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n2:pmcid: PMC0
bibo:doi: 10.18632%2Foncotarget.21586
n3:contains: _:vb71241133 _:vb71241097 _:vb71241072 _:vb71241075 _:vb71241070 _:vb71241060 _:vb71241034 _:vb71241019

Subject Item: _:vb71241019
rdf:type: n3:Section
dc:title: introduction
n3:contains: _:vb71241020 _:vb71241021 _:vb71241022 _:vb71241023 _:vb71241032 _:vb71241033 _:vb71241024 _:vb71241025 _:vb71241026 _:vb71241027 _:vb71241028 _:vb71241029 _:vb71241030 _:vb71241031

Subject Item: _:vb71241020
rdf:type: n2:Context
rdf:value: These tumors are highly aggressive and the prognosis for patients is extremely poor, with median overall survival of 14.6 months and 5-year survival rates less than 10% following standard of care treatment [>>1<<, 2]. With near 100% relapse rates and limited treatment options at the time of recurrence, GBM represents one of the biggest therapeutic challenges of our time.
n2:mentions: n4:15758009

Subject Item: _:vb71241021
rdf:type: n2:Context
rdf:value: These tumors are highly aggressive and the prognosis for patients is extremely poor, with median overall survival of 14.6 months and 5-year survival rates less than 10% following standard of care treatment [1, >>2<<]. With near 100% relapse rates and limited treatment options at the time of recurrence, GBM represents one of the biggest therapeutic challenges of our time.
n2:mentions: n4:19269895

Subject Item: _:vb71241022
rdf:type: n2:Context
rdf:value: Tumors are further protected by the blood brain barrier (BBB), a semipermeable membrane of endothelial cells connected by tight junctions, which prevents the passage of most conventional drugs to tumor sites [>>3<<, 4]. A hallmark adaptation of GBM is the development of a profoundly immunosuppressive tumor microenvironment (TME) that cripples endogenous antitumor immune responses and limits the effectiveness of immunotherapies [5, 6].
n2:mentions: n4:22154620

Subject Item: _:vb71241023
rdf:type: n2:Context
rdf:value: Tumors are further protected by the blood brain barrier (BBB), a semipermeable membrane of endothelial cells connected by tight junctions, which prevents the passage of most conventional drugs to tumor sites [3, >>4<<]. A hallmark adaptation of GBM is the development of a profoundly immunosuppressive tumor microenvironment (TME) that cripples endogenous antitumor immune responses and limits the effectiveness of immunotherapies [5, 6].
n2:mentions: n4:24028526

Subject Item: _:vb71241024
rdf:type: n2:Context
rdf:value: A hallmark adaptation of GBM is the development of a profoundly immunosuppressive tumor microenvironment (TME) that cripples endogenous antitumor immune responses and limits the effectiveness of immunotherapies [>>5<<, 6].
n2:mentions: n4:10695732

Subject Item: _:vb71241025
rdf:type: n2:Context
rdf:value: A hallmark adaptation of GBM is the development of a profoundly immunosuppressive tumor microenvironment (TME) that cripples endogenous antitumor immune responses and limits the effectiveness of immunotherapies [5, >>6<<].
n2:mentions: n4:15776005

Subject Item: _:vb71241026
rdf:type: n2:Context
rdf:value: cell death (PD) pathway is an endogenous negative feedback mechanism for T-cell activity that is often exploited by human tumors, including GBM, to suppress the antitumor efficacy of incoming CD8+ cytotoxic T lymphocytes (CTLs) [>>7<<, 8]. Immune checkpoint inhibition with monoclonal antibodies targeting the programmed cell death-1 (PD-1) protein or its ligand, PD-L1, has produced significant clinical results in the treatment of several cancers, most notably metastatic
n2:mentions: n4:26325035

Subject Item: _:vb71241027
rdf:type: n2:Context
rdf:value: cell death (PD) pathway is an endogenous negative feedback mechanism for T-cell activity that is often exploited by human tumors, including GBM, to suppress the antitumor efficacy of incoming CD8+ cytotoxic T lymphocytes (CTLs) [7, >>8<<]. Immune checkpoint inhibition with monoclonal antibodies targeting the programmed cell death-1 (PD-1) protein or its ligand, PD-L1, has produced significant clinical results in the treatment of several cancers, most notably metastatic
n2:mentions: n4:14612546

Subject Item: _:vb71241028
rdf:type: n2:Context
rdf:value: checkpoint inhibition with monoclonal antibodies targeting the programmed cell death-1 (PD-1) protein or its ligand, PD-L1, has produced significant clinical results in the treatment of several cancers, most notably metastatic melanoma [>>9<<, 10] and non-small cell lung cancer (NSCLC) [11, 12], and has shown promise in preclinical studies for the treatment of GBM [13, 14].
n2:mentions: n4:25795410

Subject Item: _:vb71241029
rdf:type: n2:Context
rdf:value: inhibition with monoclonal antibodies targeting the programmed cell death-1 (PD-1) protein or its ligand, PD-L1, has produced significant clinical results in the treatment of several cancers, most notably metastatic melanoma [9, >>10<<] and non-small cell lung cancer (NSCLC) [11, 12], and has shown promise in preclinical studies for the treatment of GBM [13, 14].
n2:mentions: n4:26027431

Subject Item: _:vb71241030
rdf:type: n2:Context
rdf:value: targeting the programmed cell death-1 (PD-1) protein or its ligand, PD-L1, has produced significant clinical results in the treatment of several cancers, most notably metastatic melanoma [9, 10] and non-small cell lung cancer (NSCLC) [>>11<<, 12], and has shown promise in preclinical studies for the treatment of GBM [13, 14].
n2:mentions: n4:26412456

Subject Item: _:vb71241031
rdf:type: n2:Context
rdf:value: the programmed cell death-1 (PD-1) protein or its ligand, PD-L1, has produced significant clinical results in the treatment of several cancers, most notably metastatic melanoma [9, 10] and non-small cell lung cancer (NSCLC) [11, >>12<<], and has shown promise in preclinical studies for the treatment of GBM [13, 14].
n2:mentions: n4:26028407

Subject Item: _:vb71241032
rdf:type: n2:Context
rdf:value: produced significant clinical results in the treatment of several cancers, most notably metastatic melanoma [9, 10] and non-small cell lung cancer (NSCLC) [11, 12], and has shown promise in preclinical studies for the treatment of GBM [>>13<<, 14]. CheckMate 143 (NCT02017717) was the first randomized phase III clinical trial of PD pathway inhibition in the setting of GBM, including a comparison of nivolumab (Opdivo) and the anti-vascular endothelial growth factor (VEGF)
n2:mentions: n4:24691018

Subject Item: _:vb71241033
rdf:type: n2:Context
rdf:value: significant clinical results in the treatment of several cancers, most notably metastatic melanoma [9, 10] and non-small cell lung cancer (NSCLC) [11, 12], and has shown promise in preclinical studies for the treatment of GBM [13, >>14<<]. CheckMate 143 (NCT02017717) was the first randomized phase III clinical trial of PD pathway inhibition in the setting of GBM, including a comparison of nivolumab (Opdivo) and the anti-vascular endothelial growth factor (VEGF) antibody,
n2:mentions: n4:23462419

