The first fusion gene was described in cancer cells in the early 1980s. The finding was based on the discovery in 1960 by Peter Nowell and David Hungerford in Philadelphia of a small abnormal marker chromosome in patients with chronic myeloid leukemia - the first consistent chromosome abnormality detected in a human malignancy, later designated the Philadelphia chromosome. In 1973, Janet Rowley in Chicago showed that the Philadelphia chromosome had originated through a translocation between chromosomes 9 and 22, and not through a simple deletion of chromosome 22 as was previously thought. Several investigators in the early 1980s showed that the Philadelphia chromosome translocation led to the formation of a new BCR/ABL1 fusion gene, composed of the 3'part of the ABL1 gene in the breakpoint on chromosome 9 and the 5' part of a gene called BCR in the breakpoint in chromosome 22. In 1985 it was clearly established that the fusion gene on chromosome 22 produced an abnormal chimeric BCR/ABL1 protein with the capacity to induce chronic myeloid leukemia.
Fusion genes have been associated with many diseases including cancer but the challenge is accurate detection at a higher throughput. NGS certainly has opened the field but inaccuracy and false negative are still a major concern if one is trying to detect fusion genes in degraded samples such as FFPE and liquid biopsy. QIAGEN has used two unique strategies such as UMI and SPE that enables accurate detection of fusion even from 10 ngs of RNA. Learn more from this video.
published: 02 Mar 2017
NGS and RNA-based sequencing, together for accurate fusion biomarker detection
Oncomine fusion detection technology allows sensitive and specific gene fusion detection with the possibility to identify fusions beyond the known ones.
published: 17 Oct 2019
Expert video report on detection of gene fusions in oncology
Frederique Penault-Llorca explains that gene fusions are rare but present in a high number of cancers and several of them are already targetable. From an array of gene fusions, she details on NTRK family which requires a specific approach regarding detection because of an agnostic biomarker’s nature. She details about techniques for detection of alterations and the recommendations for testing algorithm to apply.
Produced by ESMO, www.oncologypro.esmo.org
This video was supported with an educational grant from Bayer. The selection of study results covered in this track is exclusively under the responsibility of ESMO and the speakers selected by ESMO.
published: 07 Oct 2019
NTRK fusions: Biology and Testing Methods
Dr. Denise Croix from Roche MSA discusses NTRK fusions biology and testing methods. Content and approvals of any product related info is current as of the date of publishing.
TE-US-00861
published: 31 Aug 2020
What are NTRK Gene Fusions?
Dr. Robert Doebele explains what an NTRK gene fusion is in cancer. NTRK is an important biomarker that can impact lung what treatment options. Talk to your doctor about comprehensive biomarker testing. Visit www.lung.org/ntrk for more information.
Support for this educational program provided by Amgen, AstraZeneca, Blueprint Medicines, Bristol Myers Squibb, Genentech, Lilly Oncology, Merck, Novartis and Pfizer.
published: 02 Nov 2020
Reporter Gene Fusion Techniques
This video is made to explain two different techniques of reporter gene fusion- transcriptional and translational- by using GFP as an example.
published: 15 Dec 2018
ESMO Expert video report on Targeting NTRK gene fusions across cancers
TRK fusions are highly actionable driver alterations. A. Drilon gives an overview of their frequency in different cancer types, and explains how to screen for these alterations with next generation sequencing, immunohistochemistry or FISH. He details the targeted therapies which have shown very high and durable response rates, as well as the mechanisms of resistance and how to tackle it.
Produced by ESMO, www.oncologypro.esmo.org
published: 13 May 2019
bcr-abl Translocation Mechanism | Philadelphia Chromosome
The Philadelphia chromosome or Philadelphia translocation (Ph) is a specific genetic abnormality in chromosome 22 of leukemia cancer cells (particularly chronic myeloid leukemia (CML) cells). This chromosome is defective and unusually short because of reciprocal translocation, t(9;22)(q34;q11), of genetic material between chromosome 9 and chromosome 22, and contains a fusion gene called BCR-ABL1. This gene is the ABL1 gene of chromosome 9 juxtaposed onto the breakpoint cluster region BCR gene of chromosome 22, coding for a hybrid protein: a tyrosine kinase signalling protein that is "always on", causing the cell to divide uncontrollably by interrupting the stability of the genome and impairing various signaling pathways governing the cell cycle.
The chromosomal defect in the Philadelphia ...
Fusion genes have been associated with many diseases including cancer but the challenge is accurate detection at a higher throughput. NGS certainly has opened ...
