Deciphering the Increased Prevalence of TP53 Mutations in Metastatic Prostate Cancer

The prevalence of TP53 mutations in advanced prostate cancers (PCa) is 3 to 5 times of the quantity in primary PCa. By an integrative analysis of the Cancer Genome Atlas and Catalogue of Somatic Mutations in Cancer data, we revealed the supporting evidence for 2 complementary hypotheses: H 1 - TP53...
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Gespeichert in:

Autor*in:	Wensheng Zhang [verfasserIn] Yan Dong [verfasserIn] Oliver Sartor [verfasserIn] Kun Zhang [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2022

Übergeordnetes Werk:	In: Cancer Informatics - SAGE Publishing, 2005, 21(2022)
Übergeordnetes Werk:	volume:21 ; year:2022

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1177/11769351221087046

Katalog-ID:	DOAJ078152372

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520			\|a The prevalence of TP53 mutations in advanced prostate cancers (PCa) is 3 to 5 times of the quantity in primary PCa. By an integrative analysis of the Cancer Genome Atlas and Catalogue of Somatic Mutations in Cancer data, we revealed the supporting evidence for 2 complementary hypotheses: H 1 - TP53 abnormalities promote metastasis or therapy-resistance of PCa cells, and H 2 —part of TP53 mutations in PCa metastases occur after the diagnosis of original cancers. The plausibility of these hypotheses can explain the increased prevalence of TP53 mutations in PCa metastases. With H 1 and H 2 as the general assumptions, we developed mathematical models to decipher the change of the percentage frequency (prevalence) of TP53 mutations from primary tumors to metastases. The following results were obtained. Compared to TP53-normal patients, TP53-mutated patients had poorer biochemical relapse-free survival, higher Gleason scores, and more advanced t-stages ( P < .01). Single-nucleotide variants in metastases more frequently occurred on G bases of the coding sequence than those in primary cancers ( P = .03). The profile of TP53 hotspot mutations was significantly different between primary and metastatic PCa as demonstrated in a set of statistical tests ( P < .05). By the derived formulae, we estimated that about 40% TP53 mutation records collected from metastases occurred after the diagnosis of the original cancers. Our study provided significant insight into PCa progression. The proposed models can also be applied to decipher the prevalence of mutations on TP53 (or other driver genes) in other cancer types.
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allfields	10.1177/11769351221087046 doi (DE-627)DOAJ078152372 (DE-599)DOAJb9b02e5b8c0d4ac6b5846a38e93b77de DE-627 ger DE-627 rakwb eng RC254-282 Wensheng Zhang verfasserin aut Deciphering the Increased Prevalence of TP53 Mutations in Metastatic Prostate Cancer 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The prevalence of TP53 mutations in advanced prostate cancers (PCa) is 3 to 5 times of the quantity in primary PCa. By an integrative analysis of the Cancer Genome Atlas and Catalogue of Somatic Mutations in Cancer data, we revealed the supporting evidence for 2 complementary hypotheses: H 1 - TP53 abnormalities promote metastasis or therapy-resistance of PCa cells, and H 2 —part of TP53 mutations in PCa metastases occur after the diagnosis of original cancers. The plausibility of these hypotheses can explain the increased prevalence of TP53 mutations in PCa metastases. With H 1 and H 2 as the general assumptions, we developed mathematical models to decipher the change of the percentage frequency (prevalence) of TP53 mutations from primary tumors to metastases. The following results were obtained. Compared to TP53-normal patients, TP53-mutated patients had poorer biochemical relapse-free survival, higher Gleason scores, and more advanced t-stages ( P < .01). Single-nucleotide variants in metastases more frequently occurred on G bases of the coding sequence than those in primary cancers ( P = .03). The profile of TP53 hotspot mutations was significantly different between primary and metastatic PCa as demonstrated in a set of statistical tests ( P < .05). By the derived formulae, we estimated that about 40% TP53 mutation records collected from metastases