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10.1186%2F1479-5876-10-146
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results
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The Ki-67 protein (also known as MKI67) is a cellular marker for proliferation [>>39<<] and cell cycling [40] and is an indicator of the growth fraction of a given cell population.
n2:mentions
n3:10653597
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_:vb16980026
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The Ki-67 protein (also known as MKI67) is a cellular marker for proliferation [39] and cell cycling [>>40<<] and is an indicator of the growth fraction of a given cell population.
n2:mentions
n3:20921622
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ICOS is a T cell surface molecule structurally related to CD28 and CTLA-4 [>>41<<]. It is expressed at low levels on resting naïve T cells and is rapidly up-regulated following TCR ligation and CD28 costimulation [42].
n2:mentions
n3:11343121
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It is expressed at low levels on resting naïve T cells and is rapidly up-regulated following TCR ligation and CD28 costimulation [>>42<<]. After ipilimumab treatment, ICOS was increased significantly on CD4+ and CD8+ T cells in both 3-month and 6-month post-treatment PBMCs (p ≤ 0.0001 with a median fold-increase of 1.34 to 2.90), with higher increases on CD4+ than on CD8+
n2:mentions
n3:11046032
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_:vb16980029
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Our analysis highlighted the potential importance of EOMES, a transcription factor in the T-box family and involved in the regulation of INF-γ, granzyme B and perforin production by CD8+ T cells [>>43<<]. To better understand the potential role of EOMES+CD8+ T cells in ipilimumab treatment, we stratified pre-treatment specimens by the median % of EOMES+CD8+ T cells.
n2:mentions
n3:14605368
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discussion
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ICOS is not necessary for Th17 differentiation, but it is required for the expansion of the Th17 compartment [>>44<<]. ICOS expressing cells may also demonstrate anti-tumor reactivity and be responsible in part for the anti-tumor effects of ipilimumab [45].
n2:mentions
n3:19098919
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ICOS expressing cells may also demonstrate anti-tumor reactivity and be responsible in part for the anti-tumor effects of ipilimumab [>>45<<].
n2:mentions
n3:21708958
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_:vb16980033
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Interestingly, there was no alteration observed in the frequency of Ki67 positive cells among tumor infiltrating lymphocytes when post –tremelimumab biopsies were compared to baseline biopsies [>>34<<]. The reason for increased Ki-67 in CD4+ and CD8+ T cells in peripheral blood, but not in the tumor site might be due to the differences in the CTLA-4 blocking antibodies or the different time points for sample harvesting, or lymphocytes
n2:mentions
n3:21558401
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and CD8+ T cells in peripheral blood, but not in the tumor site might be due to the differences in the CTLA-4 blocking antibodies or the different time points for sample harvesting, or lymphocytes may proliferate in lymphoid organs [>>33<<] and the peripheral blood compartment before they infiltrate into tumor sites.
n2:mentions
n3:20150263
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The use of microarrays and T cell phenotypic analysis to confirm the changes in gene expression would not have detected the alterations seen in detailed phosphoflow assays by Comin-Anduix et al [>>32<<]. Interestingly, the microarray analysis in the current work did not show that major alterations were seen in downstream TCR and cytokine signaling molecules, so we cannot confirm or refute their data. We did not see significant changes
n2:mentions
n3:20856802
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we focused on the effects of ipilimumab on T cells as an effective immunotherapeutic agent, it might also have a wider impact on the immune system, not only on CD4+ and CD8+ T cells as in our current study, but also on CD14+ monocytes [>>32<<] and B cells [46].
n2:mentions
n3:20856802
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effects of ipilimumab on T cells as an effective immunotherapeutic agent, it might also have a wider impact on the immune system, not only on CD4+ and CD8+ T cells as in our current study, but also on CD14+ monocytes [32] and B cells [>>46<<].
