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(A) <t>Mutational</t> frequencies of the top mutated genes identified in the 72 non‐hypermutated gastric cancer (GC) tumors from PRH ( n = 72 for all genes except ARID1A ( n = 62), KMT2D ( n = 70), MYH11 ( n = 63), IRS2 ( n = 65), and CLTCL1 ( n = 61)). (B) Mutational frequencies by anatomical location of non‐hypermutated GC tumors from PRH. For Fundus/Cardia, there were 13 cases, and n = 13 for all genes, except for MYH11 , PHOX2B , and PER1 , which had n = 12. For the Body, there were 45 cases, and all genes had n = 45, except for ARID1A ( n = 38), KMT2D ( n = 43), and CACNA1D ( n = 39). For the Antrum, there were 14 cases, and all genes had n = 14, except for NOTCH1 ( n = 12), CDKN2A ( n = 13), and NFE2L2 ( n = 13).
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(A) <t>Mutational</t> frequencies of the top mutated genes identified in the 72 non‐hypermutated gastric cancer (GC) tumors from PRH ( n = 72 for all genes except ARID1A ( n = 62), KMT2D ( n = 70), MYH11 ( n = 63), IRS2 ( n = 65), and CLTCL1 ( n = 61)). (B) Mutational frequencies by anatomical location of non‐hypermutated GC tumors from PRH. For Fundus/Cardia, there were 13 cases, and n = 13 for all genes, except for MYH11 , PHOX2B , and PER1 , which had n = 12. For the Body, there were 45 cases, and all genes had n = 45, except for ARID1A ( n = 38), KMT2D ( n = 43), and CACNA1D ( n = 39). For the Antrum, there were 14 cases, and all genes had n = 14, except for NOTCH1 ( n = 12), CDKN2A ( n = 13), and NFE2L2 ( n = 13).
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(A) <t>Mutational</t> frequencies of the top mutated genes identified in the 72 non‐hypermutated gastric cancer (GC) tumors from PRH ( n = 72 for all genes except ARID1A ( n = 62), KMT2D ( n = 70), MYH11 ( n = 63), IRS2 ( n = 65), and CLTCL1 ( n = 61)). (B) Mutational frequencies by anatomical location of non‐hypermutated GC tumors from PRH. For Fundus/Cardia, there were 13 cases, and n = 13 for all genes, except for MYH11 , PHOX2B , and PER1 , which had n = 12. For the Body, there were 45 cases, and all genes had n = 45, except for ARID1A ( n = 38), KMT2D ( n = 43), and CACNA1D ( n = 39). For the Antrum, there were 14 cases, and all genes had n = 14, except for NOTCH1 ( n = 12), CDKN2A ( n = 13), and NFE2L2 ( n = 13).
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(A) <t>Mutational</t> frequencies of the top mutated genes identified in the 72 non‐hypermutated gastric cancer (GC) tumors from PRH ( n = 72 for all genes except ARID1A ( n = 62), KMT2D ( n = 70), MYH11 ( n = 63), IRS2 ( n = 65), and CLTCL1 ( n = 61)). (B) Mutational frequencies by anatomical location of non‐hypermutated GC tumors from PRH. For Fundus/Cardia, there were 13 cases, and n = 13 for all genes, except for MYH11 , PHOX2B , and PER1 , which had n = 12. For the Body, there were 45 cases, and all genes had n = 45, except for ARID1A ( n = 38), KMT2D ( n = 43), and CACNA1D ( n = 39). For the Antrum, there were 14 cases, and all genes had n = 14, except for NOTCH1 ( n = 12), CDKN2A ( n = 13), and NFE2L2 ( n = 13).
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(A) <t>Mutational</t> frequencies of the top mutated genes identified in the 72 non‐hypermutated gastric cancer (GC) tumors from PRH ( n = 72 for all genes except ARID1A ( n = 62), KMT2D ( n = 70), MYH11 ( n = 63), IRS2 ( n = 65), and CLTCL1 ( n = 61)). (B) Mutational frequencies by anatomical location of non‐hypermutated GC tumors from PRH. For Fundus/Cardia, there were 13 cases, and n = 13 for all genes, except for MYH11 , PHOX2B , and PER1 , which had n = 12. For the Body, there were 45 cases, and all genes had n = 45, except for ARID1A ( n = 38), KMT2D ( n = 43), and CACNA1D ( n = 39). For the Antrum, there were 14 cases, and all genes had n = 14, except for NOTCH1 ( n = 12), CDKN2A ( n = 13), and NFE2L2 ( n = 13).
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tcga mutation profiles  (Broad Institute Inc)
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Broad Institute Inc tcga mutation profiles
(A) <t>Mutational</t> frequencies of the top mutated genes identified in the 72 non‐hypermutated gastric cancer (GC) tumors from PRH ( n = 72 for all genes except ARID1A ( n = 62), KMT2D ( n = 70), MYH11 ( n = 63), IRS2 ( n = 65), and CLTCL1 ( n = 61)). (B) Mutational frequencies by anatomical location of non‐hypermutated GC tumors from PRH. For Fundus/Cardia, there were 13 cases, and n = 13 for all genes, except for MYH11 , PHOX2B , and PER1 , which had n = 12. For the Body, there were 45 cases, and all genes had n = 45, except for ARID1A ( n = 38), KMT2D ( n = 43), and CACNA1D ( n = 39). For the Antrum, there were 14 cases, and all genes had n = 14, except for NOTCH1 ( n = 12), CDKN2A ( n = 13), and NFE2L2 ( n = 13).
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Image Search Results