Subject Item: _:vb71241034
rdf:type: n3:Section
dc:title: future direction
n3:contains: _:vb71241036 _:vb71241037 _:vb71241038 _:vb71241039 _:vb71241035 _:vb71241052 _:vb71241053 _:vb71241054 _:vb71241055 _:vb71241048 _:vb71241049 _:vb71241050 _:vb71241051 _:vb71241044 _:vb71241045 _:vb71241046 _:vb71241047 _:vb71241040 _:vb71241041 _:vb71241042 _:vb71241043 _:vb71241056 _:vb71241057 _:vb71241058 _:vb71241059

Subject Item: _:vb71241035
rdf:type: n2:Context
rdf:value: In both primary and recurrent GBM, bevacizumab has been shown to increase PFS and improve peritumoral edema, reducing the need for immunosuppressive glucocorticoids known to interfere with the efficacy of immunotherapy [>>94<<]. Although not shown to extend OS, bevacizumab may confer additional benefits in the setting of immunotherapy. High levels of intratumoral VEGF are strongly immunosuppressive, promoting the activity of Treg cells, shifting DC populations
n2:mentions: n4:26125449

Subject Item: _:vb71241036
rdf:type: n2:Context
rdf:value: intratumoral VEGF are strongly immunosuppressive, promoting the activity of Treg cells, shifting DC populations towards an immature phenotype, and inducing apoptosis in CD8+ T-cells, effects abrogated with the use of anti-VEGF therapy [>>95<<]. The vasculature-normalizing effects of anti-VEGF therapy have also been shown to improve delivery of chemotherapeutic agents to tumor sites and enhance intratumoral immune cell infiltration, improving the efficacy of therapies like
n2:mentions: n4:20631075

Subject Item: _:vb71241037
rdf:type: n2:Context
rdf:value: effects of anti-VEGF therapy have also been shown to improve delivery of chemotherapeutic agents to tumor sites and enhance intratumoral immune cell infiltration, improving the efficacy of therapies like adoptive T-cell transfer [>>95<<, 96]. Furthermore, in a recent phase I trial of patients with metastatic melanoma, bevacizumab enhanced intratumoral lymphocyte infiltration and humoral immune responses in combination with CTLA-4 blockade [97].
n2:mentions: n4:20631075

Subject Item: _:vb71241038
rdf:type: n2:Context
rdf:value: effects of anti-VEGF therapy have also been shown to improve delivery of chemotherapeutic agents to tumor sites and enhance intratumoral immune cell infiltration, improving the efficacy of therapies like adoptive T-cell transfer [95, >>96<<]. Furthermore, in a recent phase I trial of patients with metastatic melanoma, bevacizumab enhanced intratumoral lymphocyte infiltration and humoral immune responses in combination with CTLA-4 blockade [97].
n2:mentions: n4:23045683

Subject Item: _:vb71241039
rdf:type: n2:Context
rdf:value: Furthermore, in a recent phase I trial of patients with metastatic melanoma, bevacizumab enhanced intratumoral lymphocyte infiltration and humoral immune responses in combination with CTLA-4 blockade [>>97<<]. Although bevacizumab independently has immune-modulating functions and can provide some synergistic effects in combination with nivolumab, this synergy may be further enhanced with the addition of other immune-modulating strategies.
n2:mentions: n4:27549123

Subject Item: _:vb71241040
rdf:type: n2:Context
rdf:value: Combination anti-PD-1 and anti-CTLA-4 treatment in several studies has resulted in better clinical outcomes than seen with either agent alone [>>79<<, 98]. Furthermore, CTLA-4 and PD-1 expression in peripheral blood and tumor-infiltrating lymphocytes increases with immune checkpoint inhibition, reflecting the expansion of effector T-cell populations that would otherwise have been
n2:mentions: n4:23724867

Subject Item: _:vb71241041
rdf:type: n2:Context
rdf:value: Combination anti-PD-1 and anti-CTLA-4 treatment in several studies has resulted in better clinical outcomes than seen with either agent alone [79, >>98<<]. Furthermore, CTLA-4 and PD-1 expression in peripheral blood and tumor-infiltrating lymphocytes increases with immune checkpoint inhibition, reflecting the expansion of effector T-cell populations that would otherwise have been apoptotic
n2:mentions: n4:25539810

Subject Item: _:vb71241042
rdf:type: n2:Context
rdf:value: Additionally, this increased expression of immune checkpoint molecules renders patients more susceptible to immune checkpoint blockade and represents another indication for combination treatment [>>99<<]. Combining immune checkpoint blockade with other chemotherapeutic agents has also been shown to relieve tumor-induced immunosuppression and improve immune and clinical outcomes. Combination treatment with CT-011, an anti-PD-1 antibody,
n2:mentions: n4:20160101

Subject Item: _:vb71241043
rdf:type: n2:Context
rdf:value: Combination treatment with CT-011, an anti-PD-1 antibody, and cyclophosphamide resulted in a significant decrease in intratumoral Treg cell infiltration as well as an increase in the presence of antigen-specific CD8+ T-cells [>>100<<]. Mkrtichyan and colleagues also reported that treating mice with combination cyclophosphamide and a PD-1 inhibitor reduced the presence of exhausted PD-1-expressing immune cells within the TME, allowing infiltration and proliferation of
n2:mentions: n4:21710477

Subject Item: _:vb71241044
rdf:type: n2:Context
rdf:value: mice with combination cyclophosphamide and a PD-1 inhibitor reduced the presence of exhausted PD-1-expressing immune cells within the TME, allowing infiltration and proliferation of non-exhausted, functional, PD-1-deficient T-cells [>>101<<].
n2:mentions: n4:22837483

Subject Item: _:vb71241045
rdf:type: n2:Context
rdf:value: changes in tumor cells that enhance their susceptibility to immune-mediated destruction, such as increased expression of death receptors, costimulatory molecules, stress ligands, adhesion molecules, and MHC class I molecules [>>102<<]. RT also promotes intracellular protein degradation and broadens the peptide repertoire of available tumor antigens by inducing the production of novel proteins [103].
n2:mentions: n4:23291374

Subject Item: _:vb71241046
rdf:type: n2:Context
rdf:value: RT also promotes intracellular protein degradation and broadens the peptide repertoire of available tumor antigens by inducing the production of novel proteins [>>103<<]. Although GBM is known to have fewer mutations and tumor associated antigens (TAA) compared to various other cancers [104], future immunostimulatory strategies will involve targeting predominantly tumor-generated neo-antigens instead of
n2:mentions: n4:16636135

Subject Item: _:vb71241047
rdf:type: n2:Context
rdf:value: Although GBM is known to have fewer mutations and tumor associated antigens (TAA) compared to various other cancers [>>104<<], future immunostimulatory strategies will involve targeting predominantly tumor-generated neo-antigens instead of TAA.
n2:mentions: n4:24132290

Subject Item: _:vb71241048
rdf:type: n2:Context
rdf:value: Treatment with TMZ and fractionated RT have specifically been shown to increase IFN-γ release, leading to upregulation of PD-L1 in in vitro GBM cell lines [>>105<<]. Tumor cell death induced by RT and chemotherapy releases inflammatory tumor cell debris and tumor-associated antigens into the TME, leading to increased antigen presentation and activation of adaptive immune responses [102, 106]. Other
n2:mentions: n4:28066420

