Patents by Inventor Vilmos Adleff
Vilmos Adleff has filed for patents to protect the following inventions. This listing includes patent applications that are pending as well as patents that have already been granted by the United States Patent and Trademark Office (USPTO).
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Patent number: 11845994Abstract: Recent large-scale analyses have demonstrated that the genomic landscape of human cancer is complex and variable among individuals of the same tumor type. Such underlying genetic differences may in part be responsible for the varying therapeutic responses observed in cancer patients. To examine the effect of somatic genetic changes in colorectal cancer on sensitivity to a common targeted therapy, we performed complete exome sequence and copy number analyses of 129 tumors that were KRAS wild-type and analyzed their response to anti-EGFR antibody blockade in patient-derived tumorgraft models. In addition to previously identified genes, we detected mutations in ERBB2, EGFR, FGFR1, PDGFRA, and MAP2K1 as potential mechanisms of primary resistance to this therapy. Alterations in the ectodomain of EGFR were identified in patients with acquired resistance to EGFR blockade.Type: GrantFiled: April 8, 2021Date of Patent: December 19, 2023Assignees: The Johns Hopkins University, University of TorinoInventors: Victor E. Velculescu, Eniko Papp, Vilmos Adleff, Andrea Bertotti, Livio Trusolino
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Publication number: 20220325343Abstract: This document relates to methods and materials for assessed, monitored, and/or treated mammals (e.g., humans) having cancer. For example, methods and materials for identifying a mammal as having cancer (e.g., a localized cancer) are provided. For example, methods and materials for assessing, monitoring, and/or treating a mammal having cancer are provided.Type: ApplicationFiled: June 17, 2022Publication date: October 13, 2022Inventors: Victor E. Velculescu, Stephen Cristiano, Alessandro Leal, Jillian A. Phallen, Jacob Fiksel, Vilmos Adleff, Robert B. Scharpf
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Publication number: 20210301352Abstract: Recent large-scale analyses have demonstrated that the genomic landscape of human cancer is complex and variable among individuals of the same tumor type. Such underlying genetic differences may in part be responsible for the varying therapeutic responses observed in cancer patients. To examine the effect of somatic genetic changes in colorectal cancer on sensitivity to a common targeted therapy, we performed complete exome sequence and copy number analyses of 129 tumors that were KRAS wild-type and analyzed their response to anti-EGFR antibody blockade in patient-derived tumorgraft models. In addition to previously identified genes, we detected mutations in ERBB2, EGFR, FGFR1, PDGFRA, and MAP2K1 as potential mechanisms of primary resistance to this therapy. Alterations in the ectodomain of EGFR were identified in patients with acquired resistance to EGFR blockade.Type: ApplicationFiled: April 8, 2021Publication date: September 30, 2021Inventors: Victor E. Velculescu, Eniko Papp, Vilmos Adleff, Andrea Bertotti, Livio Trusolino
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Publication number: 20210254152Abstract: This document relates to methods and materials for assessed, monitored, and/or treated mammals (e.g., humans) having cancer. For example, methods and materials for identifying a mammal as having cancer (e.g., a localized cancer) are provided. For example, methods and materials for assessing, monitoring, and/or treating a mammal having cancer are provided.Type: ApplicationFiled: March 17, 2021Publication date: August 19, 2021Inventors: Victor E. Velculescu, Stephen Cristiano, Alessandro Leal, Jillian A. Phallen, Jacob Fiksel, Vilmos Adleff, Robert B. Scharpf
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Publication number: 20210198747Abstract: This document relates to methods and materials for assessed, monitored, and/or treated mammals (e.g., humans) having cancer. For example, methods and materials for identifying a mammal as having cancer (e.g., a localized cancer) are provided. For example, methods and materials for assessing, monitoring, and/or treating a mammal having cancer are provided.Type: ApplicationFiled: May 17, 2019Publication date: July 1, 2021Inventors: Victor E. Velculescu, Stephen Cristiano, Alessandro Leal, Jillian A. Phallen, Jacob Fiksel, Vilmos Adleff, Robert B. Scharpf
