Patents by Inventor Michael Mingzhao Xing
Michael Mingzhao Xing 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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Publication number: 20240366544Abstract: The present invention relates to the field of cancer. More specifically, the present invention provides methods and compositions useful for the treatment of cancer characterized by TERT and BRAF mutations. In a specific embodiment, a method for treating a mutant telomerase reverse trancriptase (TERT) enzyme-associated cancer in a subject comprises the step of administering to the subject an anti-cancer agent that inhibits one or more of FOS, GABPB, the formation of the GABPA-GABPB complex or the binding of the GABPA-GABPB complex to a mutant TERT promoter.Type: ApplicationFiled: January 26, 2024Publication date: November 7, 2024Inventors: Michael Mingzhao Xing, Rengyun Liu
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Patent number: 11911356Abstract: The present invention relates to the field of cancer. More specifically, the present invention provides methods and compositions useful for the treatment of cancer characterized by TERT and BRAF mutations. In a specific embodiment, a method for treating a mutant telomerase reverse trancriptase (TERT) enzyme-associated cancer in a subject comprises the step of administering to the subject an anti-cancer agent that inhibits one or more of FOS, GABPB, the formation of the GABPA-GABPB complex or the binding of the GABPA-GABPB complex to a mutant TERT promoter.Type: GrantFiled: December 22, 2018Date of Patent: February 27, 2024Assignee: The Johns Hopkins UniversityInventors: Michael Mingzhao Xing, Rengyun Liu
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Patent number: 11680297Abstract: The present inventors have identified specific oncogenic pathways preferentially activated in BRAF-mutated-melanoma cells and a pathway pattern that predicts resistance of BRAF-mutated melanoma to BRAF/MEK inhibitors, providing novel clinical implications for melanoma therapy. In one embodiment, a method comprises (a) testing a sample oiBRAF-mutated melanoma cells isolated from a patient and measuring the expression levels of genes expressed in the following oncogenic pathways: TNFa, EGFR, IFNa, hypoxia, IFNy, STAT3 and Myc; (b) calculating a 7-pathway activation pattern based on the measured expression levels of step (a); and (c) identifying the patient's resistance level to BRAF/MEK inhibitor treatment based on comparison of the calculated 7-pathway activation pattern to a reference.Type: GrantFiled: September 16, 2014Date of Patent: June 20, 2023Assignee: THE JOHNS HOPKINS UNIVERSITYInventors: Michael Mingzhao Xing, Dingxie Liu
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Publication number: 20220372582Abstract: The present invention relates to the field of cancer. More specifically, the present invention provides methods and compositions related to certain promoter mutations in cancer. In one embodiment, a method for treating a subject having thyroid cancer comprises the steps of (a) obtaining a biological sample from the subject (b) performing an assay on the sample obtained from the subject to identify a mutation at 1 295 228 C>T (C228T) and 1 295 250 C>T (C250T), corresponding to ?124 C>T and ?146 C>T from the translation start site in the promoter of the telomerase reverse transcriptase (TERT) gene; (c) identifying the subject as having or likely to develop aggressive thyroid cancer if the C228T and/or C250T mutation is identified; and (d) treating the subject with one or more treatment modalities appropriate for a subject having or likely to develop aggressive thyroid cancer.Type: ApplicationFiled: June 3, 2022Publication date: November 24, 2022Inventor: Michael Mingzhao Xing
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Patent number: 10920281Abstract: The present invention relates to the field of cancer. More specifically, the present invention provides methods and compositions useful for treating thyroid cancer. In certain embodiments, the method comprises the steps of (a) treating DNA isolated from a sample collected from the patient using bisulfate; (b) measuring the DNA methylation level of the promoter region of the RASAL1 gene from the bisulfate-treated DNA using methylation-specific polymerase chain reaction (MSP), wherein the MSP creates a methylation and unmethylation band; (c) normalizing the measured DNA methylation level using an internal reference gene; (d) calculating the percentage of allelic methylation using the formula [M/(M+U]×100%, wherein M and U represent the density of the methylation and unmethylation band; and (e) predicting an increased risk of thyroid cancer in the subject if the percentage of allelic methylation is at least 40%.Type: GrantFiled: May 1, 2018Date of Patent: February 16, 2021Assignee: The Johns Hopkins UniversityInventor: Michael MingZhao Xing