(A) Mutational frequencies of the top mutated genes identified in the 72 non‐hypermutated gastric cancer (GC) tumors from PRH ( n = 72 for all genes except ARID1A ( n = 62), KMT2D ( n = 70), MYH11 ( n = 63), IRS2 ( n = 65), and CLTCL1 ( n = 61)). (B) Mutational frequencies by anatomical location of non‐hypermutated GC tumors from PRH. For Fundus/Cardia, there were 13 cases, and n = 13 for all genes, except for MYH11 , PHOX2B , and PER1 , which had n = 12. For the Body, there were 45 cases, and all genes had n = 45, except for ARID1A ( n = 38), KMT2D ( n = 43), and CACNA1D ( n = 39). For the Antrum, there were 14 cases, and all genes had n = 14, except for NOTCH1 ( n = 12), CDKN2A ( n = 13), and NFE2L2 ( n = 13).

Journal: Cancer Medicine

Article Title: Actionable Genes and Carcinogenic Pathways for Gastric Cancer in Latinos

doi: 10.1002/cam4.71216

Figure Lengend Snippet: (A) Mutational frequencies of the top mutated genes identified in the 72 non‐hypermutated gastric cancer (GC) tumors from PRH ( n = 72 for all genes except ARID1A ( n = 62), KMT2D ( n = 70), MYH11 ( n = 63), IRS2 ( n = 65), and CLTCL1 ( n = 61)). (B) Mutational frequencies by anatomical location of non‐hypermutated GC tumors from PRH. For Fundus/Cardia, there were 13 cases, and n = 13 for all genes, except for MYH11 , PHOX2B , and PER1 , which had n = 12. For the Body, there were 45 cases, and all genes had n = 45, except for ARID1A ( n = 38), KMT2D ( n = 43), and CACNA1D ( n = 39). For the Antrum, there were 14 cases, and all genes had n = 14, except for NOTCH1 ( n = 12), CDKN2A ( n = 13), and NFE2L2 ( n = 13).

Article Snippet: We examined tumor mutational profiles of GC from 106 PRH between 2015 and 2022 (provided by CARIS Life Sciences and the Precision Oncology Alliance).

Techniques:

Frequency of genetic alterations in key signaling pathways in non‐hypermutated gastric cancer cases leading to deregulation of the WNT/β‐catenin, MAPK, PI3K, TGF‐β, and p53 signaling pathways in the non‐hypermutated cases. The frequencies of alterations are expressed as a percentage of all cases. The red color denotes the overall mutational frequency, and blue denotes the amplification frequency for each gene. Figure adapted from: Nature, volume 487, pages 330–337 (2012).

Journal: Cancer Medicine

Article Title: Actionable Genes and Carcinogenic Pathways for Gastric Cancer in Latinos

doi: 10.1002/cam4.71216

Figure Lengend Snippet: Frequency of genetic alterations in key signaling pathways in non‐hypermutated gastric cancer cases leading to deregulation of the WNT/β‐catenin, MAPK, PI3K, TGF‐β, and p53 signaling pathways in the non‐hypermutated cases. The frequencies of alterations are expressed as a percentage of all cases. The red color denotes the overall mutational frequency, and blue denotes the amplification frequency for each gene. Figure adapted from: Nature, volume 487, pages 330–337 (2012).

Article Snippet: We examined tumor mutational profiles of GC from 106 PRH between 2015 and 2022 (provided by CARIS Life Sciences and the Precision Oncology Alliance).

Techniques: Protein-Protein interactions, Amplification