of this introduction to read the full article.

 

In the fall of 2015, the US Food and Drug Administration approved the addition of a novel, much-needed treatment option for patients with metastatic pancreatic cancer, a particularly hard-to-treat form of the disease, in the second-line setting following progression on gemcitabine- based chemotherapy.1 MM-398 is a modified version of the chemotherapeutic agent irinotecan, in which the drug is encapsulated in a nanoliposomal construct that is designed to improve delivery to the tumor and enhance anti-tumor efficacy while minimizing side effects in the rest of the body.

 

Click on the PDF icon at the top of this introduction to read the full article.

 

Issue
The Journal of Community and Supportive Oncology - 14(3)
Issue
The Journal of Community and Supportive Oncology - 14(3)
Page Number
91-93
Page Number
91-93
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Publications
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irinotecan, pancreatic cancer, NAPOLI-1 trial, fluorouracil, leucovorin
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irinotecan, pancreatic cancer, NAPOLI-1 trial, fluorouracil, leucovorin
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Second targeted combination regime approved for metastatic melanoma

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Second targeted combination regime approved for metastatic melanoma
Researchers are increasingly looking to rational combinations of drugs to meet the challenge of resistance to molecularly targeted anticancer therapies. The treatment of metastatic melanoma was significantly advanced with the development of BRAF inhibitors, but is still limited by the short-lived nature of the responses to these drugs and the almost universal occurrence of tumor regrowth. More durable responses could be produced by targeting multiple points in the mitogen-activated protein kinase (MAPK) signaling pathway of which BRAF is a central component. In the fall of 2015, the MEK inhibitor cobimetinib and BRAF inhibitor vemurafenib became the second such combination to receive regulatory approval in the United States following positive results from the international, phase 3, randomized coBRIM trial, which demonstrated the superiority of the combination over single-agent BRAF inhibitor therapy. It also marked the first US approval for cobimetinib.1 

 

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The Journal of Community and Supportive Oncology - 14(2)
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Page Number
51-53
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melanoma, cobimetinib, vemurafenib, molecularly targeted anticancer therapies, metastatic melanoma, BRAF inhibitors, mitogen-activated protein kinase, MAPK, MEK inhibitor
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Researchers are increasingly looking to rational combinations of drugs to meet the challenge of resistance to molecularly targeted anticancer therapies. The treatment of metastatic melanoma was significantly advanced with the development of BRAF inhibitors, but is still limited by the short-lived nature of the responses to these drugs and the almost universal occurrence of tumor regrowth. More durable responses could be produced by targeting multiple points in the mitogen-activated protein kinase (MAPK) signaling pathway of which BRAF is a central component. In the fall of 2015, the MEK inhibitor cobimetinib and BRAF inhibitor vemurafenib became the second such combination to receive regulatory approval in the United States following positive results from the international, phase 3, randomized coBRIM trial, which demonstrated the superiority of the combination over single-agent BRAF inhibitor therapy. It also marked the first US approval for cobimetinib.1 

 

Click on the PDF icon at the top of this introduction to read the full article.

 

Researchers are increasingly looking to rational combinations of drugs to meet the challenge of resistance to molecularly targeted anticancer therapies. The treatment of metastatic melanoma was significantly advanced with the development of BRAF inhibitors, but is still limited by the short-lived nature of the responses to these drugs and the almost universal occurrence of tumor regrowth. More durable responses could be produced by targeting multiple points in the mitogen-activated protein kinase (MAPK) signaling pathway of which BRAF is a central component. In the fall of 2015, the MEK inhibitor cobimetinib and BRAF inhibitor vemurafenib became the second such combination to receive regulatory approval in the United States following positive results from the international, phase 3, randomized coBRIM trial, which demonstrated the superiority of the combination over single-agent BRAF inhibitor therapy. It also marked the first US approval for cobimetinib.1 

 

Click on the PDF icon at the top of this introduction to read the full article.

