Review



fgfr2 fusion mutants  (TargetMol)


Bioz Verified Symbol TargetMol is a verified supplier
Bioz Manufacturer Symbol TargetMol manufactures this product  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
    • 91
      Buy from Supplier

    Structured Review

    TargetMol fgfr2 fusion mutants
    Study design. 474 ICCs were included in this study. Among 474 cases, 290 ICCs were analyzed both by FISH and NGS testing (DNA-based and RNA-based) for <t>FGFR2</t> genetic alterations, and the remaining 184 cases were only analyzed by FISH. In total, there were thirty patients with FGFR2 fusion/translocation and four patients with FGFR2 genetic mutations in our cohort. Further, we selected 1534 ICC patients in 10 studies from public databases and found 38 FGFR2 genetic alterations excluding fusions in 36 patients. In addition, we also collected 31 cases with FGFR2 in-frame deletions and 65 cases with FGFR2 site mutations across multiple cancers. Finally, we depicted the comutation plot of these FGFR2 translocation/fusion, in-frame deletion and site mutation cases
    Fgfr2 Fusion Mutants, supplied by TargetMol, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/fgfr2 fusion mutants/product/TargetMol
    Average 91 stars, based on 1 article reviews
    fgfr2 fusion mutants - by Bioz Stars, 2026-05
    91/100 stars

    Images

    1) Product Images from "Oncogenic activation revealed by FGFR2 genetic alterations in intrahepatic cholangiocarcinomas"

    Article Title: Oncogenic activation revealed by FGFR2 genetic alterations in intrahepatic cholangiocarcinomas

    Journal: Cell & Bioscience

    doi: 10.1186/s13578-023-01156-7

    Study design. 474 ICCs were included in this study. Among 474 cases, 290 ICCs were analyzed both by FISH and NGS testing (DNA-based and RNA-based) for FGFR2 genetic alterations, and the remaining 184 cases were only analyzed by FISH. In total, there were thirty patients with FGFR2 fusion/translocation and four patients with FGFR2 genetic mutations in our cohort. Further, we selected 1534 ICC patients in 10 studies from public databases and found 38 FGFR2 genetic alterations excluding fusions in 36 patients. In addition, we also collected 31 cases with FGFR2 in-frame deletions and 65 cases with FGFR2 site mutations across multiple cancers. Finally, we depicted the comutation plot of these FGFR2 translocation/fusion, in-frame deletion and site mutation cases
    Figure Legend Snippet: Study design. 474 ICCs were included in this study. Among 474 cases, 290 ICCs were analyzed both by FISH and NGS testing (DNA-based and RNA-based) for FGFR2 genetic alterations, and the remaining 184 cases were only analyzed by FISH. In total, there were thirty patients with FGFR2 fusion/translocation and four patients with FGFR2 genetic mutations in our cohort. Further, we selected 1534 ICC patients in 10 studies from public databases and found 38 FGFR2 genetic alterations excluding fusions in 36 patients. In addition, we also collected 31 cases with FGFR2 in-frame deletions and 65 cases with FGFR2 site mutations across multiple cancers. Finally, we depicted the comutation plot of these FGFR2 translocation/fusion, in-frame deletion and site mutation cases

