ORCID Profile
0000-0003-2258-5030
Current Organisations
Fels Institute for Cancer Research & Molecular Biology
,
Coriell Institute for Medical Research
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Publisher: American Association for Cancer Research (AACR)
Date: 06-2023
DOI: 10.1158/1078-0432.23275177
Abstract: Supplementary Figure 2: Modest treatment-induced DNA methylation changes in UC tumors.
Publisher: American Association for Cancer Research (AACR)
Date: 11-04-2023
DOI: 10.1158/1078-0432.22587060.V1
Abstract: Supplementary Figure 2: Modest treatment-induced DNA methylation changes in UC tumors.
Publisher: American Association for Cancer Research (AACR)
Date: 15-12-2012
Publisher: American Association for Cancer Research (AACR)
Date: 06-2023
DOI: 10.1158/1078-0432.23275174
Abstract: Supplementary Figure 3: Copy number variation detected by SeSAMe from DNA methylation data.
Publisher: American Association for Cancer Research (AACR)
Date: 06-2023
DOI: 10.1158/1078-0432.23275171
Abstract: Supplementary Figure 4: Weak correlation of TE expression induction with DNA methylation change and viral mimicry activation.
Publisher: American Association for Cancer Research (AACR)
Date: 11-04-2023
DOI: 10.1158/1078-0432.22587045.V1
Abstract: Supplementary Figure 7: Representative IHC staining of additional PD and SD tumors in pre-treatment and post-treatment timepoint from additional patients.
Publisher: Wiley
Date: 13-09-2017
DOI: 10.1002/IJC.31014
Publisher: American Association for Cancer Research (AACR)
Date: 11-04-2023
DOI: 10.1158/1078-0432.22587048.V1
Abstract: Supplementary Figure 6: Gene Set Enrichment Analysis reveals immune-related pathways discriminate PD and SD tumors.
Publisher: American Association for Cancer Research (AACR)
Date: 06-2023
DOI: 10.1158/1078-0432.23275186.V1
Abstract: Supplementary Figure 10: Peripheral immune cell dynamics induced by combination therapy.
Publisher: American Association for Cancer Research (AACR)
Date: 11-04-2023
DOI: 10.1158/1078-0432.22587054
Abstract: Supplementary Figure 4: Weak correlation of TE expression induction with DNA methylation change and viral mimicry activation.
Publisher: American Association for Cancer Research (AACR)
Date: 11-04-2023
DOI: 10.1158/1078-0432.22587051
Abstract: Supplementary Figure 5: Overall tumor mutation burden and frequency of mutations in cancer-associated genes in UC tumors.
Publisher: American Society of Hematology
Date: 27-08-2009
DOI: 10.1182/BLOOD-2009-01-198416
Abstract: Juvenile myelomonocytic leukemia is an aggressive myeloproliferative disorder characterized by malignant transformation in the hematopoietic stem cell compartment with proliferation of differentiated progeny. Seventy-five percent of patients harbor mutations in the NF1, NRAS, KRAS, or PTPN11 genes, which encode components of Ras signaling networks. Using single nucleotide polymorphism arrays, we identified a region of 11q isodisomy that contains the CBL gene in several JMML s les, and subsequently identified CBL mutations in 27 of 159 JMML s les. Thirteen of these mutations alter codon Y371. In this report, we also demonstrate that CBL and RAS/PTPN11 mutations were mutually exclusive in these patients. Moreover, the exclusivity of CBL mutations with respect to other Ras pathway-associated mutations indicates that CBL may have a role in deregulating this key pathway in JMML.
Publisher: American Association for Cancer Research (AACR)
Date: 11-04-2023
DOI: 10.1158/1078-0432.22587057
Abstract: Supplementary Figure 3: Copy number variation detected by SeSAMe from DNA methylation data.