Fusion genes have been associated with many diseases including cancer but the challenge is accurate detection at a higher throughput. NGS certainly has opened the field but inaccuracy and false negative are still a major concern if one is trying to detect fusion genes in degraded samples such as FFPE and liquid biopsy. QIAGEN has used two unique strategies such as UMI and SPE that enables accurate detection of fusion even from 10 ngs of RNA. Learn more from this video.
Fusion genes have been associated with many diseases including cancer but the challenge is accurate detection at a higher throughput. NGS certainly has opened the field but inaccuracy and false negative are still a major concern if one is trying to detect fusion genes in degraded samples such as FFPE and liquid biopsy. QIAGEN has used two unique strategies such as UMI and SPE that enables accurate detection of fusion even from 10 ngs of RNA. Learn more from this video.
Oncomine fusion detection technology allows sensitive and specific gene fusion detection with the possibility to identify fusions beyond the known ones.
Oncomine fusion detection technology allows sensitive and specific gene fusion detection with the possibility to identify fusions beyond the known ones.
Oncomine fusion detection technology allows sensitive and specific gene fusion detection with the possibility to identify fusions beyond the known ones.
Frederique Penault-Llorca explains that gene fusions are rare but present in a high number of cancers and several of them are already targetable. From an array ...
Frederique Penault-Llorca explains that gene fusions are rare but present in a high number of cancers and several of them are already targetable. From an array of gene fusions, she details on NTRK family which requires a specific approach regarding detection because of an agnostic biomarker’s nature. She details about techniques for detection of alterations and the recommendations for testing algorithm to apply.
Produced by ESMO, www.oncologypro.esmo.org
This video was supported with an educational grant from Bayer. The selection of study results covered in this track is exclusively under the responsibility of ESMO and the speakers selected by ESMO.
Frederique Penault-Llorca explains that gene fusions are rare but present in a high number of cancers and several of them are already targetable. From an array of gene fusions, she details on NTRK family which requires a specific approach regarding detection because of an agnostic biomarker’s nature. She details about techniques for detection of alterations and the recommendations for testing algorithm to apply.
Produced by ESMO, www.oncologypro.esmo.org
This video was supported with an educational grant from Bayer. The selection of study results covered in this track is exclusively under the responsibility of ESMO and the speakers selected by ESMO.
Dr. Denise Croix from Roche MSA discusses NTRK fusions biology and testing methods. Content and approvals of any product related info is current as of the date ...
Dr. Denise Croix from Roche MSA discusses NTRK fusions biology and testing methods. Content and approvals of any product related info is current as of the date of publishing.
TE-US-00861
Dr. Denise Croix from Roche MSA discusses NTRK fusions biology and testing methods. Content and approvals of any product related info is current as of the date of publishing.
TE-US-00861
Dr. Robert Doebele explains what an NTRK gene fusion is in cancer. NTRK is an important biomarker that can impact lung what treatment options. Talk to your doct...
Dr. Robert Doebele explains what an NTRK gene fusion is in cancer. NTRK is an important biomarker that can impact lung what treatment options. Talk to your doctor about comprehensive biomarker testing. Visit www.lung.org/ntrk for more information.
Support for this educational program provided by Amgen, AstraZeneca, Blueprint Medicines, Bristol Myers Squibb, Genentech, Lilly Oncology, Merck, Novartis and Pfizer.
Dr. Robert Doebele explains what an NTRK gene fusion is in cancer. NTRK is an important biomarker that can impact lung what treatment options. Talk to your doctor about comprehensive biomarker testing. Visit www.lung.org/ntrk for more information.
Support for this educational program provided by Amgen, AstraZeneca, Blueprint Medicines, Bristol Myers Squibb, Genentech, Lilly Oncology, Merck, Novartis and Pfizer.
TRK fusions are highly actionable driver alterations. A. Drilon gives an overview of their frequency in different cancer types, and explains how to screen for t...
TRK fusions are highly actionable driver alterations. A. Drilon gives an overview of their frequency in different cancer types, and explains how to screen for these alterations with next generation sequencing, immunohistochemistry or FISH. He details the targeted therapies which have shown very high and durable response rates, as well as the mechanisms of resistance and how to tackle it.
Produced by ESMO, www.oncologypro.esmo.org
TRK fusions are highly actionable driver alterations. A. Drilon gives an overview of their frequency in different cancer types, and explains how to screen for these alterations with next generation sequencing, immunohistochemistry or FISH. He details the targeted therapies which have shown very high and durable response rates, as well as the mechanisms of resistance and how to tackle it.
Produced by ESMO, www.oncologypro.esmo.org
The Philadelphia chromosome or Philadelphia translocation (Ph) is a specific genetic abnormality in chromosome 22 of leukemia cancer cells (particularly chronic...