    Techniques Used: Next-Generation Sequencing, Translocation Assay, Mutagenesis

    FGFR2 lesion spectrum in a large cohort of ICC and pan-cancer patients. In a total of 290 ICCs, five FGFR2 genetic alterations (except for translocation/fusion) were found, the types of genomic alterations were color coded and the length of the bar represents the frequency of mutations ( A ). In total of 1534 ICCs from ten studies, 38 FGFR2 genetic alterations excluding fusions were found and the types of genomic alterations were color coded ( B ). A consortium of 91,129 multiple tumors were collected to identify FGFR2 in-frame deletions. In total, eleven tumor types that carried FGFR2 genetic short in frame deletions were identified with ICC at the highest frequency (0.62%, 7/1122), notched rectangles represent the frame deletion represented twice, the percentages represent the frequency of the mutation ( C ). Pan-cancer study of 9999 cases from public database was analyzed to evaluate the prevalence of FGFR2 site mutations, there were 70 site mutations in 65 patients were found, and in ICC the prevalence was 1.08% ( D ). Other tumors that may show scattered FGFR2 point mutations but are not listed in the figure include: cancer of unknown (1/120, A511T), uterine corpus endometrial carcinoma (1/61, S252W), extrahepatic cholangiocarcinoma (1/351, R255W), gallbladder carcinoma (1/240, N441S), gastric cancer (1/866, K399Q), ovarian cancer(1/261, S252W) and urothelial carcinoma (1/96,Q259L)
    Figure Legend Snippet: FGFR2 lesion spectrum in a large cohort of ICC and pan-cancer patients. In a total of 290 ICCs, five FGFR2 genetic alterations (except for translocation/fusion) were found, the types of genomic alterations were color coded and the length of the bar represents the frequency of mutations ( A ). In total of 1534 ICCs from ten studies, 38 FGFR2 genetic alterations excluding fusions were found and the types of genomic alterations were color coded ( B ). A consortium of 91,129 multiple tumors were collected to identify FGFR2 in-frame deletions. In total, eleven tumor types that carried FGFR2 genetic short in frame deletions were identified with ICC at the highest frequency (0.62%, 7/1122), notched rectangles represent the frame deletion represented twice, the percentages represent the frequency of the mutation ( C ). Pan-cancer study of 9999 cases from public database was analyzed to evaluate the prevalence of FGFR2 site mutations, there were 70 site mutations in 65 patients were found, and in ICC the prevalence was 1.08% ( D ). Other tumors that may show scattered FGFR2 point mutations but are not listed in the figure include: cancer of unknown (1/120, A511T), uterine corpus endometrial carcinoma (1/61, S252W), extrahepatic cholangiocarcinoma (1/351, R255W), gallbladder carcinoma (1/240, N441S), gastric cancer (1/866, K399Q), ovarian cancer(1/261, S252W) and urothelial carcinoma (1/96,Q259L)

    Techniques Used: Translocation Assay, Mutagenesis

    Histopathological features of FGFR2 genetic alteration ICCs. FGFR2 gene fusion/translocation ICCs were enriched for specific subtypes in small duct cholangiocarcinoma (CLC) with specific immunological features showing MUC5A negativity, MUC6 negativity or sporadic positivity, and CD56 positivity. HE and IHC staining are presented at 200×, the scale represents 100 µm ( A ). ICCs with FGFR2 site mutations, in-frame deletion and frame-shift deletion presented large duct (LD) or small duct (SD) in histological subtypes. HE staining are presented at 200×, the scale represents 100 µm ( B )
    Figure Legend Snippet: Histopathological features of FGFR2 genetic alteration ICCs. FGFR2 gene fusion/translocation ICCs were enriched for specific subtypes in small duct cholangiocarcinoma (CLC) with specific immunological features showing MUC5A negativity, MUC6 negativity or sporadic positivity, and CD56 positivity. HE and IHC staining are presented at 200×, the scale represents 100 µm ( A ). ICCs with FGFR2 site mutations, in-frame deletion and frame-shift deletion presented large duct (LD) or small duct (SD) in histological subtypes. HE staining are presented at 200×, the scale represents 100 µm ( B )

    Techniques Used: Translocation Assay, Immunohistochemistry, Staining

    Underlying co-mutation features of different types of FGFR2 genetic alterations. Comutation plot of seventeen FGFR2 translocation/fusion cases ( A ), thirty-one FGFR2 in-frame deletion cases ( B ) and sixty-five FGFR2 site mutation cases ( C )
    Figure Legend Snippet: Underlying co-mutation features of different types of FGFR2 genetic alterations. Comutation plot of seventeen FGFR2 translocation/fusion cases ( A ), thirty-one FGFR2 in-frame deletion cases ( B ) and sixty-five FGFR2 site mutation cases ( C )