 

Issue
The Journal of Community and Supportive Oncology - 14(2)
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The Journal of Community and Supportive Oncology - 14(2)
Page Number
51-53
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51-53
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Second targeted combination regime approved for metastatic melanoma
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Second targeted combination regime approved for metastatic melanoma
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melanoma, cobimetinib, vemurafenib, molecularly targeted anticancer therapies, metastatic melanoma, BRAF inhibitors, mitogen-activated protein kinase, MAPK, MEK inhibitor
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melanoma, cobimetinib, vemurafenib, molecularly targeted anticancer therapies, metastatic melanoma, BRAF inhibitors, mitogen-activated protein kinase, MAPK, MEK inhibitor
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Idarucizumab given the nod as the first specific antidote for an oral anticoagulant

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Idarucizumab given the nod as the first specific antidote for an oral anticoagulant
In the fall of 2015, idarucizumab became the first drug-specific antidote to an oral anticoagulant to receive regulatory approval from the US Food and Drug Administration. Anticoagulants are designed to inhibit the formation of blood clots and prevent thrombotic disorders, but they can increase bleeding risk in patients who experience trauma or illness or who undergo invasive surgical procedures. For this reason, traditional anticoagulants have antidotes that reverse their therapeutic effects, but newer oral anticoagulants lack specific reversal agents and that has proven a barrier to their use in patients with higher bleeding risk.

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The Journal of Community and Supportive Oncology - 14(1)
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8-10
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venous thromboembolism, VTE, deep venous thrombosis, pulmonary embolism, idarucizumab, humanized monoclonal antibody fragment, reversal agent, thrombin, direct oral anticoagulants, DOACs, dabigatran, rivaroxaban, apixaban, edoxaban, andexanet alfa
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In the fall of 2015, idarucizumab became the first drug-specific antidote to an oral anticoagulant to receive regulatory approval from the US Food and Drug Administration. Anticoagulants are designed to inhibit the formation of blood clots and prevent thrombotic disorders, but they can increase bleeding risk in patients who experience trauma or illness or who undergo invasive surgical procedures. For this reason, traditional anticoagulants have antidotes that reverse their therapeutic effects, but newer oral anticoagulants lack specific reversal agents and that has proven a barrier to their use in patients with higher bleeding risk.

Click on the PDF icon at the top of this introduction to read the full article.

 

In the fall of 2015, idarucizumab became the first drug-specific antidote to an oral anticoagulant to receive regulatory approval from the US Food and Drug Administration. Anticoagulants are designed to inhibit the formation of blood clots and prevent thrombotic disorders, but they can increase bleeding risk in patients who experience trauma or illness or who undergo invasive surgical procedures. For this reason, traditional anticoagulants have antidotes that reverse their therapeutic effects, but newer oral anticoagulants lack specific reversal agents and that has proven a barrier to their use in patients with higher bleeding risk.

Click on the PDF icon at the top of this introduction to read the full article.

 

Issue
The Journal of Community and Supportive Oncology - 14(1)
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The Journal of Community and Supportive Oncology - 14(1)
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8-10
Page Number
8-10
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Idarucizumab given the nod as the first specific antidote for an oral anticoagulant
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Idarucizumab given the nod as the first specific antidote for an oral anticoagulant
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venous thromboembolism, VTE, deep venous thrombosis, pulmonary embolism, idarucizumab, humanized monoclonal antibody fragment, reversal agent, thrombin, direct oral anticoagulants, DOACs, dabigatran, rivaroxaban, apixaban, edoxaban, andexanet alfa
Legacy Keywords
venous thromboembolism, VTE, deep venous thrombosis, pulmonary embolism, idarucizumab, humanized monoclonal antibody fragment, reversal agent, thrombin, direct oral anticoagulants, DOACs, dabigatran, rivaroxaban, apixaban, edoxaban, andexanet alfa
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Filgrastim-sndz debuts as the first biosimilar approved in United States

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Filgrastim-sndz debuts as the first biosimilar approved in United States
In March this year, filgrastim-sndz became the first biosimilar to receive approval from the US Food and Drug Administration for use in the United States. Biosimilars are biological products that show comparable quality, efficacy, and safety to a reference drug that is already approved. In this case, filgrastim-sndz, by Sandoz, a Novartis company, is a biosimilar of Amgen’s filgrastim, the reference drug or originator, which is already licensed in the United States for 5 indications, including for cancer patients undergoing treatments that deplete white blood cells, as well as those preparing for autologous peripheral blood stem-cell transplant, or those with severe, chronic neutropenia.1
 
Click on the PDF icon at the top of this introduction to read the full article.
 