n2:mentions
n3:19789309
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Ipilimumab may also rescue tumor-impaired IFN-γ pathways in CD4+ T cells [>>47<<], since a number of genes associated with IFN-γ signals such as STAT1, ISG15, GBp1, and EIF2AK2 were up-regulated by ipilimumab (data not shown).
n2:mentions
n3:17488182
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Up-regulation of STAT1 has been confirmed by phosphoflow [>>32<<] after tremelimumab.
n2:mentions
n3:20856802
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Eomesodermin (EOMES) is an important transcription factor controlling the function of effector CD8+ T cells [>>43<<]. The expression of EOMES in CD8+ T cells may reflect a critical basal level of immune competence of the melanoma patient.
n2:mentions
n3:14605368
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CTLA-4 signaling may specifically target EOMES resulting in reduced IFN-γ and granzyme B expression by selectively inhibiting accumulation of EOMES mRNA and protein [>>48<<]. Ectopic expression of EOMES reversed CTLA-4 mediated inhibition of effector molecules, and CTLA-4-/ CD8+ T cells had greatly enhanced IFN-γ and granzyme B production, as well as enhanced cytolytic function and increased expression of
n2:mentions
n3:19283722
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expression of EOMES reversed CTLA-4 mediated inhibition of effector molecules, and CTLA-4-/ CD8+ T cells had greatly enhanced IFN-γ and granzyme B production, as well as enhanced cytolytic function and increased expression of EOMES [>>48<<]. The increase in IFN-γ signals and up-regulated % of granzyme B expression on EOMES+/CD8+ T cells (p = 0.003, data not shown) in our current study would suggest ipilimumab interferes with the down-regulation of EOMES and its downstream
n2:mentions
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CTLA-4 expression is associated with decreased proliferation with cell cycle arrest at the G1-S interface and diminished cytokine secretion [2,>>3<<]. It decreases cell proliferation through the inhibition of mitogen-activated (MAP) kinases but promotes T cell survival through the binding of phosphoinositol-3 kinase and activating protein kinase B (PKB/AKT) resulting in T cell anergy
n2:mentions
n3:11239447
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inhibition of mitogen-activated (MAP) kinases but promotes T cell survival through the binding of phosphoinositol-3 kinase and activating protein kinase B (PKB/AKT) resulting in T cell anergy and tolerance without the death of T cells [>>4<<]. CTLA-4 signals suppress both CD4+ and CD8+ T cell responses via a tyrosine-based inhibitory motif [5,6].
n2:mentions
n3:19052636
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CTLA-4 signals suppress both CD4+ and CD8+ T cell responses via a tyrosine-based inhibitory motif [>>5<<,6].
n2:mentions
n3:11825563
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CTLA-4 signals suppress both CD4+ and CD8+ T cell responses via a tyrosine-based inhibitory motif [5,>>6<<].
n2:mentions
n3:12087419
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CTLA-4 blockade has antitumor activity in mice, and important effects on the breaking of tolerance [>>6<<-10]. In experiments with B16 melanoma, a therapeutic effect induced by CTLA-4 blockade with a vaccine was associated with the development of autoimmune vitiligo, suggesting that expansion of T cells recognizing melanocyte lineage antigens
n2:mentions
n3:10430624 n3:1335364 n3:12087419 n3:8596936 n3:16778987
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Several autoimmune diseases were associated with the single nucleotide polymorphisms in the CTLA-4 gene, including hypothyroidism and type 1 diabetes [>>11<<]. In CTLA-4 -/- knockout mice, expansion of lymphocytes with diffuse lymphadenopathy and lymphoid infiltration of different organs occurs, consistent with a generalized expansion of T cells [12]. Similarly, both preclinical and clinical
n2:mentions
n3:12724780
Subject Item
_:vb16980050
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In CTLA-4 -/- knockout mice, expansion of lymphocytes with diffuse lymphadenopathy and lymphoid infiltration of different organs occurs, consistent with a generalized expansion of T cells [>>12<<]. Similarly, both preclinical and clinical data indicate that CTLA-4 blockade results in activation and expansion of the total CD4+ and CD8+ effector T cells [13], and the breaking of self-tolerance has been shown in patients, as
n2:mentions
n3:7481803
Subject Item
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Similarly, both preclinical and clinical data indicate that CTLA-4 blockade results in activation and expansion of the total CD4+ and CD8+ effector T cells [>>13<<], and the breaking of self-tolerance has been shown in patients, as evidenced by the occurrence of immune-related adverse events (irAEs) observed with two different CTLA-4 antibodies, ipilimumab (Bristol Myers Squibb, Princeton, NJ) [14]
n2:mentions
n3:19001145
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shown in patients, as evidenced by the occurrence of immune-related adverse events (irAEs) observed with two different CTLA-4 antibodies, ipilimumab (Bristol Myers Squibb, Princeton, NJ) [14] and tremelimumab (Pfizer, New York, NY) [>>15<<].