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Publication number: 20200323805Abstract: The present invention relates to the field of cancer. More specifically, the present invention provides methods and compositions useful for the treatment of cancer characterized by TERT and BRAF mutations. In a specific embodiment, a method for treating a mutant telomerase reverse trancriptase (TERT) enzyme-associated cancer in a subject comprises the step of administering to the subject an anti-cancer agent that inhibits one or more of FOS, GABPB, the formation of the GABPA-GABPB complex or the binding of the GABPA-GABPB complex to a mutant TERT promoter.Type: ApplicationFiled: December 22, 2018Publication date: October 15, 2020Inventors: Michael Mingzhao Xing, Rengyun Liu
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Publication number: 20200199686Abstract: The present invention relates to the field of cancer. More specifically, the present invention provides methods and compositions related to certain promoter mutations in cancer. In one embodiment, a method for treating a subject having thyroid cancer comprises the steps of (a) obtaining a biological sample from the subject; (b) performing an assay on the sample obtained from the subject to identify a mutation at 1 295 228 C>T (C228T) and 1 295 250 C>T (C250T), corresponding to ?124 C>T and ?146 C>T from the translation start site in the promoter of the telomerase reverse transcriptase (TERT) gene; (c) identifying the subject as having or likely to develop aggressive thyroid cancer if the C228T and/or C250T mutation is identified; and (d) treating the subject with one or more treatment modalities appropriate for a subject having or likely to develop aggressive thyroid cancer.Type: ApplicationFiled: December 23, 2019Publication date: June 25, 2020Inventor: Michael Mingzhao Xing
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Patent number: 10544464Abstract: The present invention relates to the field of cancer. More specifically, the present invention provides methods and compositions related to certain promoter mutations in cancer. In one embodiment, a method for treating a subject having thyroid cancer comprises the steps of (a) obtaining a biological sample from the subject; (b) performing an assay on the sample obtained from the subject to identify a mutation at 1 295 228 C>T (C228T) and 1 295 250 C>T (C250T), corresponding to ?124 C>T and ?146 C>T from the translation start site in the promoter of the telomerase reverse transcriptase (TERT) gene; (c) identifying the subject as having or likely to develop aggressive thyroid cancer if the C228T and/or C250T mutation is identified; and (d) treating the subject with one or more treatment modalities appropriate for a subject having or likely to develop aggressive thyroid cancer.Type: GrantFiled: March 27, 2014Date of Patent: January 28, 2020Assignee: The Johns Hopkins UniversityInventor: Michael Mingzhao Xing
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Publication number: 20180274042Abstract: The present invention relates to the field of cancer. More specifically, the present invention provides methods and compositions useful for treating thyroid cancer. In certain embodiments, the method comprises the steps of (a) treating DNA isolated from a sample collected from the patient using bisulfate; (b) measuring the DNA methylation level of the promoter region of the RASAL1 gene from the bisulfate-treated DNA using methylation-specific polymerase chain reaction (MSP), wherein the MSP creates a methylation and unmethylation band; (c) normalizing the measured DNA methylation level using an internal reference gene; (d) calculating the percentage of allelic methylation using the formula [M/(M+U]×100%, wherein M and U represent the density of the methylation and unmethylation band; and (e) predicting an increased risk of thyroid cancer in the subject if the percentage of allelic methylation is at least 40%.Type: ApplicationFiled: May 1, 2018Publication date: September 27, 2018Inventor: Michael MingZhao Xing
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Patent number: 10047402Abstract: The present invention relates to the field of cancer. More specifically, the present invention provides methods and compositions useful for treating thyroid cancer. In certain embodiments, the method comprises the steps of (a) treating DNA isolated from a sample collected from the patient using bisulfite; (b) measuring the DNA methylation level of the promoter region of the RASAL1 gene from the bisulfite-treated DNA using methylation-specific polymerase chain reaction (MSP), wherein the MSP creates a methylation and unmethylation band; (c) normalizing the measured DNA methylation level using an internal reference gene; (d) calculating the percentage of allelic methylation using the formula [M/(M+U]×100%, wherein M and U represent the density of the methylation and unmethylation band; and (e) predicting an increased risk of thyroid cancer in the subject if the percentage of allelic methylation is at least 40%.Type: GrantFiled: August 4, 2014Date of Patent: August 14, 2018Assignee: The Johns Hopkins UniversityInventor: Michael MingZhao Xing