    Techniques Used: Mutagenesis, Translocation Assay

    Various oncogenic activities and diverse responses to FGFR-selective small molecule kinase inhibitor (SMKI) among FGFR2 mutants. Proliferation activities of AML12 cells expressing MCS, FGFR2 and different FGFR2 mutants are shown ( A ). Representative images of transwell migration assay and average numbers of migrated AML12 cells expressing FGFR2 and different FGFR2 mutants are shown ( B ), the scale represents 100 µm. Representative images of invasion assay and average number of invasive AML12 cells expressing FGFR2 and various FGFR2 mutants are shown ( C ). Cellular skeleton staining revealed the morphological changes in AML12 cells when expressing Lenti-CMV-MCS control virus (MCS), FGFR2 and different FGFR2 mutants ( D ). Evaluation the sensitivity of RBE cells with different FGFR2 mutants to BGJ398 ( E )
    Figure Legend Snippet: Various oncogenic activities and diverse responses to FGFR-selective small molecule kinase inhibitor (SMKI) among FGFR2 mutants. Proliferation activities of AML12 cells expressing MCS, FGFR2 and different FGFR2 mutants are shown ( A ). Representative images of transwell migration assay and average numbers of migrated AML12 cells expressing FGFR2 and different FGFR2 mutants are shown ( B ), the scale represents 100 µm. Representative images of invasion assay and average number of invasive AML12 cells expressing FGFR2 and various FGFR2 mutants are shown ( C ). Cellular skeleton staining revealed the morphological changes in AML12 cells when expressing Lenti-CMV-MCS control virus (MCS), FGFR2 and different FGFR2 mutants ( D ). Evaluation the sensitivity of RBE cells with different FGFR2 mutants to BGJ398 ( E )

    Techniques Used: Expressing, Transwell Migration Assay, Invasion Assay, Staining, Control, Virus

    Frameshift mutation resulting in premature stop codons is also a potential therapeutic target. Proliferation activities of AML12 cells expression Lenti-CMV-MCS control virus (MCS), FGFR2, FGFR2-BICC1 fusion and FGFR2 I548Wfs*8 mutant are shown ( A ). Representative images of transwell migration and average numbers of migrated cells expressing above three clones ( B ), the scale represents 100 µm. Representative images of invasion and average colonies of invasion cells expressing above three clones in AML12 cells are shown ( C ). Capability of FGFR2 I548Wfs*8 rendering RBE cells sensitive to BGJ398 ( D )
    Figure Legend Snippet: Frameshift mutation resulting in premature stop codons is also a potential therapeutic target. Proliferation activities of AML12 cells expression Lenti-CMV-MCS control virus (MCS), FGFR2, FGFR2-BICC1 fusion and FGFR2 I548Wfs*8 mutant are shown ( A ). Representative images of transwell migration and average numbers of migrated cells expressing above three clones ( B ), the scale represents 100 µm. Representative images of invasion and average colonies of invasion cells expressing above three clones in AML12 cells are shown ( C ). Capability of FGFR2 I548Wfs*8 rendering RBE cells sensitive to BGJ398 ( D )

    Techniques Used: Mutagenesis, Expressing, Control, Virus, Migration, Clone Assay



    Similar Products

    fgfr2 fusion mutants  (TargetMol)
    91
    TargetMol fgfr2 fusion mutants
    Study design. 474 ICCs were included in this study. Among 474 cases, 290 ICCs were analyzed both by FISH and NGS testing (DNA-based and RNA-based) for <t>FGFR2</t> genetic alterations, and the remaining 184 cases were only analyzed by FISH. In total, there were thirty patients with FGFR2 fusion/translocation and four patients with FGFR2 genetic mutations in our cohort. Further, we selected 1534 ICC patients in 10 studies from public databases and found 38 FGFR2 genetic alterations excluding fusions in 36 patients. In addition, we also collected 31 cases with FGFR2 in-frame deletions and 65 cases with FGFR2 site mutations across multiple cancers. Finally, we depicted the comutation plot of these FGFR2 translocation/fusion, in-frame deletion and site mutation cases
    Fgfr2 Fusion Mutants, supplied by TargetMol, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/fgfr2 fusion mutants/product/TargetMol
    Average 91 stars, based on 1 article reviews
    fgfr2 fusion mutants - by Bioz Stars, 2026-05
    91/100 stars
    		  Buy from Supplier