n2:mentions
n3:19001146
Subject Item
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Ipilimumab is a fully human CTLA-4 blocking IgG1 monoclonal antibody which induces long-lasting clinical responses in a minority of patients with metastatic melanoma [>>16<<-21]. Ipilimumab with or without a gp100 peptide vaccine, compared with gp100 vaccine alone, improved overall survival (OS) in patients with previously treated metastatic melanoma [22].
n2:mentions
n3:20004617 n3:12826605 n3:19671877 n3:18838703 n3:20147741
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Ipilimumab with or without a gp100 peptide vaccine, compared with gp100 vaccine alone, improved overall survival (OS) in patients with previously treated metastatic melanoma [>>22<<]. Ipilimumab when combined with dacarbazine improved overall survival in previously untreated patients compared to dacarbazine alone [23]. These were the first randomized Phase III trials to demonstrate a significant survival impact for
n2:mentions
n3:20525992
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Ipilimumab when combined with dacarbazine improved overall survival in previously untreated patients compared to dacarbazine alone [>>23<<]. These were the first randomized Phase III trials to demonstrate a significant survival impact for patients with metastatic melanoma, yet few studies have shed light on its anti-tumor mechanism, or documented pharmacodynamic (PD) markers
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An increase in the absolute lymphocyte count (ALC) after 2 or 3 doses of the drug at weeks 4 and 7 has been documented [>>24<<], and may correlate with an improved outcome; increased CD4+ HLA-DR+ T cells have been shown in several studies to occur after ipilimumab therapy [25,26]; in several small cohort studies of brief duration, ipilimumab treatment increased
n2:mentions
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count (ALC) after 2 or 3 doses of the drug at weeks 4 and 7 has been documented [24], and may correlate with an improved outcome; increased CD4+ HLA-DR+ T cells have been shown in several studies to occur after ipilimumab therapy [>>25<<,26]; in several small cohort studies of brief duration, ipilimumab treatment increased the frequency of CD4+ICOShi T cells in tumors and in the circulation, and it also induced antibody reactivity against the cancer-testis antigen
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n3:15613700
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count (ALC) after 2 or 3 doses of the drug at weeks 4 and 7 has been documented [24], and may correlate with an improved outcome; increased CD4+ HLA-DR+ T cells have been shown in several studies to occur after ipilimumab therapy [25,>>26<<]; in several small cohort studies of brief duration, ipilimumab treatment increased the frequency of CD4+ICOShi T cells in tumors and in the circulation, and it also induced antibody reactivity against the cancer-testis antigen NY-ESO-1
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several small cohort studies of brief duration, ipilimumab treatment increased the frequency of CD4+ICOShi T cells in tumors and in the circulation, and it also induced antibody reactivity against the cancer-testis antigen NY-ESO-1 [27,>>28<<]. CTLA-4 abrogating antibodies do not impact on vaccine-specific immune responses [29] and even when administered with a peptide vaccine, tumor antigen-specific responses were only modestly increased [29,30].