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Patent number: 10982287Abstract: Recent large-scale analyses have demonstrated that the genomic landscape of human cancer is complex and variable among individuals of the same tumor type. Such underlying genetic differences may in part be responsible for the varying therapeutic responses observed in cancer patients. To examine the effect of somatic genetic changes in colorectal cancer on sensitivity to a common targeted therapy, we performed complete exome sequence and copy number analyses of 129 tumors that were KRAS wild-type and analyzed their response to anti-EGFR antibody blockade in patient-derived tumorgraft models. In addition to previously identified genes, we detected mutations in ERBB2, EGFR, FGFR1, PDGFRA, and MAP2K1 as potential mechanisms of primary resistance to this therapy. Alterations in the ectodomain of EGFR were identified in patients with acquired resistance to EGFR blockade.Type: GrantFiled: January 6, 2016Date of Patent: April 20, 2021Assignees: The Johns Hopkins University, University of TorinoInventors: Victor Velculescu, Eniko Papp, Vilmos Adleff, Andrea Bertotti, Livio Trusolino
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Patent number: 10982279Abstract: This document relates to methods and materials for assessed, monitored, and/or treated mammals (e.g., humans) having cancer. For example, methods and materials for identifying a mammal as having cancer (e.g., a localized cancer) are provided. For example, methods and materials for assessing, monitoring, and/or treating a mammal having cancer are provided.Type: GrantFiled: December 30, 2019Date of Patent: April 20, 2021Assignee: The Johns Hopkins UniversityInventors: Victor E. Velculescu, Stephen Cristiano, Alessandro Leal, Jillian A. Phallen, Jacob Fiksel, Vilmos Adleff, Robert B. Scharpf
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Publication number: 20210108256Abstract: Pancreatic adenocarcinoma has the worst overall mortality of any solid tumor, with only 7% of patients surviving after 5 years. To evaluate the clinical implications of genomic alterations in this low cellularity tumor type, we deeply sequenced the genomes of 101 enriched pancreatic adenocarcinomas from patients who underwent potentially curative resections and used non-invasive approaches to examine tumor specific mutations in the circulation of these patients. These analyses revealed somatic mutations in chromatin regulating genes including MLL and ARID1A in 20% of patients that were associated with improved survival. Liquid biopsy analyses of cell free plasma DNA revealed that 43% of patients with localized disease had detectable circulating tumor DNA (ctDNA) in their blood at the time of diagnosis. Detection of ctDNA after resection predicted clinical relapse and poor outcome, and disease recurrence by ctDNA was detected 6.5 months earlier than with standard CT imaging.Type: ApplicationFiled: October 26, 2020Publication date: April 15, 2021Inventors: Victor E. Velculescu, Mark Sausen, Vilmos Adleff, Jillian A. Phallen
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Patent number: 10975431Abstract: This document relates to methods and materials for assessed, monitored, and/or treated mammals (e.g., humans) having cancer. For example, methods and materials for identifying a mammal as having cancer (e.g., a localized cancer) are provided. For example, methods and materials for assessing, monitoring, and/or treating a mammal having cancer are provided.Type: GrantFiled: December 30, 2019Date of Patent: April 13, 2021Assignee: The Johns Hopkins UniversityInventors: Victor E. Velculescu, Stephen Cristiano, Alessandro Leal, Jillian A. Phallen, Jacob Fiksel, Vilmos Adleff, Robert B. Scharpf
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Patent number: 10815522Abstract: Pancreatic adenocarcinoma has the worst overall mortality of any solid tumor, with only 7% of patients surviving after 5 years. To evaluate the clinical implications of genomic alterations in this low cellularity tumor type, we deeply sequenced the genomes of 101 enriched pancreatic adenocarcinomas from patients who underwent potentially curative resections and used non-invasive approaches to examine tumor specific mutations in the circulation of these patients. These analyses revealed somatic mutations in chromatin regulating genes including MLL and ARID1A in 20% of patients that were associated with improved survival. Liquid biopsy analyses of cell free plasma DNA revealed that 43% of patients with localized disease had detectable circulating tumor DNA (ctDNA) in their blood at the time of diagnosis. Detection of ctDNA after resection predicted clinical relapse and poor outcome, and disease recurrence by ctDNA was detected 6.5 months earlier than with standard CT imaging.Type: GrantFiled: February 18, 2016Date of Patent: October 27, 2020Assignee: The Johns Hopkins UniversityInventors: Victor Velculescu, Mark Sausen, Vilmos Adleff, Jillian Phallen