    Image Search Results


    Study design. 474 ICCs were included in this study. Among 474 cases, 290 ICCs were analyzed both by FISH and NGS testing (DNA-based and RNA-based) for FGFR2 genetic alterations, and the remaining 184 cases were only analyzed by FISH. In total, there were thirty patients with FGFR2 fusion/translocation and four patients with FGFR2 genetic mutations in our cohort. Further, we selected 1534 ICC patients in 10 studies from public databases and found 38 FGFR2 genetic alterations excluding fusions in 36 patients. In addition, we also collected 31 cases with FGFR2 in-frame deletions and 65 cases with FGFR2 site mutations across multiple cancers. Finally, we depicted the comutation plot of these FGFR2 translocation/fusion, in-frame deletion and site mutation cases

    Journal: Cell & Bioscience

    Article Title: Oncogenic activation revealed by FGFR2 genetic alterations in intrahepatic cholangiocarcinomas

    doi: 10.1186/s13578-023-01156-7

    Figure Lengend Snippet: Study design. 474 ICCs were included in this study. Among 474 cases, 290 ICCs were analyzed both by FISH and NGS testing (DNA-based and RNA-based) for FGFR2 genetic alterations, and the remaining 184 cases were only analyzed by FISH. In total, there were thirty patients with FGFR2 fusion/translocation and four patients with FGFR2 genetic mutations in our cohort. Further, we selected 1534 ICC patients in 10 studies from public databases and found 38 FGFR2 genetic alterations excluding fusions in 36 patients. In addition, we also collected 31 cases with FGFR2 in-frame deletions and 65 cases with FGFR2 site mutations across multiple cancers. Finally, we depicted the comutation plot of these FGFR2 translocation/fusion, in-frame deletion and site mutation cases

    Article Snippet: RBEwere infected with recombinant lentiviruses expressing different FGFR2 fusion mutants, then were distributed into 96-well plates with indicated concentrations of BGJ398 (#T1975, TargetMol, USA).

    Techniques: Next-Generation Sequencing, Translocation Assay, Mutagenesis

    FGFR2 lesion spectrum in a large cohort of ICC and pan-cancer patients. In a total of 290 ICCs, five FGFR2 genetic alterations (except for translocation/fusion) were found, the types of genomic alterations were color coded and the length of the bar represents the frequency of mutations ( A ). In total of 1534 ICCs from ten studies, 38 FGFR2 genetic alterations excluding fusions were found and the types of genomic alterations were color coded ( B ). A consortium of 91,129 multiple tumors were collected to identify FGFR2 in-frame deletions. In total, eleven tumor types that carried FGFR2 genetic short in frame deletions were identified with ICC at the highest frequency (0.62%, 7/1122), notched rectangles represent the frame deletion represented twice, the percentages represent the frequency of the mutation ( C ). Pan-cancer study of 9999 cases from public database was analyzed to evaluate the prevalence of FGFR2 site mutations, there were 70 site mutations in 65 patients were found, and in ICC the prevalence was 1.08% ( D ). Other tumors that may show scattered FGFR2 point mutations but are not listed in the figure include: cancer of unknown (1/120, A511T), uterine corpus endometrial carcinoma (1/61, S252W), extrahepatic cholangiocarcinoma (1/351, R255W), gallbladder carcinoma (1/240, N441S), gastric cancer (1/866, K399Q), ovarian cancer(1/261, S252W) and urothelial carcinoma (1/96,Q259L)