Publisher: American Association for Cancer Research (AACR)
Date: 06-2023
DOI: 10.1158/1078-0432.23275153.V1
Abstract: Supplementary TablesSupplementary Table 1: Patient and tumor s le informationSupplementary Table 2: Tumor mutation burdenSupplementary Table 3: Unfiltered whole exome sequencing mutation analysisSupplementary Table 4: Filtered whole exome sequencing mutation analysisSupplementary Table 5: Immunohistochemistry scores of tumorsSupplementary Table 6: FACS panel for PBMC analysisSupplementary Table 7: Geometric mean fluorescence intensity (GMFI) from PBMC FACSSupplementary Table 8: Representativeness of Study Participants
Publisher: American Association for Cancer Research (AACR)
Date: 11-04-2023
DOI: 10.1158/1078-0432.22587054.V1
Abstract: Supplementary Figure 4: Weak correlation of TE expression induction with DNA methylation change and viral mimicry activation.
Publisher: American Association for Cancer Research (AACR)
Date: 11-04-2023
DOI: 10.1158/1078-0432.22587039.V1
Abstract: Supplementary Figure 9: CD8 infiltration in tumor is associated with survival.
Publisher: American Association for Cancer Research (AACR)
Date: 06-2023
DOI: 10.1158/1078-0432.23275177.V1
Abstract: Supplementary Figure 2: Modest treatment-induced DNA methylation changes in UC tumors.
Publisher: American Association for Cancer Research (AACR)
Date: 06-2023
DOI: 10.1158/1078-0432.23275189
Abstract: Supplementary Figure 1: Patient recruitment and s le collection overview.
Publisher: American Association for Cancer Research (AACR)
Date: 06-2023
DOI: 10.1158/1078-0432.23275183
Abstract: Supplementary Figure 11: Peripheral immune cells are activated mid-treatment cycle.
Publisher: American Association for Cancer Research (AACR)
Date: 06-2023
DOI: 10.1158/1078-0432.23275186
Abstract: Supplementary Figure 10: Peripheral immune cell dynamics induced by combination therapy.
Publisher: American Association for Cancer Research (AACR)
Date: 06-2023
DOI: 10.1158/1078-0432.C.6571947
Abstract: AbstractPurpose: On the basis of preclinical evidence of epigenetic contribution to sensitivity and resistance to immune checkpoint inhibitors (ICI), we hypothesized that guadecitabine (hypomethylating agent) and atezolizumab [anti–programmed cell death ligand 1 (PD-L1)] together would potentiate a clinical response in patients with metastatic urothelial carcinoma (UC) unresponsive to initial immune checkpoint blockade therapy. Patients and Methods: We designed a single arm phase II study (NCT03179943) with a safety run-in to identify the recommended phase II dose of the combination therapy of guadecitabine and atezolizumab. Patients with recurrent/advanced UC who had previously progressed on ICI therapy with programmed cell death protein 1 or PD-L1 targeting agents were eligible. Preplanned correlative analysis was performed to characterize peripheral immune dynamics and global DNA methylation, transcriptome, and immune infiltration dynamics of patient tumors. Results: Safety run-in enrolled 6 patients and phase II enrolled 15 patients before the trial was closed for futility. No dose-limiting toxicity was observed. Four patients, with best response of stable disease (SD), exhibited extended tumor control (8–11 months) and survival ( months). Correlative analysis revealed lack of DNA demethylation in tumors after 2 cycles of treatment. Increased peripheral immune activation and immune infiltration in tumors after treatment correlated with progression-free survival and SD. Furthermore, high IL6 and IL8 levels in the patients’ plasma was associated with short survival. Conclusions: No RECIST responses were observed after combination therapy in this trial. Although we could not detect the anticipated tumor-intrinsic effects of guadecitabine, the addition of hypomethylating agent to ICI therapy induced immune activation in a few patients, which associated with longer patient survival. /
Publisher: American Association for Cancer Research (AACR)
Date: 06-2023
DOI: 10.1158/1078-0432.23275180
Abstract: Supplementary Figure 12: HLA-DR and NKG2D abundance on peripheral lymphocytes associate with longer progression free survival.
Publisher: American Association for Cancer Research (AACR)
Date: 11-04-2023
DOI: 10.1158/1078-0432.22587042.V1
Abstract: Supplementary Figure 8: PD-L1 levels in tumor or tumor microenvironment does not associate with tumor progression or control.
Publisher: American Association for Cancer Research (AACR)
Date: 06-2023
DOI: 10.1158/1078-0432.23275183.V1
Abstract: Supplementary Figure 11: Peripheral immune cells are activated mid-treatment cycle.
