Identifying Actionable Alterations in KRAS Wild-Type Pancreatic Cancer
The 5-year relative survival rate for pancreatic cancer is currently the lowest among all cancer types with a dismal 13%. A Kirsten rat sarcoma virus ( KRAS ) gene mutation is present in approximately 90% of patients with pancreatic cancer; however, KRAS -specific drugs are not yet widely used in cl...
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| Veröffentlicht in: | Targeted oncology 2024-09, Vol.19 (5), p.679-689 |
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| creator | Elhariri, Ahmed Patel, Jaydeepbhai Mahadevia, Himil Albelal, Douaa Ahmed, Ahmed K. Jones, Jeremy C. Borad, Mitesh J. Babiker, Hani |
| description | The 5-year relative survival rate for pancreatic cancer is currently the lowest among all cancer types with a dismal 13%. A Kirsten rat sarcoma virus (
KRAS
) gene mutation is present in approximately 90% of patients with pancreatic cancer; however,
KRAS
-specific drugs are not yet widely used in clinical practice for pancreatic cancer, specifically the
KRAS
G12D
variant. Advances in genomic testing revealed an opportunity to detect genetic alterations in a subset of patients with no
KRAS
mutation termed
KRAS
wild-type. Patients with
KRAS
wild-type tumors have a propensity to express driver alterations, hence paving the way for utilizing a targeted therapy approach either via clinical trials or standard-of-care drugs. These alterations include fusions, amplifications, translocations, rearrangements and microsatellite instability-high tumors and can be as high as 11% in some studies. Here, we discuss some of the most notable alterations in
KRAS
wild-type and highlight promising clinical trials. |
| doi_str_mv | 10.1007/s11523-024-01088-3 |
| format | Article |
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KRAS
) gene mutation is present in approximately 90% of patients with pancreatic cancer; however,
KRAS
-specific drugs are not yet widely used in clinical practice for pancreatic cancer, specifically the
KRAS
G12D
variant. Advances in genomic testing revealed an opportunity to detect genetic alterations in a subset of patients with no
KRAS
mutation termed
KRAS
wild-type. Patients with
KRAS
wild-type tumors have a propensity to express driver alterations, hence paving the way for utilizing a targeted therapy approach either via clinical trials or standard-of-care drugs. These alterations include fusions, amplifications, translocations, rearrangements and microsatellite instability-high tumors and can be as high as 11% in some studies. Here, we discuss some of the most notable alterations in
KRAS
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KRAS
) gene mutation is present in approximately 90% of patients with pancreatic cancer; however,
KRAS
-specific drugs are not yet widely used in clinical practice for pancreatic cancer, specifically the
KRAS
G12D
variant. Advances in genomic testing revealed an opportunity to detect genetic alterations in a subset of patients with no
KRAS
mutation termed
KRAS
wild-type. Patients with
KRAS
wild-type tumors have a propensity to express driver alterations, hence paving the way for utilizing a targeted therapy approach either via clinical trials or standard-of-care drugs. These alterations include fusions, amplifications, translocations, rearrangements and microsatellite instability-high tumors and can be as high as 11% in some studies. Here, we discuss some of the most notable alterations in
KRAS
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Patel, Jaydeepbhai ; Mahadevia, Himil ; Albelal, Douaa ; Ahmed, Ahmed K. ; Jones, Jeremy C. ; Borad, Mitesh J. ; Babiker, Hani</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c256t-f6d2ecf8e7d4400339833b60cfd7359c4615fb0f637c6439d5a7458dbffdd5863</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Biomedicine</topic><topic>Cancer therapies</topic><topic>Case reports</topic><topic>Chemotherapy</topic><topic>Clinical trials</topic><topic>Cyclin-dependent kinases</topic><topic>Fibroblasts</topic><topic>Genes</topic><topic>Growth factors</topic><topic>Hematology</topic><topic>Humans</topic><topic>Kinases</topic><topic>Lymphoma</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Metastasis</topic><topic>Mutation</topic><topic>Oncology</topic><topic>Pancreatic cancer</topic><topic>Pancreatic Neoplasms - drug therapy</topic><topic>Pancreatic Neoplasms - genetics</topic><topic>Proteins</topic><topic>Proto-Oncogene Proteins p21(ras) - genetics</topic><topic>Review Article</topic><topic>Sarcoma</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Elhariri, Ahmed</creatorcontrib><creatorcontrib>Patel, Jaydeepbhai</creatorcontrib><creatorcontrib>Mahadevia, Himil</creatorcontrib><creatorcontrib>Albelal, Douaa</creatorcontrib><creatorcontrib>Ahmed, Ahmed K.</creatorcontrib><creatorcontrib>Jones, Jeremy C.</creatorcontrib><creatorcontrib>Borad, Mitesh J.</creatorcontrib><creatorcontrib>Babiker, Hani</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>Targeted oncology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Elhariri, Ahmed</au><au>Patel, Jaydeepbhai</au><au>Mahadevia, Himil</au><au>Albelal, Douaa</au><au>Ahmed, Ahmed K.</au><au>Jones, Jeremy C.</au><au>Borad, Mitesh J.</au><au>Babiker, Hani</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Identifying Actionable Alterations in KRAS Wild-Type Pancreatic Cancer</atitle><jtitle>Targeted oncology</jtitle><stitle>Targ Oncol</stitle><addtitle>Target Oncol</addtitle><date>2024-09-01</date><risdate>2024</risdate><volume>19</volume><issue>5</issue><spage>679</spage><epage>689</epage><pages>679-689</pages><issn>1776-2596</issn><issn>1776-260X</issn><eissn>1776-260X</eissn><abstract>The 5-year relative survival rate for pancreatic cancer is currently the lowest among all cancer types with a dismal 13%. A Kirsten rat sarcoma virus (
KRAS
) gene mutation is present in approximately 90% of patients with pancreatic cancer; however,
KRAS
-specific drugs are not yet widely used in clinical practice for pancreatic cancer, specifically the
KRAS
G12D
variant. Advances in genomic testing revealed an opportunity to detect genetic alterations in a subset of patients with no
KRAS
mutation termed
KRAS
wild-type. Patients with
KRAS
wild-type tumors have a propensity to express driver alterations, hence paving the way for utilizing a targeted therapy approach either via clinical trials or standard-of-care drugs. These alterations include fusions, amplifications, translocations, rearrangements and microsatellite instability-high tumors and can be as high as 11% in some studies. Here, we discuss some of the most notable alterations in
KRAS
wild-type and highlight promising clinical trials.</abstract><cop>Cham</cop><pub>Springer International Publishing</pub><pmid>39123077</pmid><doi>10.1007/s11523-024-01088-3</doi><tpages>11</tpages></addata></record> |
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| subjects | Biomedicine Cancer therapies Case reports Chemotherapy Clinical trials Cyclin-dependent kinases Fibroblasts Genes Growth factors Hematology Humans Kinases Lymphoma Medicine Medicine & Public Health Metastasis Mutation Oncology Pancreatic cancer Pancreatic Neoplasms - drug therapy Pancreatic Neoplasms - genetics Proteins Proto-Oncogene Proteins p21(ras) - genetics Review Article Sarcoma Tumors |
| title | Identifying Actionable Alterations in KRAS Wild-Type Pancreatic Cancer |
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