Subject Item: _:vb71241049
rdf:type: n2:Context
rdf:value: Tumor cell death induced by RT and chemotherapy releases inflammatory tumor cell debris and tumor-associated antigens into the TME, leading to increased antigen presentation and activation of adaptive immune responses [>>102<<, 106]. Other therapies to consider that promote the activation and recruitment of inflammatory cells to the TME include DC-based vaccination, oncolytic virotherapy (OVT), and adoptive T-cell transfer [107–109]. Tumor cell PD-L1 expression
n2:mentions: n4:23291374

Subject Item: _:vb71241050
rdf:type: n2:Context
rdf:value: Tumor cell death induced by RT and chemotherapy releases inflammatory tumor cell debris and tumor-associated antigens into the TME, leading to increased antigen presentation and activation of adaptive immune responses [102, >>106<<]. Other therapies to consider that promote the activation and recruitment of inflammatory cells to the TME include DC-based vaccination, oncolytic virotherapy (OVT), and adoptive T-cell transfer [107–109]. Tumor cell PD-L1 expression has
n2:mentions: n4:24048442

Subject Item: _:vb71241051
rdf:type: n2:Context
rdf:value: Other therapies to consider that promote the activation and recruitment of inflammatory cells to the TME include DC-based vaccination, oncolytic virotherapy (OVT), and adoptive T-cell transfer [>>107<<–109]. Tumor cell PD-L1 expression has been shown to preclude the effectiveness of adoptive T-cell therapy by promoting apoptosis of transferred cells, an effect that can be abrogated with the addition of PD-1 blocking antibodies [110]. In
n2:mentions: n4:14559843 n4:22915761 n4:11244031

Subject Item: _:vb71241052
rdf:type: n2:Context
rdf:value: Tumor cell PD-L1 expression has been shown to preclude the effectiveness of adoptive T-cell therapy by promoting apoptosis of transferred cells, an effect that can be abrogated with the addition of PD-1 blocking antibodies [>>110<<]. In a preclinical study of mice bearing B7-H1/SCCVII tumors treated with adoptive T-cell transfer, anti-PD-1 therapy, or both, combination treatment was required to achieve ultimate tumor regression and prolonged animal survival [108].
n2:mentions: n4:12091876

Subject Item: _:vb71241053
rdf:type: n2:Context
rdf:value: In a preclinical study of mice bearing B7-H1/SCCVII tumors treated with adoptive T-cell transfer, anti-PD-1 therapy, or both, combination treatment was required to achieve ultimate tumor regression and prolonged animal survival [>>108<<]. Given the mechanisms underlying PD-L1 upregulation, patients with stronger IFN-γ-releasing adaptive immune responses and more intense intra- and peritumoral inflammation would be expected to exhibit higher levels of PD-L1 expression,
n2:mentions: n4:14559843

Subject Item: _:vb71241054
rdf:type: n2:Context
rdf:value: This represents another mechanism of synergy whereby immunotherapies that enhance IFN-γ secretion, such as OVT, will locally sensitize tumors to PD blockade [>>109<<]. In a recent study of combination OVT and PD blockade, an oncolytic measles virus was shown to upregulate expression of PD-L1 in human GBM cells, and combination therapy led to prolonged survival of C57BL/6 mice bearing syngeneic
n2:mentions: n4:11244031

Subject Item: _:vb71241055
rdf:type: n2:Context
rdf:value: Tumor analysis in treated mice revealed an elevated influx of inflammatory immune cells, particularly antigen-specific CD8+ CTLs [>>111<<]. Treatment with nivolumab has also been associated with activation of a variety of genes associated with innate immunity and IFN-γ-releasing natural killer (NK) cell function, introducing the possibility of combination treatment with NK
n2:mentions: n4:27663389

Subject Item: _:vb71241056
rdf:type: n2:Context
rdf:value: been associated with activation of a variety of genes associated with innate immunity and IFN-γ-releasing natural killer (NK) cell function, introducing the possibility of combination treatment with NK cell-directed therapies as well [>>73<<, 98, 100].
n2:mentions: n4:27169994

Subject Item: _:vb71241057
rdf:type: n2:Context
rdf:value: associated with activation of a variety of genes associated with innate immunity and IFN-γ-releasing natural killer (NK) cell function, introducing the possibility of combination treatment with NK cell-directed therapies as well [73, >>98<<, 100].
n2:mentions: n4:25539810

Subject Item: _:vb71241058
rdf:type: n2:Context
rdf:value: with activation of a variety of genes associated with innate immunity and IFN-γ-releasing natural killer (NK) cell function, introducing the possibility of combination treatment with NK cell-directed therapies as well [73, 98, >>100<<].
n2:mentions: n4:21710477

Subject Item: _:vb71241059
rdf:type: n2:Context
rdf:value: of primary disease provide tumor debulking leading to GBM cell death, elaboration of tumor-associated antigens, and the release of TILs into the periphery, increasing their availability for interaction with circulating nivolumab [>>112<<].
n2:mentions: n4:18478111

Subject Item: _:vb71241060
rdf:type: n3:Section
dc:title: clinical management of gbm
n3:contains: _:vb71241061 _:vb71241062 _:vb71241063 _:vb71241068 _:vb71241069 _:vb71241064 _:vb71241065 _:vb71241066 _:vb71241067

Subject Item: _:vb71241061
rdf:type: n2:Context
rdf:value: The current standard of care for newly diagnosed GBM is maximal surgical resection and concurrent radiotherapy (RT) and temozolomide (TMZ) chemotherapy, followed by 6 months of adjuvant TMZ [>>1<<]. A recent phase III trial evaluating the addition of tumor treating fields (TTFs) to the TMZ and radiation protocol showed increased OS from 16 months to 21 months in newly diagnosed GBM [16].
n2:mentions: n4:15758009

Subject Item: _:vb71241062
rdf:type: n2:Context
rdf:value: A recent phase III trial evaluating the addition of tumor treating fields (TTFs) to the TMZ and radiation protocol showed increased OS from 16 months to 21 months in newly diagnosed GBM [>>16<<]. However, even with the best available treatment, GBM has a near 100% relapse rate with a median time to recurrence of 7 months [2]. Treatment options at this time are limited; repeat surgery is considered for approximately 25% of
n2:mentions: n4:26670971

Subject Item: _:vb71241063
rdf:type: n2:Context
rdf:value: However, even with the best available treatment, GBM has a near 100% relapse rate with a median time to recurrence of 7 months [>>2<<]. Treatment options at this time are limited; repeat surgery is considered for approximately 25% of patients and re-irradiation is only possible as a palliative option in rare cases [17]. Chemotherapy response rates, including to TMZ,
n2:mentions: n4:19269895

Subject Item: _:vb71241064
rdf:type: n2:Context
rdf:value: Treatment options at this time are limited; repeat surgery is considered for approximately 25% of patients and re-irradiation is only possible as a palliative option in rare cases [>>17<<]. Chemotherapy response rates, including to TMZ, typically do not exceed 10% and none have been shown to prolong OS [18–22]. Although two large randomized trials failed to show increased OS with addition of bevacizumab, an anti-VEGF
n2:mentions: n4:23136223