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Patent number: 9907813Abstract: Dual suppression of the MAP kinase and PI3K/Akt pathways showed synergistic or greatly enhanced anti-melanoma cell effects, compared to suppression of a single pathway, including the inhibition of cell proliferation, transformation and invasion, induction of G0/G1 cell cycle arrest and, importantly, cell apoptosis. Remarkably, suppression of either pathway induces the expression of thyroid iodide-handling genes and dual suppression of the two pathways synergistically and robustly induces expression of these genes, accompanied by uptake of radioiodine in the cells. These genes include sodium/iodide symporter, thyroid-stimulating hormone receptor, thyroglobulin, thyroperoxidase, pendrin gene, thyroid transcription factors (e.g., TTF-1, TTF-2, PAX8) and other thyroid genes.Type: GrantFiled: January 21, 2016Date of Patent: March 6, 2018Assignee: The Johns Hopkins UniversityInventor: Michael Mingzhao Xing
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Patent number: 9850544Abstract: We examined IQGAP1 copy gain and its relationship with clinicopathologic outcomes of thyroid cancer and investigated its role in cell invasion and molecules involved in the process. We found IQGAP1 copy number (CN) gain?3 in 1 of 30 (3%) of benign thyroid tumor, 24 of 74 (32%) follicular variant papillary thyroid cancer (FVPTC), 44 of 107 (41%) follicular thyroid cancer (FTC), 8 of 16 (50%) tall cell papillary thyroid cancer (PTC), and 27 of 41 (66%) anaplastic thyroid cancer, in increasing order of invasiveness of these tumors. A similar tumor distribution trend of CN?4 was also seen. IQGAP1 copy gain was positively correlated with IQGAP1 protein expression. It was significantly associated with extrathyroidal and vascular invasion of FVPTC and FTC and, remarkably, a 50%-60% rate of multifocality and recurrence of BRAF mutation-positive PTC (P=0.01 and 0.02, respectively). The siRNA knockdown of IQGAP1 dramatically inhibited thyroid cancer cell invasion and colony formation.Type: GrantFiled: August 28, 2015Date of Patent: December 26, 2017Assignee: The Johns Hopkins UniversityInventor: Michael Mingzhao Xing
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Publication number: 20170014441Abstract: Dual suppression of the MAP kinase and PI3K/Akt pathways showed synergistic or greatly enhanced anti-melanoma cell effects, compared to suppression of a single pathway, including the inhibition of cell proliferation, transformation and invasion, induction of G0/G1 cell cycle arrest and, importantly, cell apoptosis. Remarkably, suppression of either pathway induces the expression of thyroid iodide-handling genes and dual suppression of the two pathways synergistically and robustly induces expression of these genes, accompanied by uptake of radioiodine in the cells. These genes include sodium/iodide symporter, thyroid-stimulating hormone receptor, thyroglobulin, thyroperoxidase, pendrin gene, thyroid transcription factors (e.g., TTF-1, TTF-2, PAX8) and other thyroid genes.Type: ApplicationFiled: January 21, 2016Publication date: January 19, 2017Inventor: Michael Mingzhao Xing
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Publication number: 20160222466Abstract: The present inventors have identified specific oncogenic pathways preferentially activated in BRAF-mutated-melanoma cells and a pathway pattern that predicts resistance of BRAF-mutated melanoma to BRAF/MEK inhibitors, providing novel clinical implications for melanoma therapy. In one embodiment, a method comprises (a) testing a sample oiBRAF-mutated melanoma cells isolated from a patient and measuring the expression levels of genes expressed in the following oncogenic pathways: TNFa, EGFR, IFNa, hypoxia, IFNy, STAT3 and Myc; (b) calculating a 7-pathway activation pattern based on the measured expression levels of step (a); and (c) identifying the patient's resistance level to BRAF/MEK inhibitor treatment based on comparison of the calculated 7-pathway activation pattern to a reference.Type: ApplicationFiled: September 16, 2014Publication date: August 4, 2016Applicant: THE JOHNS HOPKINS UNIVERSITYInventors: Michael Mingzhao Xing, Dingxie Liu
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Publication number: 20160177400Abstract: The present invention relates to the field of cancer. More specifically, the present invention provides methods and compositions useful for treating thyroid cancer. In certain embodiments, the method comprises the steps of (a) treating DNA isolated from a sample collected from the patient using bisulfite; (b) measuring the DNA methylation level of the promoter region of the RASAL1 gene from the bisulfite-treated DNA using methylation-specific polymerase chain reaction (MSP), wherein the MSP creates a methylation and unmethylation band; (c) normalizing the measured DNA methylation level using an internal reference gene; (d) calculating the percentage of allelic methylation using the formula [M/(M+U]×100%, wherein M and U represent the density of the methylation and unmethylation band; and (e) predicting an increased risk of thyroid cancer in the subject if the percentage of allelic methylation is at least 40%.Type: ApplicationFiled: August 4, 2014Publication date: June 23, 2016Inventor: Michael MingZhao Xing