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The Journal of Community and Supportive Oncology - 13(12)
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Page Number
420-422
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Biosimilars, filgrastim, figrastim-sndz, granulocyte-colony stimulating factor, G-CSF
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In March this year, filgrastim-sndz became the first biosimilar to receive approval from the US Food and Drug Administration for use in the United States. Biosimilars are biological products that show comparable quality, efficacy, and safety to a reference drug that is already approved. In this case, filgrastim-sndz, by Sandoz, a Novartis company, is a biosimilar of Amgen’s filgrastim, the reference drug or originator, which is already licensed in the United States for 5 indications, including for cancer patients undergoing treatments that deplete white blood cells, as well as those preparing for autologous peripheral blood stem-cell transplant, or those with severe, chronic neutropenia.1
 
Click on the PDF icon at the top of this introduction to read the full article.
 
In March this year, filgrastim-sndz became the first biosimilar to receive approval from the US Food and Drug Administration for use in the United States. Biosimilars are biological products that show comparable quality, efficacy, and safety to a reference drug that is already approved. In this case, filgrastim-sndz, by Sandoz, a Novartis company, is a biosimilar of Amgen’s filgrastim, the reference drug or originator, which is already licensed in the United States for 5 indications, including for cancer patients undergoing treatments that deplete white blood cells, as well as those preparing for autologous peripheral blood stem-cell transplant, or those with severe, chronic neutropenia.1
 
Click on the PDF icon at the top of this introduction to read the full article.
 
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The Journal of Community and Supportive Oncology - 13(12)
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The Journal of Community and Supportive Oncology - 13(12)
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420-422
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420-422
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Filgrastim-sndz debuts as the first biosimilar approved in United States
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Filgrastim-sndz debuts as the first biosimilar approved in United States
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Biosimilars, filgrastim, figrastim-sndz, granulocyte-colony stimulating factor, G-CSF
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Approval reinstates gefitinib as a therapy for lung cancer

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Approval reinstates gefitinib as a therapy for lung cancer
This past summer, the United States joined more than 60 countries worldwide in approving the epidermal growth factor receptor (EGFR) inhibitor gefitinib for the treatment of patients with non-small-cell lung cancer (NSCLC) who harbor certain EGFR mutations. The approval marked “restoration of fortune” for the drug, which originally received accelerated approval from the US Food and Drug Administration (FDA) in 2003 for the treatment of advanced NSCLC after progression on platinum doublet chemotherapy and docetaxel but was voluntarily withdrawn from the market after subsequent confirmatory randomized trials failed to verify a survival benefit.

 

Click on the PDF icon at the top of this introduction to read the full article.

 

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The Journal of Community and Supportive Oncology - 13(11)
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385-387
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non-small-cell lung cancer, NSCLC, EGFR, epidermal growth factor receptor, ISEL study, gefitinibtyrosine kinase inhibitor, TKI
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This past summer, the United States joined more than 60 countries worldwide in approving the epidermal growth factor receptor (EGFR) inhibitor gefitinib for the treatment of patients with non-small-cell lung cancer (NSCLC) who harbor certain EGFR mutations. The approval marked “restoration of fortune” for the drug, which originally received accelerated approval from the US Food and Drug Administration (FDA) in 2003 for the treatment of advanced NSCLC after progression on platinum doublet chemotherapy and docetaxel but was voluntarily withdrawn from the market after subsequent confirmatory randomized trials failed to verify a survival benefit.

 

Click on the PDF icon at the top of this introduction to read the full article.

 

This past summer, the United States joined more than 60 countries worldwide in approving the epidermal growth factor receptor (EGFR) inhibitor gefitinib for the treatment of patients with non-small-cell lung cancer (NSCLC) who harbor certain EGFR mutations. The approval marked “restoration of fortune” for the drug, which originally received accelerated approval from the US Food and Drug Administration (FDA) in 2003 for the treatment of advanced NSCLC after progression on platinum doublet chemotherapy and docetaxel but was voluntarily withdrawn from the market after subsequent confirmatory randomized trials failed to verify a survival benefit.

 

Click on the PDF icon at the top of this introduction to read the full article.