Publisher: American Association for Cancer Research (AACR)
Date: 06-2023
DOI: 10.1158/1078-0432.23275162.V1
Abstract: Supplementary Figure 7: Representative IHC staining of additional PD and SD tumors in pre-treatment and post-treatment timepoint from additional patients.
Publisher: American Association for Cancer Research (AACR)
Date: 11-04-2023
DOI: 10.1158/1078-0432.22587063.V1
Abstract: Supplementary Figure 12: HLA-DR and NKG2D abundance on peripheral lymphocytes associate with longer progression free survival.
Publisher: American Association for Cancer Research (AACR)
Date: 11-04-2023
DOI: 10.1158/1078-0432.22587042
Abstract: Supplementary Figure 8: PD-L1 levels in tumor or tumor microenvironment does not associate with tumor progression or control.
Publisher: Informa UK Limited
Date: 30-04-2009
DOI: 10.4161/EPI.4.3.8694
Publisher: American Association for Cancer Research (AACR)
Date: 06-2023
DOI: 10.1158/1078-0432.23275156.V1
Abstract: Supplementary Figure 9: CD8 infiltration in tumor is associated with survival.
Publisher: American Association for Cancer Research (AACR)
Date: 11-04-2023
DOI: 10.1158/1078-0432.22587045
Abstract: Supplementary Figure 7: Representative IHC staining of additional PD and SD tumors in pre-treatment and post-treatment timepoint from additional patients.
Publisher: American Association for Cancer Research (AACR)
Date: 11-04-2023
DOI: 10.1158/1078-0432.22587036.V1
Abstract: Supplementary TablesSupplementary Table 1: Patient and tumor s le informationSupplementary Table 2: Tumor mutation burdenSupplementary Table 3: Unfiltered whole exome sequencing mutation analysisSupplementary Table 4: Filtered whole exome sequencing mutation analysisSupplementary Table 5: Immunohistochemistry scores of tumorsSupplementary Table 6: FACS panel for PBMC analysisSupplementary Table 7: Geometric mean fluorescence intensity (GMFI) from PBMC FACSSupplementary Table 8: Representativeness of Study Participants
Publisher: American Association for Cancer Research (AACR)
Date: 11-04-2023
DOI: 10.1158/1078-0432.22587057.V1
Abstract: Supplementary Figure 3: Copy number variation detected by SeSAMe from DNA methylation data.
Publisher: American Association for Cancer Research (AACR)
Date: 11-04-2023
DOI: 10.1158/1078-0432.22587048
Abstract: Supplementary Figure 6: Gene Set Enrichment Analysis reveals immune-related pathways discriminate PD and SD tumors.
Publisher: American Association for Cancer Research (AACR)
Date: 06-2023
DOI: 10.1158/1078-0432.23275174.V1
Abstract: Supplementary Figure 3: Copy number variation detected by SeSAMe from DNA methylation data.
Publisher: American Association for Cancer Research (AACR)
Date: 06-2023
DOI: 10.1158/1078-0432.23275156
Abstract: Supplementary Figure 9: CD8 infiltration in tumor is associated with survival.
Publisher: American Association for Cancer Research (AACR)
Date: 06-2023
DOI: 10.1158/1078-0432.23275153
Abstract: Supplementary TablesSupplementary Table 1: Patient and tumor s le informationSupplementary Table 2: Tumor mutation burdenSupplementary Table 3: Unfiltered whole exome sequencing mutation analysisSupplementary Table 4: Filtered whole exome sequencing mutation analysisSupplementary Table 5: Immunohistochemistry scores of tumorsSupplementary Table 6: FACS panel for PBMC analysisSupplementary Table 7: Geometric mean fluorescence intensity (GMFI) from PBMC FACSSupplementary Table 8: Representativeness of Study Participants
Publisher: American Association for Cancer Research (AACR)
Date: 06-2023
DOI: 10.1158/1078-0432.23275168.V1
Abstract: Supplementary Figure 5: Overall tumor mutation burden and frequency of mutations in cancer-associated genes in UC tumors.