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Patent number: 9273318Abstract: Dual suppression of the MAP kinase and PI3K/Akt pathways showed synergistic or greatly enhanced anti-melanoma cell effects, compared to suppression of a single pathway, including the inhibition of cell proliferation, transformation and invasion, induction of G0/G1 cell cycle arrest and, importantly, cell apoptosis. Remarkably, suppression of either pathway induces the expression of thyroid iodide-handling genes and dual suppression of the two pathways synergistically and robustly induces expression of these genes, accompanied by uptake of radioiodine in the cells. These genes include sodium/iodide symporter, thyroid-stimulating hormone receptor, thyroglobulin, thyroperoxidase, pendrin gene, thyroid transcription factors (e.g., TTF-1, TTF-2, PAX8) and other thyroid genes.Type: GrantFiled: January 6, 2014Date of Patent: March 1, 2016Assignee: The Johns Hopkins UniversityInventor: Michael Mingzhao Xing
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Publication number: 20160040250Abstract: The present invention relates to the field of cancer. More specifically, the present invention provides methods and compositions related to certain promoter mutations in cancer. In one embodiment, a method for treating a subject having thyroid cancer comprises the steps of (a) obtaining a biological sample from the subject; (b) performing an assay on the sample obtained from the subject to identify a mutation at 1 295 228 C>T (C228T) and 1 295 250 C>T (C250T), corresponding to ?124 C>T and ?146 C>T from the translation start site in the promoter of the telomerase reverse transcriptase (TERT) gene; (c) identifying the subject as having or likely to develop aggressive thyroid cancer if the C228T and/or C250T mutation is identified; and (d) treating the subject with one or more treatment modalities appropriate for a subject having or likely to develop aggressive thyroid cancer.Type: ApplicationFiled: March 27, 2014Publication date: February 11, 2016Inventor: Michael Mingzhao Xing
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Patent number: 9150929Abstract: The present invention relates to diagnostic, therapeutic and prognostic methods for thyroid cancers. In one embodiment, the present invention provides a method for treating a an anaplastic thyroid cancer (ATC) patient comprising the step of administering to the patient an effective amount of an anaplastic lymphoma kinase (ALK) inhibitor. In another embodiment, a method for diagnosing ATC in patient comprises the step of performing an assay on a biological sample from the patient to identify the presence or absence of a C3592T and/or a G3602A mutation in exon 23 of the ALK gene according to SEQ ID NO:6, wherein the presence of either of both of the mutations correlates with a diagnosis of ATC in the patient.Type: GrantFiled: May 7, 2012Date of Patent: October 6, 2015Assignee: The Johns Hopkins UniversityInventors: Michael Mingzhao Xing, Murugan Avaniyapuram Kannan
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Patent number: 8980554Abstract: A frequent SNP A259G (K87E) genotype switch in the MMP8 gene in has been found to modify the clinical behavior of cancers. The modification varies based on the patient's genotype for the SNP, and whether homozygous or heterozygous. One particular genotype for this SNP leads to more aggressive tumor behavior and worst clinical outcome than the others.Type: GrantFiled: July 26, 2011Date of Patent: March 17, 2015Assignee: The Johns Hopkins UniversityInventor: Michael Mingzhao Xing
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Publication number: 20140301943Abstract: Dual suppression of the MAP kinase and PI3K/Akt pathways showed synergistic or greatly enhanced anti-melanoma cell effects, compared to suppression of a single pathway, including the inhibition of cell proliferation, transformation and invasion, induction of G0/G1 cell cycle arrest and, importantly, cell apoptosis. Remarkably, suppression of either pathway induces the expression of thyroid iodide-handling genes and dual suppression of the two pathways synergistically and robustly induces expression of these genes, accompanied by uptake of radioiodine in the cells. These genes include sodium/iodide symporter, thyroid-stimulating hormone receptor, thyroglobulin, thyroperoxidase, pendrin gene, thyroid transcription factors (e.g., TTF-1, TTF-2, PAX8) and other thyroid genes.Type: ApplicationFiled: January 6, 2014Publication date: October 9, 2014Applicant: The Johns Hopkins UniversityInventor: Michael Mingzhao Xing