Subject Item: _:vb71241065
rdf:type: n2:Context
rdf:value: Chemotherapy response rates, including to TMZ, typically do not exceed 10% and none have been shown to prolong OS [>>18<<–22]. Although two large randomized trials failed to show increased OS with addition of bevacizumab, an anti-VEGF monoclonal antibody, to the current treatment strategy [23, 24], it is regularly used in the treatment of recurrent GBM due
n2:mentions: n4:18356283 n4:10944597 n4:21603247 n4:20308655 n4:17108063

Subject Item: _:vb71241066
rdf:type: n2:Context
rdf:value: Although two large randomized trials failed to show increased OS with addition of bevacizumab, an anti-VEGF monoclonal antibody, to the current treatment strategy [>>23<<, 24], it is regularly used in the treatment of recurrent GBM due to a demonstrated ability to prolong progression-free survival (PFS), reduce the use of immunosuppressive corticosteroids, and improve patient quality of life, both as a
n2:mentions: n4:24552317

Subject Item: _:vb71241067
rdf:type: n2:Context
rdf:value: Although two large randomized trials failed to show increased OS with addition of bevacizumab, an anti-VEGF monoclonal antibody, to the current treatment strategy [23, >>24<<], it is regularly used in the treatment of recurrent GBM due to a demonstrated ability to prolong progression-free survival (PFS), reduce the use of immunosuppressive corticosteroids, and improve patient quality of life, both as a
n2:mentions: n4:24552318

Subject Item: _:vb71241068
rdf:type: n2:Context
rdf:value: due to a demonstrated ability to prolong progression-free survival (PFS), reduce the use of immunosuppressive corticosteroids, and improve patient quality of life, both as a monotherapy and in combination with other cytotoxic agents [>>25<<–28]. Overall, the median survival for patients with recurrent disease typically ranges between 6.6 and 9.6 months, with one recent study showing overall survival rates of slightly over one year for patients treated with TTFs [29].
n2:mentions: n4:17317837 n4:19114704 n4:17947719 n4:19720927

Subject Item: _:vb71241069
rdf:type: n2:Context
rdf:value: Overall, the median survival for patients with recurrent disease typically ranges between 6.6 and 9.6 months, with one recent study showing overall survival rates of slightly over one year for patients treated with TTFs [>>29<<].
n2:mentions: n4:28664468

Subject Item: _:vb71241070
rdf:type: n3:Section
dc:title: gbm and immunotherapy
n3:contains: _:vb71241071

Subject Item: _:vb71241071
rdf:type: n2:Context
rdf:value: The field of immunotherapy centers on the natural ability of the host immune system to identify and destroy malignant cells, an ability that is often impaired in the setting of cancer, particularly GBM [>>6<<]. Immunotherapies are targeted towards activating and enhancing endogenous host immune responses.
n2:mentions: n4:15776005

Subject Item: _:vb71241072
rdf:type: n3:Section
dc:title: endogenous pd pathway
n3:contains: _:vb71241073 _:vb71241074

Subject Item: _:vb71241073
rdf:type: n2:Context
rdf:value: mechanism for T-cell activity that functions in the healthy host to minimize tissue damage incurred with prolonged inflammatory responses and prevent the development of autoimmunity by inducing peripheral tolerance to self-antigens [>>7<<, 30]. An overview of the endogenous PD pathway is shown in Figure 2.
n2:mentions: n4:26325035

Subject Item: _:vb71241074
rdf:type: n2:Context
rdf:value: mechanism for T-cell activity that functions in the healthy host to minimize tissue damage incurred with prolonged inflammatory responses and prevent the development of autoimmunity by inducing peripheral tolerance to self-antigens [7, >>30<<]. An overview of the endogenous PD pathway is shown in Figure 2.
n2:mentions: n4:14579280

Subject Item: _:vb71241075
rdf:type: n3:Section
dc:title: pd pathway in cancer
n3:contains: _:vb71241080 _:vb71241081 _:vb71241082 _:vb71241083 _:vb71241084 _:vb71241085 _:vb71241086 _:vb71241087 _:vb71241076 _:vb71241077 _:vb71241078 _:vb71241079 _:vb71241096 _:vb71241088 _:vb71241089 _:vb71241090 _:vb71241091 _:vb71241092 _:vb71241093 _:vb71241094 _:vb71241095

Subject Item: _:vb71241076
rdf:type: n2:Context
rdf:value: Seldom present on healthy cells in the steady state, PD-L1 is often expressed by both tumor cells and tumor-infiltrating lymphocytes (TILs) in a variety of human cancers, including GBM [>>31<<–34]. In a recent study of human GBM, 88% of tumors expressed PD-L1 [31], further supporting an exploration of the role of the PD pathway in malignant glioma.
n2:mentions: n4:23478000 n4:25355681 n4:17404099 n4:16611412

Subject Item: _:vb71241077
rdf:type: n2:Context
rdf:value: In a recent study of human GBM, 88% of tumors expressed PD-L1 [>>31<<], further supporting an exploration of the role of the PD pathway in malignant glioma.
n2:mentions: n4:25355681

Subject Item: _:vb71241078
rdf:type: n2:Context
rdf:value: Induction of tumor PD-L1 expression likely occurs in response to inflammation induced by host antitumor immune responses [>>34<<] and through tumor-specific mutations, such as loss of the tumor-suppressor PTEN or enhanced ALK gene signaling [35, 36].
n2:mentions: n4:17404099

Subject Item: _:vb71241079
rdf:type: n2:Context
rdf:value: of tumor PD-L1 expression likely occurs in response to inflammation induced by host antitumor immune responses [34] and through tumor-specific mutations, such as loss of the tumor-suppressor PTEN or enhanced ALK gene signaling [>>35<<, 36]. An overview of the PD-1 pathway in cancer is shown in Figure 3.
n2:mentions: n4:23785454

Subject Item: _:vb71241080
rdf:type: n2:Context
rdf:value: of tumor PD-L1 expression likely occurs in response to inflammation induced by host antitumor immune responses [34] and through tumor-specific mutations, such as loss of the tumor-suppressor PTEN or enhanced ALK gene signaling [35, >>36<<]. An overview of the PD-1 pathway in cancer is shown in Figure 3.
n2:mentions: n4:17159987

Subject Item: _:vb71241081
rdf:type: n2:Context
rdf:value: PD signaling in the setting of cancer represents an adaptation through which tumors can exploit endogenous cellular feedback mechanisms to suppress antitumor immune responses in a mechanism termed “adaptive resistance” [>>7<<]. Tumor PD-L1 binds to PD-1 receptors on infiltrating effector T-cells, inhibiting their cytotoxic activity and thereby rendering malignant cells resistant to CTL-mediated destruction [37].
n2:mentions: n4:26325035

Subject Item: _:vb71241082
rdf:type: n2:Context
rdf:value: Tumor PD-L1 binds to PD-1 receptors on infiltrating effector T-cells, inhibiting their cytotoxic activity and thereby rendering malignant cells resistant to CTL-mediated destruction [>>37<<]. Elevated tumor PD-L1 expression has been associated with aggressive disease and poor prognoses in several cancers including renal [38], pancreatic [34], breast [32], ovarian [39], esophageal [40], and gastric cancers [41]. Patients with
n2:mentions: n4:19423728