 

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The Journal of Community and Supportive Oncology - 13(11)
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The Journal of Community and Supportive Oncology - 13(11)
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385-387
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385-387
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Approval reinstates gefitinib as a therapy for lung cancer
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Approval reinstates gefitinib as a therapy for lung cancer
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non-small-cell lung cancer, NSCLC, EGFR, epidermal growth factor receptor, ISEL study, gefitinibtyrosine kinase inhibitor, TKI
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non-small-cell lung cancer, NSCLC, EGFR, epidermal growth factor receptor, ISEL study, gefitinibtyrosine kinase inhibitor, TKI
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Dinutuximab combination therapy becomes first approval for high-risk neuroblastoma

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Dinutuximab combination therapy becomes first approval for high-risk neuroblastoma
The approval of dinutuximab by the US Food and Drug Administration marks the third approval for a pediatric cancer and the first for patients with high-risk neuroblastoma.1 Dinutuximab is an immunotherapeutic agent; a monoclonal antibody (mAb) targeting a glycolipid that is highly expressed on the surface of neuroblastoma cells.

The mAb was approved in combination with the cytokines granulocyte macrophage colony-stimulating factor (GM-CSF) and interleukin-2 (IL-2), and the oral retinoid isotretinoin (RA). The approval was based on a pivotal, phase 3, multicenter, open-label, randomized trial conducted by the Children’s Oncology Group between October 2001 and January 2009 that was stopped early after the combination demonstrated superiority over standard therapy with respect to event-free survival (EFS).2

Two hundred and twenty-six patients (mostly pediatric patients, though age up to 31 years at diagnosis was allowed) with high-risk neuroblastoma were enrolled based on the following criteria: age of ≤31 years at diagnosis; completion of induction therapy, autologous stem-cell transplant (SCT), and radiation therapy, with autologous SCT performed within 9 months of initiation of induction therapy; achievement of at least partial response prior to autologous SCT; enrollment between 50-100 days after final autologous SCT; absence of progressive disease; adequate organ function; life expectancy of at least 2 months; and prior enrollment in the COG biology study (ANBL00B1). An additional 25 patients with biopsy-proven residual disease after autologous SCT were also enrolled, but were nonrandomly assigned to the immunotherapy arm and were excluded from the primary outcome analysis. Patients with systemic infections or a requirement for concomitant systemic corticosteroids or immunosuppressant usage were ineligible. 

 

Click on the PDF icon at the top of this introduction to read the full article.

 

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The Journal of Community and Supportive Oncology - 13(10)
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344-346
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dinutuximab, neuroblastoma, immunotherapeutic agent, monoclonal antibody, mAb, cytokine, granulocyte macrophage colony-stimulating factor, GM-CSF, interleukin-2, IL-2, retinoid isotretinoin, RA, glycolipid disialoganglioside, GD2
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The approval of dinutuximab by the US Food and Drug Administration marks the third approval for a pediatric cancer and the first for patients with high-risk neuroblastoma.1 Dinutuximab is an immunotherapeutic agent; a monoclonal antibody (mAb) targeting a glycolipid that is highly expressed on the surface of neuroblastoma cells.

The mAb was approved in combination with the cytokines granulocyte macrophage colony-stimulating factor (GM-CSF) and interleukin-2 (IL-2), and the oral retinoid isotretinoin (RA). The approval was based on a pivotal, phase 3, multicenter, open-label, randomized trial conducted by the Children’s Oncology Group between October 2001 and January 2009 that was stopped early after the combination demonstrated superiority over standard therapy with respect to event-free survival (EFS).2

Two hundred and twenty-six patients (mostly pediatric patients, though age up to 31 years at diagnosis was allowed) with high-risk neuroblastoma were enrolled based on the following criteria: age of ≤31 years at diagnosis; completion of induction therapy, autologous stem-cell transplant (SCT), and radiation therapy, with autologous SCT performed within 9 months of initiation of induction therapy; achievement of at least partial response prior to autologous SCT; enrollment between 50-100 days after final autologous SCT; absence of progressive disease; adequate organ function; life expectancy of at least 2 months; and prior enrollment in the COG biology study (ANBL00B1). An additional 25 patients with biopsy-proven residual disease after autologous SCT were also enrolled, but were nonrandomly assigned to the immunotherapy arm and were excluded from the primary outcome analysis. Patients with systemic infections or a requirement for concomitant systemic corticosteroids or immunosuppressant usage were ineligible. 