    Journal: Cell & Bioscience

    Article Title: Oncogenic activation revealed by FGFR2 genetic alterations in intrahepatic cholangiocarcinomas

    doi: 10.1186/s13578-023-01156-7

    Figure Lengend Snippet: FGFR2 lesion spectrum in a large cohort of ICC and pan-cancer patients. In a total of 290 ICCs, five FGFR2 genetic alterations (except for translocation/fusion) were found, the types of genomic alterations were color coded and the length of the bar represents the frequency of mutations ( A ). In total of 1534 ICCs from ten studies, 38 FGFR2 genetic alterations excluding fusions were found and the types of genomic alterations were color coded ( B ). A consortium of 91,129 multiple tumors were collected to identify FGFR2 in-frame deletions. In total, eleven tumor types that carried FGFR2 genetic short in frame deletions were identified with ICC at the highest frequency (0.62%, 7/1122), notched rectangles represent the frame deletion represented twice, the percentages represent the frequency of the mutation ( C ). Pan-cancer study of 9999 cases from public database was analyzed to evaluate the prevalence of FGFR2 site mutations, there were 70 site mutations in 65 patients were found, and in ICC the prevalence was 1.08% ( D ). Other tumors that may show scattered FGFR2 point mutations but are not listed in the figure include: cancer of unknown (1/120, A511T), uterine corpus endometrial carcinoma (1/61, S252W), extrahepatic cholangiocarcinoma (1/351, R255W), gallbladder carcinoma (1/240, N441S), gastric cancer (1/866, K399Q), ovarian cancer(1/261, S252W) and urothelial carcinoma (1/96,Q259L)

    Article Snippet: RBEwere infected with recombinant lentiviruses expressing different FGFR2 fusion mutants, then were distributed into 96-well plates with indicated concentrations of BGJ398 (#T1975, TargetMol, USA).

    Techniques: Translocation Assay, Mutagenesis

    Histopathological features of FGFR2 genetic alteration ICCs. FGFR2 gene fusion/translocation ICCs were enriched for specific subtypes in small duct cholangiocarcinoma (CLC) with specific immunological features showing MUC5A negativity, MUC6 negativity or sporadic positivity, and CD56 positivity. HE and IHC staining are presented at 200×, the scale represents 100 µm ( A ). ICCs with FGFR2 site mutations, in-frame deletion and frame-shift deletion presented large duct (LD) or small duct (SD) in histological subtypes. HE staining are presented at 200×, the scale represents 100 µm ( B )

    Journal: Cell & Bioscience

    Article Title: Oncogenic activation revealed by FGFR2 genetic alterations in intrahepatic cholangiocarcinomas

    doi: 10.1186/s13578-023-01156-7

    Figure Lengend Snippet: Histopathological features of FGFR2 genetic alteration ICCs. FGFR2 gene fusion/translocation ICCs were enriched for specific subtypes in small duct cholangiocarcinoma (CLC) with specific immunological features showing MUC5A negativity, MUC6 negativity or sporadic positivity, and CD56 positivity. HE and IHC staining are presented at 200×, the scale represents 100 µm ( A ). ICCs with FGFR2 site mutations, in-frame deletion and frame-shift deletion presented large duct (LD) or small duct (SD) in histological subtypes. HE staining are presented at 200×, the scale represents 100 µm ( B )

    Article Snippet: RBEwere infected with recombinant lentiviruses expressing different FGFR2 fusion mutants, then were distributed into 96-well plates with indicated concentrations of BGJ398 (#T1975, TargetMol, USA).

    Techniques: Translocation Assay, Immunohistochemistry, Staining

    Underlying co-mutation features of different types of FGFR2 genetic alterations. Comutation plot of seventeen FGFR2 translocation/fusion cases ( A ), thirty-one FGFR2 in-frame deletion cases ( B ) and sixty-five FGFR2 site mutation cases ( C )

    Journal: Cell & Bioscience

    Article Title: Oncogenic activation revealed by FGFR2 genetic alterations in intrahepatic cholangiocarcinomas

    doi: 10.1186/s13578-023-01156-7

    Figure Lengend Snippet: Underlying co-mutation features of different types of FGFR2 genetic alterations. Comutation plot of seventeen FGFR2 translocation/fusion cases ( A ), thirty-one FGFR2 in-frame deletion cases ( B ) and sixty-five FGFR2 site mutation cases ( C )

    Article Snippet: RBEwere infected with recombinant lentiviruses expressing different FGFR2 fusion mutants, then were distributed into 96-well plates with indicated concentrations of BGJ398 (#T1975, TargetMol, USA).