Subject Item: _:vb71241083
rdf:type: n2:Context
rdf:value: Elevated tumor PD-L1 expression has been associated with aggressive disease and poor prognoses in several cancers including renal [>>38<<], pancreatic [34], breast [32], ovarian [39], esophageal [40], and gastric cancers [41].
n2:mentions: n4:15569934

Subject Item: _:vb71241084
rdf:type: n2:Context
rdf:value: Elevated tumor PD-L1 expression has been associated with aggressive disease and poor prognoses in several cancers including renal [38], pancreatic [>>34<<], breast [32], ovarian [39], esophageal [40], and gastric cancers [41].
n2:mentions: n4:17404099

Subject Item: _:vb71241085
rdf:type: n2:Context
rdf:value: Elevated tumor PD-L1 expression has been associated with aggressive disease and poor prognoses in several cancers including renal [38], pancreatic [34], breast [>>32<<], ovarian [39], esophageal [40], and gastric cancers [41].
n2:mentions: n4:16611412

Subject Item: _:vb71241086
rdf:type: n2:Context
rdf:value: Elevated tumor PD-L1 expression has been associated with aggressive disease and poor prognoses in several cancers including renal [38], pancreatic [34], breast [32], ovarian [>>39<<], esophageal [40], and gastric cancers [41].
n2:mentions: n4:17360651

Subject Item: _:vb71241087
rdf:type: n2:Context
rdf:value: Elevated tumor PD-L1 expression has been associated with aggressive disease and poor prognoses in several cancers including renal [38], pancreatic [34], breast [32], ovarian [39], esophageal [>>40<<], and gastric cancers [41].
n2:mentions: n4:15837746

Subject Item: _:vb71241088
rdf:type: n2:Context
rdf:value: Elevated tumor PD-L1 expression has been associated with aggressive disease and poor prognoses in several cancers including renal [38], pancreatic [34], breast [32], ovarian [39], esophageal [40], and gastric cancers [>>41<<]. Patients with PD-L1-positive tumors displayed local evidence of impaired cellular immune responses, including a paucity of TILs or an abundance of heavily immunosuppressed and dysfunctional effector cells [34, 39]. However, in other
n2:mentions: n4:16530813

Subject Item: _:vb71241089
rdf:type: n2:Context
rdf:value: Patients with PD-L1-positive tumors displayed local evidence of impaired cellular immune responses, including a paucity of TILs or an abundance of heavily immunosuppressed and dysfunctional effector cells [>>34<<, 39]. However, in other studies of NSCLC [42], colorectal cancer [33], and melanoma [43], tumor PD-L1 expression was associated with evidence of strong ongoing antitumor immune responses and correlated with a positive prognosis. These
n2:mentions: n4:17404099

Subject Item: _:vb71241090
rdf:type: n2:Context
rdf:value: Patients with PD-L1-positive tumors displayed local evidence of impaired cellular immune responses, including a paucity of TILs or an abundance of heavily immunosuppressed and dysfunctional effector cells [34, >>39<<]. However, in other studies of NSCLC [42], colorectal cancer [33], and melanoma [43], tumor PD-L1 expression was associated with evidence of strong ongoing antitumor immune responses and correlated with a positive prognosis. These
n2:mentions: n4:17360651

Subject Item: _:vb71241091
rdf:type: n2:Context
rdf:value: However, in other studies of NSCLC [>>42<<], colorectal cancer [33], and melanoma [43], tumor PD-L1 expression was associated with evidence of strong ongoing antitumor immune responses and correlated with a positive prognosis.
n2:mentions: n4:24217091

Subject Item: _:vb71241092
rdf:type: n2:Context
rdf:value: However, in other studies of NSCLC [42], colorectal cancer [>>33<<], and melanoma [43], tumor PD-L1 expression was associated with evidence of strong ongoing antitumor immune responses and correlated with a positive prognosis.
n2:mentions: n4:23478000

Subject Item: _:vb71241093
rdf:type: n2:Context
rdf:value: Furthermore, in some of these cases, infiltrating effector cells lacked PD-1 expression entirely, rendering them functionally insensitive to PD-L1-mediated inhibition [>>33<<].
n2:mentions: n4:23478000

Subject Item: _:vb71241094
rdf:type: n2:Context
rdf:value: Several studies have correlated elevated pretreatment levels of PD-L1 with a worse prognosis [>>44<<, 45], whereas others have found no prognostic predictive value [31].
n2:mentions: n4:26323609

Subject Item: _:vb71241095
rdf:type: n2:Context
rdf:value: Several studies have correlated elevated pretreatment levels of PD-L1 with a worse prognosis [44, >>45<<], whereas others have found no prognostic predictive value [31].
n2:mentions: n4:23986257

Subject Item: _:vb71241096
rdf:type: n2:Context
rdf:value: Several studies have correlated elevated pretreatment levels of PD-L1 with a worse prognosis [44, 45], whereas others have found no prognostic predictive value [>>31<<].
n2:mentions: n4:25355681

Subject Item: _:vb71241097
rdf:type: n3:Section
dc:title: clinically targeting pd pathway in cancer
n3:contains: _:vb71241098 _:vb71241099 _:vb71241100 _:vb71241101 _:vb71241102 _:vb71241103 _:vb71241104 _:vb71241105 _:vb71241106 _:vb71241107 _:vb71241108 _:vb71241109 _:vb71241110 _:vb71241111 _:vb71241112 _:vb71241113 _:vb71241114 _:vb71241115 _:vb71241116 _:vb71241117 _:vb71241118 _:vb71241119 _:vb71241120 _:vb71241121 _:vb71241122 _:vb71241123 _:vb71241124 _:vb71241125 _:vb71241126 _:vb71241127 _:vb71241128 _:vb71241129 _:vb71241130 _:vb71241131 _:vb71241132

Subject Item: _:vb71241098
rdf:type: n2:Context
rdf:value: Human ex vivo studies have demonstrated reversal of PD pathway-mediated T-cell exhaustion and enhancement of lymphocyte proliferation and cytokine production after administration of monoclonal antibodies targeting either PD-1 or PD-L1 [>>46<<–51]. Preclinical studies in mouse tumor models have established the in vivo safety and efficacy of these agents, yielding significant tumor regression and prolonged animal survival in the setting of many cancers, including GBM [14, 52,
n2:mentions: n4:19651643 n4:12538684 n4:12704383 n4:16482562 n4:17898045 n4:15705911

Subject Item: _:vb71241099
rdf:type: n2:Context
rdf:value: Preclinical studies in mouse tumor models have established the in vivo safety and efficacy of these agents, yielding significant tumor regression and prolonged animal survival in the setting of many cancers, including GBM [>>14<<, 52, 53]. In phase III clinical trials, anti-PD pathway therapies have produced substantial clinical responses in a subset of patients with variety of cancers [9–12, 54–56], culminating in FDA approval of two immune checkpoint inhibitors,
n2:mentions: n4:23462419

Subject Item: _:vb71241100
rdf:type: n2:Context
rdf:value: Preclinical studies in mouse tumor models have established the in vivo safety and efficacy of these agents, yielding significant tumor regression and prolonged animal survival in the setting of many cancers, including GBM [14, >>52<<, 53]. In phase III clinical trials, anti-PD pathway therapies have produced substantial clinical responses in a subset of patients with variety of cancers [9–12, 54–56], culminating in FDA approval of two immune checkpoint inhibitors,
n2:mentions: n4:26546453

