A Balancing Act: p53 Activity from Tumor Suppression to Pathology and Therapeutic Implications
TP53 , encoding the p53 transcription factor, is the most frequently mutated tumor suppressor gene across all human cancer types. While p53 has long been appreciated to induce antiproliferative cell cycle arrest, apoptosis, and senescence programs in response to diverse stress signals, various studi...
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| Veröffentlicht in: | Annual review of pathology 2022-01, Vol.17 (1), p.205-226 |
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| creator | Wang, Mengxiong Attardi, Laura D |
| description | TP53
, encoding the p53 transcription factor, is the most frequently mutated tumor suppressor gene across all human cancer types. While p53 has long been appreciated to induce antiproliferative cell cycle arrest, apoptosis, and senescence programs in response to diverse stress signals, various studies in recent years have revealed additional important functions for p53 that likely also contribute to tumor suppression, including roles in regulating tumor metabolism, ferroptosis, signaling in the tumor microenvironment, and stem cell self-renewal differentiation. Not only does
p53
loss or mutation cause cancer, but hyperactive p53 also drives various pathologies, including developmental phenotypes, premature aging, neurodegeneration, and side effects of cancer therapies. These findings underscore the importance of balanced p53 activity and influence our thinking of how to best develop cancer therapies based on modulating the p53 pathway. |
| doi_str_mv | 10.1146/annurev-pathol-042320-025840 |
| format | Article |
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, encoding the p53 transcription factor, is the most frequently mutated tumor suppressor gene across all human cancer types. While p53 has long been appreciated to induce antiproliferative cell cycle arrest, apoptosis, and senescence programs in response to diverse stress signals, various studies in recent years have revealed additional important functions for p53 that likely also contribute to tumor suppression, including roles in regulating tumor metabolism, ferroptosis, signaling in the tumor microenvironment, and stem cell self-renewal differentiation. Not only does
p53
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, encoding the p53 transcription factor, is the most frequently mutated tumor suppressor gene across all human cancer types. While p53 has long been appreciated to induce antiproliferative cell cycle arrest, apoptosis, and senescence programs in response to diverse stress signals, various studies in recent years have revealed additional important functions for p53 that likely also contribute to tumor suppression, including roles in regulating tumor metabolism, ferroptosis, signaling in the tumor microenvironment, and stem cell self-renewal differentiation. Not only does
p53
loss or mutation cause cancer, but hyperactive p53 also drives various pathologies, including developmental phenotypes, premature aging, neurodegeneration, and side effects of cancer therapies. These findings underscore the importance of balanced p53 activity and influence our thinking of how to best develop cancer therapies based on modulating the p53 pathway.</description><subject>Apoptosis - genetics</subject><subject>cancer</subject><subject>Cell Cycle Checkpoints - genetics</subject><subject>developmental disease</subject><subject>DNE</subject><subject>GOF</subject><subject>Humans</subject><subject>Neoplasms - genetics</subject><subject>Neoplasms - metabolism</subject><subject>Neoplasms - therapy</subject><subject>p53</subject><subject>Signal Transduction - genetics</subject><subject>therapeutic strategies</subject><subject>transcription factor</subject><subject>Tumor Microenvironment</subject><subject>tumor suppression</subject><subject>Tumor Suppressor Protein p53 - genetics</subject><subject>Tumor Suppressor Protein p53 - metabolism</subject><issn>1553-4006</issn><issn>1553-4014</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqVkLtOwzAUhi0EoqXwCsgDA0vAt7gOYgkVN6kSSJQVy0mc1iiJg50U9e1xSenOdM7wX_R_AFxgdIUx49eqaXqn11GrupWtIsQIJShCJBYMHYAxjmMaMYTZ4f5HfAROvP9EiFEuxDEYUcaThHAyBh8pvFOVanLTLGGadzewjen2MWvTbWDpbA0XfW0dfOvb1mnvjW1gZ-Hrb71dbqBqCrhYaada3Xcmh891W5lcdUHoT8FRqSqvz3Z3At4f7hezp2j-8vg8S-eRYgnrIpLHlCYxC_sKlBAlqOAiI0RwTElRcJpwInA2paWiKiMlokQkhShIGI9UwukEXA65rbNfvfadrI3PdRWWadt7GehMAweEp0F6O0hzZ713upStM7VyG4mR3BKWO8JyICwHwnIgHOznu6Y-q3WxN_8hDYJ0EGxjVBWCjP72_yv5AU0nkRI</recordid><startdate>20220124</startdate><enddate>20220124</enddate><creator>Wang, Mengxiong</creator><creator>Attardi, Laura D</creator><general>Annual Reviews</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20220124</creationdate><title>A Balancing Act: p53 Activity from Tumor Suppression to Pathology and Therapeutic Implications</title><author>Wang, Mengxiong ; Attardi, Laura D</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-a494t-2c533954146d092a83868b2286132dd6396281b73fa3ab2f03289d8d24230a963</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Apoptosis - genetics</topic><topic>cancer</topic><topic>Cell Cycle Checkpoints - genetics</topic><topic>developmental disease</topic><topic>DNE</topic><topic>GOF</topic><topic>Humans</topic><topic>Neoplasms - genetics</topic><topic>Neoplasms - metabolism</topic><topic>Neoplasms - therapy</topic><topic>p53</topic><topic>Signal Transduction - genetics</topic><topic>therapeutic strategies</topic><topic>transcription factor</topic><topic>Tumor Microenvironment</topic><topic>tumor suppression</topic><topic>Tumor Suppressor Protein p53 - genetics</topic><topic>Tumor Suppressor Protein p53 - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Mengxiong</creatorcontrib><creatorcontrib>Attardi, Laura D</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Annual review of pathology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Mengxiong</au><au>Attardi, Laura D</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A Balancing Act: p53 Activity from Tumor Suppression to Pathology and Therapeutic Implications</atitle><jtitle>Annual review of pathology</jtitle><addtitle>Annu Rev Pathol</addtitle><date>2022-01-24</date><risdate>2022</risdate><volume>17</volume><issue>1</issue><spage>205</spage><epage>226</epage><pages>205-226</pages><issn>1553-4006</issn><eissn>1553-4014</eissn><abstract>TP53
, encoding the p53 transcription factor, is the most frequently mutated tumor suppressor gene across all human cancer types. While p53 has long been appreciated to induce antiproliferative cell cycle arrest, apoptosis, and senescence programs in response to diverse stress signals, various studies in recent years have revealed additional important functions for p53 that likely also contribute to tumor suppression, including roles in regulating tumor metabolism, ferroptosis, signaling in the tumor microenvironment, and stem cell self-renewal differentiation. Not only does
p53
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| ispartof | Annual review of pathology, 2022-01, Vol.17 (1), p.205-226 |
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| source | Annual Reviews Complete A-Z List; MEDLINE |
| subjects | Apoptosis - genetics cancer Cell Cycle Checkpoints - genetics developmental disease DNE GOF Humans Neoplasms - genetics Neoplasms - metabolism Neoplasms - therapy p53 Signal Transduction - genetics therapeutic strategies transcription factor Tumor Microenvironment tumor suppression Tumor Suppressor Protein p53 - genetics Tumor Suppressor Protein p53 - metabolism |
| title | A Balancing Act: p53 Activity from Tumor Suppression to Pathology and Therapeutic Implications |
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