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CTLA-4 abrogating antibodies do not impact on vaccine-specific immune responses [>>29<<] and even when administered with a peptide vaccine, tumor antigen-specific responses were only modestly increased [29,30].
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CTLA-4 abrogating antibodies do not impact on vaccine-specific immune responses [29] and even when administered with a peptide vaccine, tumor antigen-specific responses were only modestly increased [>>29<<,30]. Recall responses to viral and other antigens were not altered by ipilimumab. In patients receiving another CTLA-4 abrogating antibody, tremelimumab, the ratio of intratumoral T cells to FoxP3 positive T regulatory cells was increased
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CTLA-4 abrogating antibodies do not impact on vaccine-specific immune responses [29] and even when administered with a peptide vaccine, tumor antigen-specific responses were only modestly increased [29,>>30<<]. Recall responses to viral and other antigens were not altered by ipilimumab. In patients receiving another CTLA-4 abrogating antibody, tremelimumab, the ratio of intratumoral T cells to FoxP3 positive T regulatory cells was increased
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In patients receiving another CTLA-4 abrogating antibody, tremelimumab, the ratio of intratumoral T cells to FoxP3 positive T regulatory cells was increased after treatment only in regressing lesions [>>30<<], suggesting a therapeutic impact of CTLA-4 abrogation on T cells infiltrating the tumor.
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The same investigators also demonstrated that peripheral blood Th17 cells were induced by tremelimumab [>>31<<], and that certain signaling pathways downstream of the TCR and cytokine receptor were also influenced by CTLA-4 blockade, such as increased pp38, pSTAT1 and pSTAT3, and decreased pLck, pERK1/2 and pSTAT5 levels [32].
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by tremelimumab [31], and that certain signaling pathways downstream of the TCR and cytokine receptor were also influenced by CTLA-4 blockade, such as increased pp38, pSTAT1 and pSTAT3, and decreased pLck, pERK1/2 and pSTAT5 levels [>>32<<]. CTLA-4 blockade also induced cell proliferation in the spleen, a secondary lymphoid organ, shown by molecular imaging with the PET probe 18 F-FLT [33].
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CTLA-4 blockade also induced cell proliferation in the spleen, a secondary lymphoid organ, shown by molecular imaging with the PET probe 18 F-FLT [>>33<<]. Those investigators also reported significantly increased intratumoral CD4+ and mostly CD8+ T cell infiltration, with increased HLA-DR and CD45RO double positive cells in post tremelimumab biopsies [34] and increased expression of FoxP3.
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Those investigators also reported significantly increased intratumoral CD4+ and mostly CD8+ T cell infiltration, with increased HLA-DR and CD45RO double positive cells in post tremelimumab biopsies [>>34<<] and increased expression of FoxP3.
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material and methods
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The demographic and clinic outcomes of the patients in the current study are shown in Table 1, which have been previously reported [>>26<<] with updated follow-up:
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Briefly, the extracted poly-(A) RNA was specifically converted to cDNA, amplified and labeled with biotin following the procedure initially described by Van Gelder et al. [>>35<<]. Biotin-labeled cDNA was hybridized onto Affymetrix U133 Plus 2.0 microarrays. Microarray data were then analyzed using Affymetrix Expression Console. Gene detect calls were obtained using the Affymetrix MAS5 algorithm [36] to filter
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Gene detect calls were obtained using the Affymetrix MAS5 algorithm [>>36<<] to filter genes that are not expressed across the board and express value or signal intensity was calculated by the robust multi-array analysis method (RMA) developed by Irizarry et al [37].
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obtained using the Affymetrix MAS5 algorithm [36] to filter genes that are not expressed across the board and express value or signal intensity was calculated by the robust multi-array analysis method (RMA) developed by Irizarry et al [>>37<<]. Differential gene expressions were then assessed using Student’s t-test and false discovery rate (FDR) was estimated [38].
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Differential gene expressions were then assessed using Student’s t-test and false discovery rate (FDR) was estimated [>>38<<].
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