occurred after the diagnosis of the original cancers. Our study provided significant insight into PCa progression. The proposed models can also be applied to decipher the prevalence of mutations on TP53 (or other driver genes) in other cancer types. Neoplasms. Tumors. Oncology. Including cancer and carcinogens Yan Dong verfasserin aut Oliver Sartor verfasserin aut Kun Zhang verfasserin aut In Cancer Informatics SAGE Publishing, 2005 21(2022) (DE-627)500019932 (DE-600)2202739-7 11769351 nnns volume:21 year:2022 https://doi.org/10.1177/11769351221087046 kostenfrei https://doaj.org/article/b9b02e5b8c0d4ac6b5846a38e93b77de kostenfrei https://doi.org/10.1177/11769351221087046 kostenfrei https://doaj.org/toc/1176-9351 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_374 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_2704 GBV_ILN_2707 GBV_ILN_2890 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 21 2022
spelling	10.1177/11769351221087046 doi (DE-627)DOAJ078152372 (DE-599)DOAJb9b02e5b8c0d4ac6b5846a38e93b77de DE-627 ger DE-627 rakwb eng RC254-282 Wensheng Zhang verfasserin aut Deciphering the Increased Prevalence of TP53 Mutations in Metastatic Prostate Cancer 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The prevalence of TP53 mutations in advanced prostate cancers (PCa) is 3 to 5 times of the quantity in primary PCa. By an integrative analysis of the Cancer Genome Atlas and Catalogue of Somatic Mutations in Cancer data, we revealed the supporting evidence for 2 complementary hypotheses: H 1 - TP53 abnormalities promote metastasis or therapy-resistance of PCa cells, and H 2 —part of TP53 mutations in PCa metastases occur after the diagnosis of original cancers. The plausibility of these hypotheses can explain the increased prevalence of TP53 mutations in PCa metastases. With H 1 and H 2 as the general assumptions, we developed mathematical models to decipher the change of the percentage frequency (prevalence) of TP53 mutations from primary tumors to metastases. The following results were obtained. Compared to TP53-normal patients, TP53-mutated patients had poorer biochemical relapse-free survival, higher Gleason scores, and more advanced t-stages ( P < .01). Single-nucleotide variants in metastases more frequently occurred on G bases of the coding sequence than those in primary cancers ( P = .03). The profile of TP53 hotspot mutations was significantly different between primary and metastatic PCa as demonstrated in a set of statistical tests ( P < .05). By the derived formulae, we estimated that about 40% TP53 mutation records collected from metastases occurred after the diagnosis of the original cancers. Our study provided significant insight into PCa progression. The proposed models can also be applied to decipher the prevalence of mutations on TP53 (or other driver genes) in other cancer types. Neoplasms. Tumors. Oncology. Including cancer and carcinogens Yan Dong verfasserin aut Oliver Sartor verfasserin aut Kun Zhang verfasserin aut In Cancer Informatics SAGE Publishing, 2005 21(2022) (DE-627)500019932 (DE-600)2202739-7 11769351 nnns volume:21 year:2022 https://doi.org/10.1177/11769351221087046 kostenfrei https://doaj.org/article/b9b02e5b8c0d4ac6b5846a38e93b77de kostenfrei https://doi.org/10.1177/11769351221087046 kostenfrei https://doaj.org/toc/1176-9351 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_374 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_2704 GBV_ILN_2707 GBV_ILN_2890 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 21 2022
allfields_unstemmed	10.1177/11769351221087046 doi (DE-627)DOAJ078152372 (DE-599)DOAJb9b02e5b8c0d4ac6b5846a38e93b77de DE-627 ger DE-627 rakwb eng RC254-282 Wensheng Zhang verfasserin aut Deciphering the Increased Prevalence of TP53 Mutations in Metastatic Prostate Cancer 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The prevalence of TP53 mutations in advanced prostate cancers (PCa) is 3 to 5 times of the quantity in primary PCa. By an integrative analysis of the Cancer Genome Atlas and Catalogue of Somatic Mutations in Cancer data, we revealed the supporting evidence for 2 complementary hypotheses: H 1 - TP53 abnormalities promote metastasis or therapy-resistance of PCa cells, and H 2 —part of TP53 mutations