    Techniques: Mutagenesis, Translocation Assay

    Various oncogenic activities and diverse responses to FGFR-selective small molecule kinase inhibitor (SMKI) among FGFR2 mutants. Proliferation activities of AML12 cells expressing MCS, FGFR2 and different FGFR2 mutants are shown ( A ). Representative images of transwell migration assay and average numbers of migrated AML12 cells expressing FGFR2 and different FGFR2 mutants are shown ( B ), the scale represents 100 µm. Representative images of invasion assay and average number of invasive AML12 cells expressing FGFR2 and various FGFR2 mutants are shown ( C ). Cellular skeleton staining revealed the morphological changes in AML12 cells when expressing Lenti-CMV-MCS control virus (MCS), FGFR2 and different FGFR2 mutants ( D ). Evaluation the sensitivity of RBE cells with different FGFR2 mutants to BGJ398 ( E )

    Journal: Cell & Bioscience

    Article Title: Oncogenic activation revealed by FGFR2 genetic alterations in intrahepatic cholangiocarcinomas

    doi: 10.1186/s13578-023-01156-7

    Figure Lengend Snippet: Various oncogenic activities and diverse responses to FGFR-selective small molecule kinase inhibitor (SMKI) among FGFR2 mutants. Proliferation activities of AML12 cells expressing MCS, FGFR2 and different FGFR2 mutants are shown ( A ). Representative images of transwell migration assay and average numbers of migrated AML12 cells expressing FGFR2 and different FGFR2 mutants are shown ( B ), the scale represents 100 µm. Representative images of invasion assay and average number of invasive AML12 cells expressing FGFR2 and various FGFR2 mutants are shown ( C ). Cellular skeleton staining revealed the morphological changes in AML12 cells when expressing Lenti-CMV-MCS control virus (MCS), FGFR2 and different FGFR2 mutants ( D ). Evaluation the sensitivity of RBE cells with different FGFR2 mutants to BGJ398 ( E )

    Article Snippet: RBEwere infected with recombinant lentiviruses expressing different FGFR2 fusion mutants, then were distributed into 96-well plates with indicated concentrations of BGJ398 (#T1975, TargetMol, USA).

    Techniques: Expressing, Transwell Migration Assay, Invasion Assay, Staining, Control, Virus

    Frameshift mutation resulting in premature stop codons is also a potential therapeutic target. Proliferation activities of AML12 cells expression Lenti-CMV-MCS control virus (MCS), FGFR2, FGFR2-BICC1 fusion and FGFR2 I548Wfs*8 mutant are shown ( A ). Representative images of transwell migration and average numbers of migrated cells expressing above three clones ( B ), the scale represents 100 µm. Representative images of invasion and average colonies of invasion cells expressing above three clones in AML12 cells are shown ( C ). Capability of FGFR2 I548Wfs*8 rendering RBE cells sensitive to BGJ398 ( D )

    Journal: Cell & Bioscience

    Article Title: Oncogenic activation revealed by FGFR2 genetic alterations in intrahepatic cholangiocarcinomas

    doi: 10.1186/s13578-023-01156-7

    Figure Lengend Snippet: Frameshift mutation resulting in premature stop codons is also a potential therapeutic target. Proliferation activities of AML12 cells expression Lenti-CMV-MCS control virus (MCS), FGFR2, FGFR2-BICC1 fusion and FGFR2 I548Wfs*8 mutant are shown ( A ). Representative images of transwell migration and average numbers of migrated cells expressing above three clones ( B ), the scale represents 100 µm. Representative images of invasion and average colonies of invasion cells expressing above three clones in AML12 cells are shown ( C ). Capability of FGFR2 I548Wfs*8 rendering RBE cells sensitive to BGJ398 ( D )

    Article Snippet: RBEwere infected with recombinant lentiviruses expressing different FGFR2 fusion mutants, then were distributed into 96-well plates with indicated concentrations of BGJ398 (#T1975, TargetMol, USA).

    Techniques: Mutagenesis, Expressing, Control, Virus, Migration, Clone Assay