Subject Item: _:vb71241101
rdf:type: n2:Context
rdf:value: Preclinical studies in mouse tumor models have established the in vivo safety and efficacy of these agents, yielding significant tumor regression and prolonged animal survival in the setting of many cancers, including GBM [14, 52, >>53<<]. In phase III clinical trials, anti-PD pathway therapies have produced substantial clinical responses in a subset of patients with variety of cancers [9–12, 54–56], culminating in FDA approval of two immune checkpoint inhibitors,
n2:mentions: n4:26266810

Subject Item: _:vb71241102
rdf:type: n2:Context
rdf:value: In phase III clinical trials, anti-PD pathway therapies have produced substantial clinical responses in a subset of patients with variety of cancers [>>9<<–12, 54–56], culminating in FDA approval of two immune checkpoint inhibitors, pembrolizumab and nivolumab, both anti-PD-1 monoclonal antibodies, in the treatment of unresectable or metastatic melanoma (pembrolizumab and nivolumab) and
n2:mentions: n4:25795410 n4:26412456 n4:26028407 n4:26027431

Subject Item: _:vb71241103
rdf:type: n2:Context
rdf:value: In phase III clinical trials, anti-PD pathway therapies have produced substantial clinical responses in a subset of patients with variety of cancers [9–12, >>54<<–56], culminating in FDA approval of two immune checkpoint inhibitors, pembrolizumab and nivolumab, both anti-PD-1 monoclonal antibodies, in the treatment of unresectable or metastatic melanoma (pembrolizumab and nivolumab) and NSCLC
n2:mentions: n4:25399552 n4:25891173 n4:25452452

Subject Item: _:vb71241104
rdf:type: n2:Context
rdf:value: A list of all currently active clinical trials of PD-1/PD-L1 inhibitors in patients with malignant glioma is shown in Table 1 [>>59<<–68].
n2:mentions: n4:27114589

Subject Item: _:vb71241105
rdf:type: n2:Context
rdf:value: Patients With GlioblastomaMEDI4736, radiotherapy, bevacizumabNCT02336165Active, Not Recruiting[65, 66]Recurrent GlioblastomaII82Pembrolizumab +/- Bevacizumab for Recurrent GBMPembrolizumab, bevacizumabNCT02337491Active, Not Recruiting[>>67<<]Recurrent GlioblastomaII30*Autologous Dendritic Cells Pulsed With Tumor Lysate Antigen Vaccine and Nivolumab in Treating Patients With Recurrent GlioblastomaAutologous DCs pulsed with tumor lysate antigen vaccine, nivolumabNCT03014804Not
n2:mentions: n4:27114589

Subject Item: _:vb71241106
rdf:type: n2:Context
rdf:value: expansion and activation of antigen-specific CD8+ CTLs, reduced Treg cell activity, IFN-γ secretion and expression of IFN-γ-inducible genes, and subsequent IFN-γ-induced upregulation of PD-L1 expression on both tumor cells and TILs [>>9<<, 69–75]. Biopsies of regressing lesions demonstrate dense intratumoral CD8+ infiltrates [69, 73], and elevations in peripheral blood lymphocyte counts are observed as well [71, 75, 76].
n2:mentions: n4:25795410

Subject Item: _:vb71241107
rdf:type: n2:Context
rdf:value: expansion and activation of antigen-specific CD8+ CTLs, reduced Treg cell activity, IFN-γ secretion and expression of IFN-γ-inducible genes, and subsequent IFN-γ-induced upregulation of PD-L1 expression on both tumor cells and TILs [9, >>69<<–75]. Biopsies of regressing lesions demonstrate dense intratumoral CD8+ infiltrates [69, 73], and elevations in peripheral blood lymphocyte counts are observed as well [71, 75, 76].
n2:mentions: n4:24332512 n4:24127452 n4:23724846 n4:27169994 n4:25428504 n4:25428505

Subject Item: _:vb71241108
rdf:type: n2:Context
rdf:value: Biopsies of regressing lesions demonstrate dense intratumoral CD8+ infiltrates [>>69<<, 73], and elevations in peripheral blood lymphocyte counts are observed as well [71, 75, 76].
n2:mentions: n4:23724846

Subject Item: _:vb71241109
rdf:type: n2:Context
rdf:value: Biopsies of regressing lesions demonstrate dense intratumoral CD8+ infiltrates [69, >>73<<], and elevations in peripheral blood lymphocyte counts are observed as well [71, 75, 76].
n2:mentions: n4:27169994

Subject Item: _:vb71241110
rdf:type: n2:Context
rdf:value: Biopsies of regressing lesions demonstrate dense intratumoral CD8+ infiltrates [69, 73], and elevations in peripheral blood lymphocyte counts are observed as well [>>71<<, 75, 76]. Patients not responding to treatment characteristically have lacked this evidence of immune activation and possess reduced numbers of peripheral blood antigen-specific T-cells, instead accumulating immunosuppressive regulatory
n2:mentions: n4:24332512

Subject Item: _:vb71241111
rdf:type: n2:Context
rdf:value: Biopsies of regressing lesions demonstrate dense intratumoral CD8+ infiltrates [69, 73], and elevations in peripheral blood lymphocyte counts are observed as well [71, >>75<<, 76]. Patients not responding to treatment characteristically have lacked this evidence of immune activation and possess reduced numbers of peripheral blood antigen-specific T-cells, instead accumulating immunosuppressive regulatory
n2:mentions: n4:24127452

Subject Item: _:vb71241112
rdf:type: n2:Context
rdf:value: Biopsies of regressing lesions demonstrate dense intratumoral CD8+ infiltrates [69, 73], and elevations in peripheral blood lymphocyte counts are observed as well [71, 75, >>76<<]. Patients not responding to treatment characteristically have lacked this evidence of immune activation and possess reduced numbers of peripheral blood antigen-specific T-cells, instead accumulating immunosuppressive regulatory T-cells
n2:mentions: n4:18483370

Subject Item: _:vb71241113
rdf:type: n2:Context
rdf:value: Patients not responding to treatment characteristically have lacked this evidence of immune activation and possess reduced numbers of peripheral blood antigen-specific T-cells, instead accumulating immunosuppressive regulatory T-cells [>>77<<].
n2:mentions: n4:24145345

Subject Item: _:vb71241114
rdf:type: n2:Context
rdf:value: Immune checkpoint inhibition has been shown to be particularly effective in patients with elevated pretreatment levels of tumor PD-L1 expression [>>9<<, 11, 55, 70, 71, 74, 77–83].
n2:mentions: n4:25795410

Subject Item: _:vb71241115
rdf:type: n2:Context
rdf:value: Immune checkpoint inhibition has been shown to be particularly effective in patients with elevated pretreatment levels of tumor PD-L1 expression [9, >>11<<, 55, 70, 71, 74, 77–83].
n2:mentions: n4:26412456

Subject Item: _:vb71241116
rdf:type: n2:Context
rdf:value: Immune checkpoint inhibition has been shown to be particularly effective in patients with elevated pretreatment levels of tumor PD-L1 expression [9, 11, >>55<<, 70, 71, 74, 77–83].
n2:mentions: n4:25452452