Publisher: American Association for Cancer Research (AACR)
Date: 06-2023
DOI: 10.1158/1078-0432.23275180.V1
Abstract: Supplementary Figure 12: HLA-DR and NKG2D abundance on peripheral lymphocytes associate with longer progression free survival.
Publisher: American Association for Cancer Research (AACR)
Date: 11-04-2023
DOI: 10.1158/1078-0432.22587066.V1
Abstract: Supplementary Figure 11: Peripheral immune cells are activated mid-treatment cycle.
Publisher: American Association for Cancer Research (AACR)
Date: 06-2023
DOI: 10.1158/1078-0432.23275165.V1
Abstract: Supplementary Figure 6: Gene Set Enrichment Analysis reveals immune-related pathways discriminate PD and SD tumors.
Publisher: American Association for Cancer Research (AACR)
Date: 16-03-2023
DOI: 10.1158/1078-0432.CCR-22-3642
Abstract: On the basis of preclinical evidence of epigenetic contribution to sensitivity and resistance to immune checkpoint inhibitors (ICI), we hypothesized that guadecitabine (hypomethylating agent) and atezolizumab [anti–programmed cell death ligand 1 (PD-L1)] together would potentiate a clinical response in patients with metastatic urothelial carcinoma (UC) unresponsive to initial immune checkpoint blockade therapy. We designed a single arm phase II study (NCT03179943) with a safety run-in to identify the recommended phase II dose of the combination therapy of guadecitabine and atezolizumab. Patients with recurrent/advanced UC who had previously progressed on ICI therapy with programmed cell death protein 1 or PD-L1 targeting agents were eligible. Preplanned correlative analysis was performed to characterize peripheral immune dynamics and global DNA methylation, transcriptome, and immune infiltration dynamics of patient tumors. Safety run-in enrolled 6 patients and phase II enrolled 15 patients before the trial was closed for futility. No dose-limiting toxicity was observed. Four patients, with best response of stable disease (SD), exhibited extended tumor control (8–11 months) and survival (& months). Correlative analysis revealed lack of DNA demethylation in tumors after 2 cycles of treatment. Increased peripheral immune activation and immune infiltration in tumors after treatment correlated with progression-free survival and SD. Furthermore, high IL6 and IL8 levels in the patients’ plasma was associated with short survival. No RECIST responses were observed after combination therapy in this trial. Although we could not detect the anticipated tumor-intrinsic effects of guadecitabine, the addition of hypomethylating agent to ICI therapy induced immune activation in a few patients, which associated with longer patient survival.
Publisher: American Association for Cancer Research (AACR)
Date: 11-04-2023
DOI: 10.1158/1078-0432.22587072
Abstract: Supplementary Figure 1: Patient recruitment and s le collection overview.
Publisher: American Association for Cancer Research (AACR)
Date: 06-2023
DOI: 10.1158/1078-0432.C.6571947.V2
Abstract: AbstractPurpose: On the basis of preclinical evidence of epigenetic contribution to sensitivity and resistance to immune checkpoint inhibitors (ICI), we hypothesized that guadecitabine (hypomethylating agent) and atezolizumab [anti–programmed cell death ligand 1 (PD-L1)] together would potentiate a clinical response in patients with metastatic urothelial carcinoma (UC) unresponsive to initial immune checkpoint blockade therapy. Patients and Methods: We designed a single arm phase II study (NCT03179943) with a safety run-in to identify the recommended phase II dose of the combination therapy of guadecitabine and atezolizumab. Patients with recurrent/advanced UC who had previously progressed on ICI therapy with programmed cell death protein 1 or PD-L1 targeting agents were eligible. Preplanned correlative analysis was performed to characterize peripheral immune dynamics and global DNA methylation, transcriptome, and immune infiltration dynamics of patient tumors. Results: Safety run-in enrolled 6 patients and phase II enrolled 15 patients before the trial was closed for futility. No dose-limiting toxicity was observed. Four patients, with best response of stable disease (SD), exhibited extended tumor control (8–11 months) and survival ( months). Correlative analysis revealed lack of DNA demethylation in tumors after 2 cycles of treatment. Increased peripheral immune activation and immune infiltration in tumors after treatment correlated with progression-free survival and SD. Furthermore, high IL6 and IL8 levels in the patients’ plasma was associated with short survival. Conclusions: No RECIST responses were observed after combination therapy in this trial. Although we could not detect the anticipated tumor-intrinsic effects of guadecitabine, the addition of hypomethylating agent to ICI therapy induced immune activation in a few patients, which associated with longer patient survival. /
Publisher: American Association for Cancer Research (AACR)
Date: 11-04-2023
DOI: 10.1158/1078-0432.22587039
Abstract: Supplementary Figure 9: CD8 infiltration in tumor is associated with survival.