 

Click on the PDF icon at the top of this introduction to read the full article.

 

The approval of dinutuximab by the US Food and Drug Administration marks the third approval for a pediatric cancer and the first for patients with high-risk neuroblastoma.1 Dinutuximab is an immunotherapeutic agent; a monoclonal antibody (mAb) targeting a glycolipid that is highly expressed on the surface of neuroblastoma cells.

The mAb was approved in combination with the cytokines granulocyte macrophage colony-stimulating factor (GM-CSF) and interleukin-2 (IL-2), and the oral retinoid isotretinoin (RA). The approval was based on a pivotal, phase 3, multicenter, open-label, randomized trial conducted by the Children’s Oncology Group between October 2001 and January 2009 that was stopped early after the combination demonstrated superiority over standard therapy with respect to event-free survival (EFS).2

Two hundred and twenty-six patients (mostly pediatric patients, though age up to 31 years at diagnosis was allowed) with high-risk neuroblastoma were enrolled based on the following criteria: age of ≤31 years at diagnosis; completion of induction therapy, autologous stem-cell transplant (SCT), and radiation therapy, with autologous SCT performed within 9 months of initiation of induction therapy; achievement of at least partial response prior to autologous SCT; enrollment between 50-100 days after final autologous SCT; absence of progressive disease; adequate organ function; life expectancy of at least 2 months; and prior enrollment in the COG biology study (ANBL00B1). An additional 25 patients with biopsy-proven residual disease after autologous SCT were also enrolled, but were nonrandomly assigned to the immunotherapy arm and were excluded from the primary outcome analysis. Patients with systemic infections or a requirement for concomitant systemic corticosteroids or immunosuppressant usage were ineligible. 

 

Click on the PDF icon at the top of this introduction to read the full article.

 

Issue
The Journal of Community and Supportive Oncology - 13(10)
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The Journal of Community and Supportive Oncology - 13(10)
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344-346
Page Number
344-346
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Dinutuximab combination therapy becomes first approval for high-risk neuroblastoma
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Dinutuximab combination therapy becomes first approval for high-risk neuroblastoma
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dinutuximab, neuroblastoma, immunotherapeutic agent, monoclonal antibody, mAb, cytokine, granulocyte macrophage colony-stimulating factor, GM-CSF, interleukin-2, IL-2, retinoid isotretinoin, RA, glycolipid disialoganglioside, GD2
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dinutuximab, neuroblastoma, immunotherapeutic agent, monoclonal antibody, mAb, cytokine, granulocyte macrophage colony-stimulating factor, GM-CSF, interleukin-2, IL-2, retinoid isotretinoin, RA, glycolipid disialoganglioside, GD2
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Nivolumab: first immunotherapy approved for lung cancer

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Nivolumab: first immunotherapy approved for lung cancer
The approval of nivolumab in early 2015 by the US Food and Drug Administration (FDA) for the treatment of squamous cell non-small-cell lung cancer (NSCLC) marks a second approval for this drug, following a 2014 approval for metastatic melanoma. Approved 3 months ahead of schedule, nivolumab is the first immunotherapy to be approved for the treatment of lung cancer. The drug can help to reinstate the antitumor immune response by targeting the programmed cell death-1 (PD-1) receptor, an “immune checkpoint” protein found on the surface of activated T cells that is involved in inhibiting T-cell activity.

 

Click on the PDF icon at the top of this introduction to read the full article.

 

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The Journal of Community and Supportive Oncology - 13(9)
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Page Number
312-315
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nivolumab, non-small-cell-lung cancer, NSCLC, immunotherapy, PD-1, PD-L1, CTLA-4, checkpoint inhibitor, CheckMate
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The approval of nivolumab in early 2015 by the US Food and Drug Administration (FDA) for the treatment of squamous cell non-small-cell lung cancer (NSCLC) marks a second approval for this drug, following a 2014 approval for metastatic melanoma. Approved 3 months ahead of schedule, nivolumab is the first immunotherapy to be approved for the treatment of lung cancer. The drug can help to reinstate the antitumor immune response by targeting the programmed cell death-1 (PD-1) receptor, an “immune checkpoint” protein found on the surface of activated T cells that is involved in inhibiting T-cell activity.