Subject Item: _:vb71241117
rdf:type: n2:Context
rdf:value: Immune checkpoint inhibition has been shown to be particularly effective in patients with elevated pretreatment levels of tumor PD-L1 expression [9, 11, 55, >>70<<, 71, 74, 77–83].
n2:mentions: n4:25428504

Subject Item: _:vb71241118
rdf:type: n2:Context
rdf:value: Immune checkpoint inhibition has been shown to be particularly effective in patients with elevated pretreatment levels of tumor PD-L1 expression [9, 11, 55, 70, >>71<<, 74, 77–83].
n2:mentions: n4:24332512

Subject Item: _:vb71241119
rdf:type: n2:Context
rdf:value: Immune checkpoint inhibition has been shown to be particularly effective in patients with elevated pretreatment levels of tumor PD-L1 expression [9, 11, 55, 70, 71, >>74<<, 77–83]. In one such study of NSCLC, treatment with the anti-PD-1 antibody nivolumab was shown to be more effective than docetaxel chemotherapy in patients with PD-L1 positive, but not PD-L1 negative, tumors at all classified levels of
n2:mentions: n4:25428505

Subject Item: _:vb71241120
rdf:type: n2:Context
rdf:value: Immune checkpoint inhibition has been shown to be particularly effective in patients with elevated pretreatment levels of tumor PD-L1 expression [9, 11, 55, 70, 71, 74, >>77<<–83]. In one such study of NSCLC, treatment with the anti-PD-1 antibody nivolumab was shown to be more effective than docetaxel chemotherapy in patients with PD-L1 positive, but not PD-L1 negative, tumors at all classified levels of PD-L1
n2:mentions: n4:23724867 n4:25891174 n4:22658127 n4:24145345 n4:24714771 n4:25428503 n4:25704439

Subject Item: _:vb71241121
rdf:type: n2:Context
rdf:value: anti-PD-1 antibody nivolumab was shown to be more effective than docetaxel chemotherapy in patients with PD-L1 positive, but not PD-L1 negative, tumors at all classified levels of PD-L1 expression (≥1%, ≥5%, and ≥10% of tumor cells) [>>11<<]. Similarly, in a phase I trial of nivolumab in 90 patients with unresectable melanoma, overall response rates were observed in 67% of patients with PD-L1-positive tumors (≥5%) as compared to 19% of patients with PD-L1-negative tumors [9].
n2:mentions: n4:26412456

Subject Item: _:vb71241122
rdf:type: n2:Context
rdf:value: Similarly, in a phase I trial of nivolumab in 90 patients with unresectable melanoma, overall response rates were observed in 67% of patients with PD-L1-positive tumors (≥5%) as compared to 19% of patients with PD-L1-negative tumors [>>9<<]. However, even patients with PD-L1-negative tumors have been shown to receive some survival benefit from anti-PD-1 therapy [12, 54, 56, 70].
n2:mentions: n4:25795410

Subject Item: _:vb71241123
rdf:type: n2:Context
rdf:value: However, even patients with PD-L1-negative tumors have been shown to receive some survival benefit from anti-PD-1 therapy [>>12<<, 54, 56, 70].
n2:mentions: n4:26028407

Subject Item: _:vb71241124
rdf:type: n2:Context
rdf:value: However, even patients with PD-L1-negative tumors have been shown to receive some survival benefit from anti-PD-1 therapy [12, >>54<<, 56, 70]. For example, in another phase III clinical trial of nivolumab vs docetaxel in NSCLC patients, prolonged survival was seen in patients treated with nivolumab, regardless of tumor cell PD-L1 expression [12]. The possibility exists
n2:mentions: n4:25399552

Subject Item: _:vb71241125
rdf:type: n2:Context
rdf:value: However, even patients with PD-L1-negative tumors have been shown to receive some survival benefit from anti-PD-1 therapy [12, 54, >>56<<, 70]. For example, in another phase III clinical trial of nivolumab vs docetaxel in NSCLC patients, prolonged survival was seen in patients treated with nivolumab, regardless of tumor cell PD-L1 expression [12]. The possibility exists
n2:mentions: n4:25891173

Subject Item: _:vb71241126
rdf:type: n2:Context
rdf:value: However, even patients with PD-L1-negative tumors have been shown to receive some survival benefit from anti-PD-1 therapy [12, 54, 56, >>70<<]. For example, in another phase III clinical trial of nivolumab vs docetaxel in NSCLC patients, prolonged survival was seen in patients treated with nivolumab, regardless of tumor cell PD-L1 expression [12]. The possibility exists that in
n2:mentions: n4:25428504

Subject Item: _:vb71241127
rdf:type: n2:Context
rdf:value: For example, in another phase III clinical trial of nivolumab vs docetaxel in NSCLC patients, prolonged survival was seen in patients treated with nivolumab, regardless of tumor cell PD-L1 expression [>>12<<]. The possibility exists that in this and other similar cases, PD blockade exerts therapeutic effects, at least partially, by preventing TILs from interacting with PD-L1 expressed by other infiltrating immune cells, such as dendritic
n2:mentions: n4:26028407

Subject Item: _:vb71241128
rdf:type: n2:Context
rdf:value: tumors, in which positive treatment responses were significantly associated with higher baseline levels of TIL-expressed PD-L1; in this study, there was no correlation between treatment response and PD-L1 expression on tumor cells. [>>70<<] Other studies have similarly documented associations between PD-L1 expression by peripheral blood lymphocytes, like CD4+ and CD8+ T-cells, and treatment response to immune checkpoint blockade [71].
n2:mentions: n4:25428504

Subject Item: _:vb71241129
rdf:type: n2:Context
rdf:value: [70] Other studies have similarly documented associations between PD-L1 expression by peripheral blood lymphocytes, like CD4+ and CD8+ T-cells, and treatment response to immune checkpoint blockade [>>71<<]. However so far, there are no published studies evaluating T-cell response following treatment with checkpoint inhibitors in GBM.
n2:mentions: n4:24332512

Subject Item: _:vb71241130
rdf:type: n2:Context
rdf:value: In some cases, anti-PD therapy has been associated with accelerated disease progression and reduced OS, in a phenomenon known as hyperprogressive disease (HPD) [>>84<<–87]. Observed in a small subset of patients, HPD occurs in many different tumor types and has been shown to be independent of initial tumor burden. Although the mechanism of HPD remains unknown, it has been linked with several genetic
n2:mentions: n4:28351930 n4:26951310 n4:28419181 n4:27827313

Subject Item: _:vb71241131
rdf:type: n2:Context
rdf:value: Although the mechanism of HPD remains unknown, it has been linked with several genetic changes and is associated with advanced patient age, raising concerns for PD blockade in the elderly population [>>84<<, 85].
n2:mentions: n4:28351930

Subject Item: _:vb71241132
rdf:type: n2:Context
rdf:value: Although the mechanism of HPD remains unknown, it has been linked with several genetic changes and is associated with advanced patient age, raising concerns for PD blockade in the elderly population [84, >>85<<].
n2:mentions: n4:27827313

Subject Item: _:vb71241133
rdf:type: n3:Section
dc:title: insight into trial failure
n3:contains: _:vb71241136 _:vb71241137 _:vb71241138 _:vb71241139 _:vb71241134 _:vb71241135