Publisher: American Association for Cancer Research (AACR)
Date: 11-04-2023
DOI: 10.1158/1078-0432.C.6571947.V1
Abstract: AbstractPurpose: On the basis of preclinical evidence of epigenetic contribution to sensitivity and resistance to immune checkpoint inhibitors (ICI), we hypothesized that guadecitabine (hypomethylating agent) and atezolizumab [anti–programmed cell death ligand 1 (PD-L1)] together would potentiate a clinical response in patients with metastatic urothelial carcinoma (UC) unresponsive to initial immune checkpoint blockade therapy. Patients and Methods: We designed a single arm phase II study (NCT03179943) with a safety run-in to identify the recommended phase II dose of the combination therapy of guadecitabine and atezolizumab. Patients with recurrent/advanced UC who had previously progressed on ICI therapy with programmed cell death protein 1 or PD-L1 targeting agents were eligible. Preplanned correlative analysis was performed to characterize peripheral immune dynamics and global DNA methylation, transcriptome, and immune infiltration dynamics of patient tumors. Results: Safety run-in enrolled 6 patients and phase II enrolled 15 patients before the trial was closed for futility. No dose-limiting toxicity was observed. Four patients, with best response of stable disease (SD), exhibited extended tumor control (8–11 months) and survival ( months). Correlative analysis revealed lack of DNA demethylation in tumors after 2 cycles of treatment. Increased peripheral immune activation and immune infiltration in tumors after treatment correlated with progression-free survival and SD. Furthermore, high IL6 and IL8 levels in the patients’ plasma was associated with short survival. Conclusions: No RECIST responses were observed after combination therapy in this trial. Although we could not detect the anticipated tumor-intrinsic effects of guadecitabine, the addition of hypomethylating agent to ICI therapy induced immune activation in a few patients, which associated with longer patient survival. /
Publisher: American Association for Cancer Research (AACR)
Date: 06-2023
DOI: 10.1158/1078-0432.23275159.V1
Abstract: Supplementary Figure 8: PD-L1 levels in tumor or tumor microenvironment does not associate with tumor progression or control.
Publisher: American Association for Cancer Research (AACR)
Date: 11-04-2023
DOI: 10.1158/1078-0432.22587036
Abstract: Supplementary TablesSupplementary Table 1: Patient and tumor s le informationSupplementary Table 2: Tumor mutation burdenSupplementary Table 3: Unfiltered whole exome sequencing mutation analysisSupplementary Table 4: Filtered whole exome sequencing mutation analysisSupplementary Table 5: Immunohistochemistry scores of tumorsSupplementary Table 6: FACS panel for PBMC analysisSupplementary Table 7: Geometric mean fluorescence intensity (GMFI) from PBMC FACSSupplementary Table 8: Representativeness of Study Participants
Publisher: American Association for Cancer Research (AACR)
Date: 06-2023
DOI: 10.1158/1078-0432.23275165
Abstract: Supplementary Figure 6: Gene Set Enrichment Analysis reveals immune-related pathways discriminate PD and SD tumors.
Publisher: American Association for Cancer Research (AACR)
Date: 06-2023
DOI: 10.1158/1078-0432.23275168
Abstract: Supplementary Figure 5: Overall tumor mutation burden and frequency of mutations in cancer-associated genes in UC tumors.
Publisher: American Association for Cancer Research (AACR)
Date: 06-2023
DOI: 10.1158/1078-0432.23275162
Abstract: Supplementary Figure 7: Representative IHC staining of additional PD and SD tumors in pre-treatment and post-treatment timepoint from additional patients.