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Publication number: 20200149118Abstract: This document relates to methods and materials for assessed, monitored, and/or treated mammals (e.g., humans) having cancer. For example, methods and materials for identifying a mammal as having cancer (e.g., a localized cancer) are provided. For example, methods and materials for assessing, monitoring, and/or treating a mammal having cancer are provided.Type: ApplicationFiled: December 30, 2019Publication date: May 14, 2020Inventors: Victor E. Velculescu, Stephen Cristiano, Alessandro Leal, Jillian A. Phallen, Jacob Fiksel, Vilmos Adleff, Robert B. Scharpf
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Publication number: 20200131571Abstract: This document relates to methods and materials for assessed, monitored, and/or treated mammals (e.g., humans) having cancer. For example, methods and materials for identifying a mammal as having cancer (e.g., a localized cancer) are provided. For example, methods and materials for assessing, monitoring, and/or treating a mammal having cancer are provided.Type: ApplicationFiled: December 30, 2019Publication date: April 30, 2020Inventors: Victor E. Velculescu, Stephen Cristiano, Alessandro Leal, Jillian A. Phallen, Jacob Fiksel, Vilmos Adleff, Robert B. Scharpf
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Publication number: 20180346987Abstract: Recent large-scale analyses have demonstrated that the genomic landscape of human cancer is complex and variable among individuals of the same tumor type. Such underlying genetic differences may in part be responsible for the varying therapeutic responses observed in cancer patients. To examine the effect of somatic genetic changes in colorectal cancer on sensitivity to a common targeted therapy, we performed complete exome sequence and copy number analyses of 129 tumors that were KRAS wild-type and analyzed their response to anti-EGFR antibody blockade in patient-derived tumorgraft models. In addition to previously identified genes, we detected mutations in ERBB2, EGFR, FGFR1, PDGFRA, and MAP2K1 as potential mechanisms of primary resistance to this therapy. Alterations in the ectodomain of EGFR were identified in patients with acquired resistance to EGFR blockade.Type: ApplicationFiled: January 6, 2016Publication date: December 6, 2018Inventors: Victor VELCULESCU, Eniko PAPP, Vilmos ADLEFF, Andrea BERTOTTI, Livio TRUSOLINO
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Publication number: 20180155770Abstract: Pancreatic adenocarcinoma has the worst overall mortality of any solid tumor, with only 7% of patients surviving after 5 years. To evaluate the clinical implications of genomic alterations in this low cellularity tumor type, we deeply sequenced the genomes of 101 enriched pancreatic adenocarcinomas from patients who underwent potentially curative resections and used non-invasive approaches to examine tumor specific mutations in the circulation of these patients. These analyses revealed somatic mutations in chromatin regulating genes including MLL and ARID1A in 20% of patients that were associated with improved survival. Liquid biopsy analyses of cell free plasma DNA revealed that 43% of patients with localized disease had detectable circulating tumor DNA (ctDNA) in their blood at the time of diagnosis. Detection of ctDNA after resection predicted clinical relapse and poor outcome, and disease recurrence by ctDNA was detected 6.5 months earlier than with standard CT imaging.Type: ApplicationFiled: February 18, 2016Publication date: June 7, 2018Inventors: Victor Velculescu, Mark Sausen, Vilmos Adleff, Jillian Phallen
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Publication number: 20170327898Abstract: The evolutionary origin of high-grade serous ovarian carcinoma remains largely unknown. The vast majority of tumor-specific genomic alterations from ovarian cancers are present in fallopian tube STIC lesions (average of 55 sequence alterations per tumor), including those affecting TP53, BRCA1, BRCA2 or PTEN genes. A quantitative evolutionary analysis indicated that tumors of the fallopian tube were the likely precursors of ovarian cancer and could directly give rise to metastatic lesions. These analyses suggest that there may be less than two years between the development of a STIC and the initiation of fallopian tube tumors, ovarian tumors or other metastases. Thus there may be a short window between the development of a STIC and the initiation of ovarian tumors or other metastases, highlighting the importance of the prevention, early detection and therapeutic intervention of this disease.Type: ApplicationFiled: May 16, 2017Publication date: November 16, 2017Inventors: Victor Velculescu, Eniko Papp, Vilmos Adleff