The Philadelphia chromosome or Philadelphia translocation (Ph) is a specific genetic abnormality in chromosome 22 of leukemia cancer cells (particularly chronic myeloid leukemia (CML) cells). This chromosome is defective and unusually short because of reciprocal translocation, t(9;22)(q34;q11), of genetic material between chromosome 9 and chromosome 22, and contains a fusion gene called BCR-ABL1. This gene is the ABL1 gene of chromosome 9 juxtaposed onto the breakpoint cluster region BCR gene of chromosome 22, coding for a hybrid protein: a tyrosine kinase signalling protein that is "always on", causing the cell to divide uncontrollably by interrupting the stability of the genome and impairing various signaling pathways governing the cell cycle.
The chromosomal defect in the Philadelphia chromosome is a reciprocal translocation, in which parts of two chromosomes, 9 and 22, swap places. The result is that a fusion gene is created by juxtaposing the ABL1 gene on chromosome 9 (region q34) to a part of the BCR (breakpoint cluster region) gene on chromosome 22 (region q11). This is a reciprocal translocation, creating an elongated chromosome 9 (termed a derivative chromosome, or der 9), and a truncated chromosome 22 (the Philadelphia chromosome, 22q-).In agreement with the International System for Human Cytogenetic Nomenclature (ISCN), this chromosomal translocation is designated as t(9;22)(q34;q11). The symbol ABL1 is derived from Abelson, the name of a leukemia virus which carries a similar protein. The symbol BCR is derived from breakpoint cluster region, a gene which encodes a protein that acts as a guanine nucleotide exchange factor for Rho GTPase proteins .
Translocation results in an oncogenic BCR-ABL1 gene fusion that can be found on the shorter derivative chromosome 22. This gene encodes for a BCR-ABL1 fusion protein. Depending on the precise location of fusion, the molecular weight of this protein can range from 185 to 210 kDa. Consequently, the hybrid BCR-ABL1 fusion protein is referred to as p210 or p185.
The Philadelphia chromosome or Philadelphia translocation (Ph) is a specific genetic abnormality in chromosome 22 of leukemia cancer cells (particularly chronic myeloid leukemia (CML) cells). This chromosome is defective and unusually short because of reciprocal translocation, t(9;22)(q34;q11), of genetic material between chromosome 9 and chromosome 22, and contains a fusion gene called BCR-ABL1. This gene is the ABL1 gene of chromosome 9 juxtaposed onto the breakpoint cluster region BCR gene of chromosome 22, coding for a hybrid protein: a tyrosine kinase signalling protein that is "always on", causing the cell to divide uncontrollably by interrupting the stability of the genome and impairing various signaling pathways governing the cell cycle.
The chromosomal defect in the Philadelphia chromosome is a reciprocal translocation, in which parts of two chromosomes, 9 and 22, swap places. The result is that a fusion gene is created by juxtaposing the ABL1 gene on chromosome 9 (region q34) to a part of the BCR (breakpoint cluster region) gene on chromosome 22 (region q11). This is a reciprocal translocation, creating an elongated chromosome 9 (termed a derivative chromosome, or der 9), and a truncated chromosome 22 (the Philadelphia chromosome, 22q-).In agreement with the International System for Human Cytogenetic Nomenclature (ISCN), this chromosomal translocation is designated as t(9;22)(q34;q11). The symbol ABL1 is derived from Abelson, the name of a leukemia virus which carries a similar protein. The symbol BCR is derived from breakpoint cluster region, a gene which encodes a protein that acts as a guanine nucleotide exchange factor for Rho GTPase proteins .
Translocation results in an oncogenic BCR-ABL1 gene fusion that can be found on the shorter derivative chromosome 22. This gene encodes for a BCR-ABL1 fusion protein. Depending on the precise location of fusion, the molecular weight of this protein can range from 185 to 210 kDa. Consequently, the hybrid BCR-ABL1 fusion protein is referred to as p210 or p185.
Fusion genes have been associated with many diseases including cancer but the challenge is accurate detection at a higher throughput. NGS certainly has opened the field but inaccuracy and false negative are still a major concern if one is trying to detect fusion genes in degraded samples such as FFPE and liquid biopsy. QIAGEN has used two unique strategies such as UMI and SPE that enables accurate detection of fusion even from 10 ngs of RNA. Learn more from this video.
Oncomine fusion detection technology allows sensitive and specific gene fusion detection with the possibility to identify fusions beyond the known ones.
