Bavituximab plus paclitaxel and carboplatin for the treatment of advanced non-small-cell lung cancer

Digumarti, Raghunadharao; Bapsy, P. P.; Suresh, A.; Bhattacharyya, G.S.; Dasappa, Lokanatha; Shan, Joseph; Gerber, David E.

doi:10.1016/j.lungcan.2014.08.010

Cited by 36 publications

(33 citation statements)

References 41 publications

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“…117 This treatment appears promising. [118][119][120] Recent reports suggest that the PtdSer in the tumor-associated endothelial cells and the PtdSer exposed on tumor cells after treatment with anticancer drugs create an immune-suppressive tumor environment; the antibody against PtdSer reverses this effect, creating anti-tumor immunity. 121 It will be interesting to study whether the flippase and scramblases discussed in this review are involved in the PtdSer exposure on tumor-associated endothelial cells.…”

Section: Perspectivesmentioning

confidence: 99%

Exposure of phosphatidylserine on the cell surface

et al. 2016

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Section: Perspectivesmentioning

confidence: 99%

Exposure of phosphatidylserine on the cell surface

et al. 2016

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“…In a 2014 phase II clinical trial among 49 locally advanced or metastatic non-small-cell lung cancer patients, bavituximab combined with carboplatin and paclitaxel treatment resulted in a 41% response rate and was considered to show tolerable safety and efficacy. 44 More recently, a phase I clinical trial with bavituximab in combination with paclitaxel has shown more promising results among 14 HER2-negative metastatic breast cancer patients, with an 85% response rate. 45 In addition, an ongoing phase III trial involving the treatment of advanced non-small-cell lung cancer with bavituximab and docetaxel is currently in progress.…”

Section: Alteration Of the Phospholipid Code During Tumor Progressionmentioning

confidence: 99%

The phospholipid code: a key component of dying cell recognition, tumor progression and host–microbe interactions

2015

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A significant effort is made by the cell to maintain certain phospholipids at specific sites. It is well described that proteins involved in intracellular signaling can be targeted to the plasma membrane and organelles through phospholipid-binding domains. Thus, the accumulation of a specific combination of phospholipids, denoted here as the 'phospholipid code', is key in initiating cellular processes. Interestingly, a variety of extracellular proteins and pathogen-derived proteins can also recognize or modify phospholipids to facilitate the recognition of dying cells, tumorigenesis and host-microbe interactions. In this article, we discuss the importance of the phospholipid code in a range of physiological and pathological processes.

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“…In summary, we have shown that PS-targeting antibodies improve the efficacy of anti-CTLA-4 or anti-PD-1 therapy in murine models of melanoma, suggesting that these combinations have the potential to improve outcome in patients with advanced-stage melanoma. Bavituximab, a chimeric PS-targeting antibody, is currently being evaluated in late-stage clinical trials for the treatment of cancer patients with solid tumors (46,54), and strong antitumor activity has been demonstrated in melanoma clinical trials using checkpoint inhibitor antibodies targeting CTLA-4 (10), PD-1 (12,13), and PD-L1 (55). It is increasingly apparent that successful immunotherapy requires tumor cell killing, induction of proinflammatory immune responses, and concomitant reduction of immunosuppressive signals leading to increased tumor infiltration by activated T cells.…”

Section: Discussionmentioning

confidence: 99%

“…Preclinical studies have shown that PS-targeting antibodies localize to PS-expressing tumors and tumor endothelial cells and elicit strong antitumor effects when combined with chemotherapy or radiotherapy (33,41,42,44). A PS-targeting antibody, bavituximab, is currently being tested in multiple advanced stage clinical trials for the treatment of solid tumors (45,46).…”

Section: Introductionmentioning

confidence: 99%

Antibody-Mediated Phosphatidylserine Blockade Enhances the Antitumor Responses to CTLA-4 and PD-1 Antibodies in Melanoma

Freimark

Gong

et al. 2016

Cancer Immunology Research

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In tumor-bearing animals, the membrane phospholipid phosphatidylserine (PS) suppresses immune responses, suggesting that PS signaling could counteract the antitumor effect of antibody-driven immune checkpoint blockade. Here, we show that treating melanoma-bearing mice with a PS-targeting antibody enhances the antitumor activity of downstream checkpoint inhibition. Combining PS-targeting antibodies with CTLA-4 or PD-1 blockade resulted in significantly greater inhibition of tumor growth than did single-agent therapy. Moreover, combination therapy enhanced CD4 þ and CD8 þ tumor-infiltrating lymphocyte numbers; elevated the fraction of cells expressing the proinflammatory cytokines IL2, IFNg, and TNFa; and increased the ratio of CD8 T cells to myeloid-derived suppressor cells and regulatory T cells in tumors. Similar changes in immune cell profiles were observed in splenocytes. Taken together, these data show that antibody-mediated PS blockade enhances the antitumor efficacy of immune checkpoint inhibition.

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Bavituximab plus paclitaxel and carboplatin for the treatment of advanced non-small-cell lung cancer

Cited by 36 publications

References 41 publications

Exposure of phosphatidylserine on the cell surface

Exposure of phosphatidylserine on the cell surface

The phospholipid code: a key component of dying cell recognition, tumor progression and host–microbe interactions

Antibody-Mediated Phosphatidylserine Blockade Enhances the Antitumor Responses to CTLA-4 and PD-1 Antibodies in Melanoma

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