 

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The approval of nivolumab in early 2015 by the US Food and Drug Administration (FDA) for the treatment of squamous cell non-small-cell lung cancer (NSCLC) marks a second approval for this drug, following a 2014 approval for metastatic melanoma. Approved 3 months ahead of schedule, nivolumab is the first immunotherapy to be approved for the treatment of lung cancer. The drug can help to reinstate the antitumor immune response by targeting the programmed cell death-1 (PD-1) receptor, an “immune checkpoint” protein found on the surface of activated T cells that is involved in inhibiting T-cell activity.

 

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The Journal of Community and Supportive Oncology - 13(9)
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The Journal of Community and Supportive Oncology - 13(9)
Page Number
312-315
Page Number
312-315
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Nivolumab: first immunotherapy approved for lung cancer
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Nivolumab: first immunotherapy approved for lung cancer
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nivolumab, non-small-cell-lung cancer, NSCLC, immunotherapy, PD-1, PD-L1, CTLA-4, checkpoint inhibitor, CheckMate
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nivolumab, non-small-cell-lung cancer, NSCLC, immunotherapy, PD-1, PD-L1, CTLA-4, checkpoint inhibitor, CheckMate
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JCSO 2015;13:312-315
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Panobinostat: a novel mechanism of action shows promise in multiple myeloma

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Panobinostat: a novel mechanism of action shows promise in multiple myeloma

Following an initial “no” vote from the Oncologic Drugs Advisory Committee (ODAC) in late 2014, the US Food and Drug Administration eventually awarded accelerated approval in February 2015 to the histone deacetylase (HDAC) inhibitor panobinostat for use in select patients with relapsed multiple myeloma. Panobinostat has a novel mechanism of action that demonstrates synergy with the proteasome inhibitor bortezomib and the immunomodulatory agent dexamethasone, which translated into improved progression-free survival (PFS) for patients with multiple myeloma who had received at least 2 prior therapies, according to data from a prespecified subgroup analysis from the Panorama-1 trial.

 

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The Journal of Community and Supportive Oncology - 13(8)
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278-281
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panobinostat, multiple myeloma, bortezomib, dexamethasone, Panorama-1, histone deacetylases, HDACs
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Following an initial “no” vote from the Oncologic Drugs Advisory Committee (ODAC) in late 2014, the US Food and Drug Administration eventually awarded accelerated approval in February 2015 to the histone deacetylase (HDAC) inhibitor panobinostat for use in select patients with relapsed multiple myeloma. Panobinostat has a novel mechanism of action that demonstrates synergy with the proteasome inhibitor bortezomib and the immunomodulatory agent dexamethasone, which translated into improved progression-free survival (PFS) for patients with multiple myeloma who had received at least 2 prior therapies, according to data from a prespecified subgroup analysis from the Panorama-1 trial.

 

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Following an initial “no” vote from the Oncologic Drugs Advisory Committee (ODAC) in late 2014, the US Food and Drug Administration eventually awarded accelerated approval in February 2015 to the histone deacetylase (HDAC) inhibitor panobinostat for use in select patients with relapsed multiple myeloma. Panobinostat has a novel mechanism of action that demonstrates synergy with the proteasome inhibitor bortezomib and the immunomodulatory agent dexamethasone, which translated into improved progression-free survival (PFS) for patients with multiple myeloma who had received at least 2 prior therapies, according to data from a prespecified subgroup analysis from the Panorama-1 trial.

 

Click on the PDF icon at the top of this introduction to read the full article.

 

Issue
The Journal of Community and Supportive Oncology - 13(8)
Issue
The Journal of Community and Supportive Oncology - 13(8)
Page Number
278-281
Page Number
278-281
Publications
Publications
Topics
Article Type
Display Headline
Panobinostat: a novel mechanism of action shows promise in multiple myeloma
Display Headline
Panobinostat: a novel mechanism of action shows promise in multiple myeloma
Legacy Keywords
panobinostat, multiple myeloma, bortezomib, dexamethasone, Panorama-1, histone deacetylases, HDACs
Legacy Keywords
panobinostat, multiple myeloma, bortezomib, dexamethasone, Panorama-1, histone deacetylases, HDACs
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JCSO 2015;13(8):278-281
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