Frederique Penault-Llorca explains that gene fusions are rare but present in a high number of cancers and several of them are already targetable. From an array of gene fusions, she details on NTRK family which requires a specific approach regarding detection because of an agnostic biomarker’s nature. She details about techniques for detection of alterations and the recommendations for testing algorithm to apply.
Produced by ESMO, www.oncologypro.esmo.org
This video was supported with an educational grant from Bayer. The selection of study results covered in this track is exclusively under the responsibility of ESMO and the speakers selected by ESMO.
Dr. Denise Croix from Roche MSA discusses NTRK fusions biology and testing methods. Content and approvals of any product related info is current as of the date of publishing.
TE-US-00861
Dr. Robert Doebele explains what an NTRK gene fusion is in cancer. NTRK is an important biomarker that can impact lung what treatment options. Talk to your doctor about comprehensive biomarker testing. Visit www.lung.org/ntrk for more information.
Support for this educational program provided by Amgen, AstraZeneca, Blueprint Medicines, Bristol Myers Squibb, Genentech, Lilly Oncology, Merck, Novartis and Pfizer.
TRK fusions are highly actionable driver alterations. A. Drilon gives an overview of their frequency in different cancer types, and explains how to screen for these alterations with next generation sequencing, immunohistochemistry or FISH. He details the targeted therapies which have shown very high and durable response rates, as well as the mechanisms of resistance and how to tackle it.
Produced by ESMO, www.oncologypro.esmo.org
The Philadelphia chromosome or Philadelphia translocation (Ph) is a specific genetic abnormality in chromosome 22 of leukemia cancer cells (particularly chronic myeloid leukemia (CML) cells). This chromosome is defective and unusually short because of reciprocal translocation, t(9;22)(q34;q11), of genetic material between chromosome 9 and chromosome 22, and contains a fusion gene called BCR-ABL1. This gene is the ABL1 gene of chromosome 9 juxtaposed onto the breakpoint cluster region BCR gene of chromosome 22, coding for a hybrid protein: a tyrosine kinase signalling protein that is "always on", causing the cell to divide uncontrollably by interrupting the stability of the genome and impairing various signaling pathways governing the cell cycle.
The chromosomal defect in the Philadelphia chromosome is a reciprocal translocation, in which parts of two chromosomes, 9 and 22, swap places. The result is that a fusion gene is created by juxtaposing the ABL1 gene on chromosome 9 (region q34) to a part of the BCR (breakpoint cluster region) gene on chromosome 22 (region q11). This is a reciprocal translocation, creating an elongated chromosome 9 (termed a derivative chromosome, or der 9), and a truncated chromosome 22 (the Philadelphia chromosome, 22q-).In agreement with the International System for Human Cytogenetic Nomenclature (ISCN), this chromosomal translocation is designated as t(9;22)(q34;q11). The symbol ABL1 is derived from Abelson, the name of a leukemia virus which carries a similar protein. The symbol BCR is derived from breakpoint cluster region, a gene which encodes a protein that acts as a guanine nucleotide exchange factor for Rho GTPase proteins .
Translocation results in an oncogenic BCR-ABL1 gene fusion that can be found on the shorter derivative chromosome 22. This gene encodes for a BCR-ABL1 fusion protein. Depending on the precise location of fusion, the molecular weight of this protein can range from 185 to 210 kDa. Consequently, the hybrid BCR-ABL1 fusion protein is referred to as p210 or p185.
The first fusion gene was described in cancer cells in the early 1980s. The finding was based on the discovery in 1960 by Peter Nowell and David Hungerford in Philadelphia of a small abnormal marker chromosome in patients with chronic myeloid leukemia - the first consistent chromosome abnormality detected in a human malignancy, later designated the Philadelphia chromosome. In 1973, Janet Rowley in Chicago showed that the Philadelphia chromosome had originated through a translocation between chromosomes 9 and 22, and not through a simple deletion of chromosome 22 as was previously thought. Several investigators in the early 1980s showed that the Philadelphia chromosome translocation led to the formation of a new BCR/ABL1 fusion gene, composed of the 3'part of the ABL1 gene in the breakpoint on chromosome 9 and the 5' part of a gene called BCR in the breakpoint in chromosome 22. In 1985 it was clearly established that the fusion gene on chromosome 22 produced an abnormal chimeric BCR/ABL1 protein with the capacity to induce chronic myeloid leukemia.
Some of the key facts of the Chronic Myeloid LeukemiaMarketReport. ... In November 2024, The U.S ... This translocation leads to the formation of a fusion gene called BCR-ABL1, which produces a protein that promotes the excessive growth of myeloid cells ... 1.
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