Subject Item: _:vb71241134
rdf:type: n2:Context
rdf:value: it is widely known that patients suffering from GBM experience global immune dysfunction and possess reduced levels of circulating CD4+ and CD8+ lymphocytes, an effect compounded by lymphocyte-depleting treatments such as chemotherapy [>>88<<, 89]. The treatment of CNS pathology, including malignant glioma, has been historically limited by poor drug penetration of the BBB [4], which is significantly prohibitive for compounds of size greater than 400-600 Da [90].
n2:mentions: n4:27964820

Subject Item: _:vb71241135
rdf:type: n2:Context
rdf:value: is widely known that patients suffering from GBM experience global immune dysfunction and possess reduced levels of circulating CD4+ and CD8+ lymphocytes, an effect compounded by lymphocyte-depleting treatments such as chemotherapy [88, >>89<<]. The treatment of CNS pathology, including malignant glioma, has been historically limited by poor drug penetration of the BBB [4], which is significantly prohibitive for compounds of size greater than 400-600 Da [90].
n2:mentions: n4:20179016

Subject Item: _:vb71241136
rdf:type: n2:Context
rdf:value: The treatment of CNS pathology, including malignant glioma, has been historically limited by poor drug penetration of the BBB [>>4<<], which is significantly prohibitive for compounds of size greater than 400-600 Da [90].
n2:mentions: n4:24028526

Subject Item: _:vb71241137
rdf:type: n2:Context
rdf:value: The treatment of CNS pathology, including malignant glioma, has been historically limited by poor drug penetration of the BBB [4], which is significantly prohibitive for compounds of size greater than 400-600 Da [>>90<<]. The calculated molecular mass of nivolumab is 146 kDa [57], supporting the assertion that antibody-mediated inhibition of the PD-1/PD-L1 axis occurs external to tumor sites and that effector T-cells, activated against tumor-associated
n2:mentions: n4:19534732

Subject Item: _:vb71241138
rdf:type: n2:Context
rdf:value: antibody-mediated inhibition of the PD-1/PD-L1 axis occurs external to tumor sites and that effector T-cells, activated against tumor-associated antigens in peripheral lymphoid tissues, enter the TME precoated with anti-PD-1 antibodies [>>52<<]. With tumor progression and particularly in the setting of recurrent disease, any PD-1-expressing lymphocytes activated against tumor antigens would be expected to have already migrated to tumor sites, where they are inaccessible to
n2:mentions: n4:26546453

Subject Item: _:vb71241139
rdf:type: n2:Context
rdf:value: Studies of T-cell function in the setting of chronic antigen exposure have suggested that these “exhausted” T-cells expressing high levels of PD-1 have poor effector functions that may not be fully restored with PD-1 blockade [>>91<<–93]. PD-1 blockade can “remove the brakes” placed on host immune responses by PD pathway signaling at tumor sites, however the ultimate antitumor effect is constrained by the host’s ability to generate adaptive immune responses against
n2:mentions: n4:20514052 n4:23460533 n4:18809920

Subject Item: _:vb639783846
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 34
n2:hasRelevantPaperId: n4:15758009

Subject Item: _:vb639783847
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 21
n2:hasRelevantPaperId: n4:27157931

Subject Item: _:vb639783848
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 20
n2:hasRelevantPaperId: n4:30742122

Subject Item: _:vb639783849
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 20
n2:hasRelevantPaperId: n4:20129251

Subject Item: _:vb639783850
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 20
n2:hasRelevantPaperId: n4:19269895

Subject Item: _:vb639783851
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 20
n2:hasRelevantPaperId: n4:29106665

Subject Item: _:vb639783852
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 17
n2:hasRelevantPaperId: n4:25355681

Subject Item: _:vb639783853
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 16
n2:hasRelevantPaperId: n4:28029927

Subject Item: _:vb639783854
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 15
n2:hasRelevantPaperId: n4:24120142

Subject Item: _:vb639783855
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 15
n2:hasRelevantPaperId: n4:24552317

Subject Item: _:vb639783856
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 14
n2:hasRelevantPaperId: n4:28371827

Subject Item: _:vb639783857
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 14
n2:hasRelevantPaperId: n4:28844499

Subject Item: _:vb639783858
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 14
n2:hasRelevantPaperId: n4:27001570

Subject Item: _:vb639783859
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 13
n2:hasRelevantPaperId: n4:28810147

Subject Item: _:vb639783860
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 13
n2:hasRelevantPaperId: n4:26323609

Subject Item: _:vb639783861
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 13
n2:hasRelevantPaperId: n4:30742119

Subject Item: _:vb639783862
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 13
n2:hasRelevantPaperId: n4:29643471

Subject Item: _:vb639783863
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 12
n2:hasRelevantPaperId: n4:18772890

Subject Item: _:vb639783864
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 12
n2:hasRelevantPaperId: n4:29260225

Subject Item: _:vb639783865
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 12
n2:hasRelevantPaperId: n4:28426845

Subject Item: _:vb639783866
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 12
n2:hasRelevantPaperId: n4:28697342

Subject Item: _:vb639783867
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 12
n2:hasRelevantPaperId: n4:28724573

Subject Item: _:vb639783868
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 12
n2:hasRelevantPaperId: n4:24691018

Subject Item: _:vb639783869
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 12
n2:hasRelevantPaperId: n4:30742120

Subject Item: _:vb639783870
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 11
n2:hasRelevantPaperId: n4:23462419

Subject Item: _:vb639783871
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 11
n2:hasRelevantPaperId: n4:29943666

Subject Item: _:vb639783872
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 11
n2:hasRelevantPaperId: n4:22437870

Subject Item: _:vb639783873
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 11
n2:hasRelevantPaperId: n4:26546453

Subject Item: _:vb639783874
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 10
n2:hasRelevantPaperId: n4:29437767

Subject Item: _:vb639783875
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 10
n2:hasRelevantPaperId: n4:25765070

Subject Item: _:vb639783876
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 10
n2:hasRelevantPaperId: n4:23945592

Subject Item: _:vb639783877
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 10
n2:hasRelevantPaperId: n4:26713745

Subject Item: _:vb639783878
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 9
n2:hasRelevantPaperId: n4:26030524

Subject Item: _:vb639783879
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 9
n2:hasRelevantPaperId: n4:27683556

Subject Item: _:vb639783880
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 9
n2:hasRelevantPaperId: n4:26027431

Subject Item: _:vb639783881
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 9
n2:hasRelevantPaperId: n4:29432077

Subject Item: _:vb639783882
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 8
n2:hasRelevantPaperId: n4:29843811

Subject Item: _:vb639783883
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 8
n2:hasRelevantPaperId: n4:30777100

Subject Item: _:vb639783884
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 8
n2:hasRelevantPaperId: n4:18669428

Subject Item: _:vb639783885
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 8
n2:hasRelevantPaperId: n4:24552318

Subject Item: _:vb639783886
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 8
n2:hasRelevantPaperId: n4:16199517

Subject Item: _:vb639783887
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 8
n2:hasRelevantPaperId: n4:23613317

Subject Item: _:vb639783888
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 8
n2:hasRelevantPaperId: n4:26059190

Subject Item: _:vb639783889
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