Publisher: American Association for Cancer Research (AACR)
Date: 11-04-2023
DOI: 10.1158/1078-0432.22587063
Abstract: Supplementary Figure 12: HLA-DR and NKG2D abundance on peripheral lymphocytes associate with longer progression free survival.
Publisher: American Society of Clinical Oncology (ASCO)
Date: 12-2015
Abstract: BRAF V600E mutation is seen in 5% to 8% of patients with metastatic colorectal cancer (CRC) and is associated with poor prognosis. Vemurafenib, an oral BRAF V600 inhibitor, has pronounced activity in patients with metastatic melanoma, but its activity in patients with BRAF V600E–positive metastatic CRC was unknown. In this multi-institutional, open-label study, patients with metastatic CRC with BRAF V600 mutations were recruited to an expansion cohort at the previously determined maximum-tolerated dose of 960 mg orally twice a day. Twenty-one patients were enrolled, of whom 20 had received at least one prior metastatic chemotherapy regimen. Grade 3 toxicities included keratoacanthomas, rash, fatigue, and arthralgia. Of the 21 patients treated, one patient had a confirmed partial response (5% 95% CI, 1% to 24%) and seven other patients had stable disease by RECIST criteria. Median progression-free survival was 2.1 months. Patterns of concurrent mutations, microsatellite instability status, CpG island methylation status, PTEN loss, EGFR expression, and copy number alterations were not associated with clinical benefit. In contrast to prior expectations, concurrent KRAS and NRAS mutations were detected at low allele frequency in a subset of the patients' tumors (median, 0.21% allele frequency) and were apparent mechanisms of acquired resistance in vemurafenib-sensitive patient-derived xenograft models. In marked contrast to the results seen in patients with BRAF V600E–mutant melanoma, single-agent vemurafenib did not show meaningful clinical activity in patients with BRAF V600E mutant CRC. Combination strategies are now under development and may be informed by the presence of intratumor heterogeneity of KRAS and NRAS mutations.
Publisher: American Association for Cancer Research (AACR)
Date: 11-04-2023
DOI: 10.1158/1078-0432.22587069.V1
Abstract: Supplementary Figure 10: Peripheral immune cell dynamics induced by combination therapy.
Publisher: American Association for Cancer Research (AACR)
Date: 11-04-2023
DOI: 10.1158/1078-0432.22587066
Abstract: Supplementary Figure 11: Peripheral immune cells are activated mid-treatment cycle.
Publisher: American Association for Cancer Research (AACR)
Date: 11-04-2023
DOI: 10.1158/1078-0432.22587060
Abstract: Supplementary Figure 2: Modest treatment-induced DNA methylation changes in UC tumors.
Publisher: American Association for Cancer Research (AACR)
Date: 06-2023
DOI: 10.1158/1078-0432.23275189.V1
Abstract: Supplementary Figure 1: Patient recruitment and s le collection overview.
Publisher: American Association for Cancer Research (AACR)
Date: 06-2023
DOI: 10.1158/1078-0432.23275171.V1
Abstract: Supplementary Figure 4: Weak correlation of TE expression induction with DNA methylation change and viral mimicry activation.
Publisher: American Association for Cancer Research (AACR)
Date: 11-04-2023
DOI: 10.1158/1078-0432.22587051.V1
Abstract: Supplementary Figure 5: Overall tumor mutation burden and frequency of mutations in cancer-associated genes in UC tumors.
Publisher: American Association for Cancer Research (AACR)
Date: 06-2023
DOI: 10.1158/1078-0432.23275159
Abstract: Supplementary Figure 8: PD-L1 levels in tumor or tumor microenvironment does not associate with tumor progression or control.
Publisher: American Association for Cancer Research (AACR)
Date: 11-04-2023
DOI: 10.1158/1078-0432.22587069
Abstract: Supplementary Figure 10: Peripheral immune cell dynamics induced by combination therapy.
Publisher: American Association for Cancer Research (AACR)
Date: 11-04-2023
DOI: 10.1158/1078-0432.22587072.V1
Abstract: Supplementary Figure 1: Patient recruitment and s le collection overview.
Location: No location found
Location: United States of America
Location: United States of America
Location: United States of America
No related grants have been discovered for Jean-Pierre Issa.