in PCa metastases occur after the diagnosis of original cancers. The plausibility of these hypotheses can explain the increased prevalence of TP53 mutations in PCa metastases. With H 1 and H 2 as the general assumptions, we developed mathematical models to decipher the change of the percentage frequency (prevalence) of TP53 mutations from primary tumors to metastases. The following results were obtained. Compared to TP53-normal patients, TP53-mutated patients had poorer biochemical relapse-free survival, higher Gleason scores, and more advanced t-stages ( P < .01). Single-nucleotide variants in metastases more frequently occurred on G bases of the coding sequence than those in primary cancers ( P = .03). The profile of TP53 hotspot mutations was significantly different between primary and metastatic PCa as demonstrated in a set of statistical tests ( P < .05). By the derived formulae, we estimated that about 40% TP53 mutation records collected from metastases occurred after the diagnosis of the original cancers. Our study provided significant insight into PCa progression. The proposed models can also be applied to decipher the prevalence of mutations on TP53 (or other driver genes) in other cancer types. Neoplasms. Tumors. Oncology. Including cancer and carcinogens Yan Dong verfasserin aut Oliver Sartor verfasserin aut Kun Zhang verfasserin aut In Cancer Informatics SAGE Publishing, 2005 21(2022) (DE-627)500019932 (DE-600)2202739-7 11769351 nnns volume:21 year:2022 https://doi.org/10.1177/11769351221087046 kostenfrei https://doaj.org/article/b9b02e5b8c0d4ac6b5846a38e93b77de kostenfrei https://doi.org/10.1177/11769351221087046 kostenfrei https://doaj.org/toc/1176-9351 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_374 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_2704 GBV_ILN_2707 GBV_ILN_2890 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 21 2022
allfieldsGer	10.1177/11769351221087046 doi (DE-627)DOAJ078152372 (DE-599)DOAJb9b02e5b8c0d4ac6b5846a38e93b77de DE-627 ger DE-627 rakwb eng RC254-282 Wensheng Zhang verfasserin aut Deciphering the Increased Prevalence of TP53 Mutations in Metastatic Prostate Cancer 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The prevalence of TP53 mutations in advanced prostate cancers (PCa) is 3 to 5 times of the quantity in primary PCa. By an integrative analysis of the Cancer Genome Atlas and Catalogue of Somatic Mutations in Cancer data, we revealed the supporting evidence for 2 complementary hypotheses: H 1 - TP53 abnormalities promote metastasis or therapy-resistance of PCa cells, and H 2 —part of TP53 mutations in PCa metastases occur after the diagnosis of original cancers. The plausibility of these hypotheses can explain the increased prevalence of TP53 mutations in PCa metastases. With H 1 and H 2 as the general assumptions, we developed mathematical models to decipher the change of the percentage frequency (prevalence) of TP53 mutations from primary tumors to metastases. The following results were obtained. Compared to TP53-normal patients, TP53-mutated patients had poorer biochemical relapse-free survival, higher Gleason scores, and more advanced t-stages ( P < .01). Single-nucleotide variants in metastases more frequently occurred on G bases of the coding sequence than those in primary cancers ( P = .03). The profile of TP53 hotspot mutations was significantly different between primary and metastatic PCa as demonstrated in a set of statistical tests ( P < .05). By the derived formulae, we estimated that about 40% TP53 mutation records collected from metastases occurred after the diagnosis of the original cancers. Our study provided significant insight into PCa progression. The proposed models can also be applied to decipher the prevalence of mutations on TP53 (or other driver genes) in other cancer types. Neoplasms. Tumors. Oncology. Including cancer and carcinogens Yan Dong verfasserin aut Oliver Sartor verfasserin aut Kun Zhang verfasserin aut In Cancer Informatics SAGE Publishing, 2005 21(2022) (DE-627)500019932 (DE-600)2202739-7 11769351 nnns volume:21 year:2022 https://doi.org/10.1177/11769351221087046 kostenfrei https://doaj.org/article/b9b02e5b8c0d4ac6b5846a38e93b77de kostenfrei https://doi.org/10.1177/11769351221087046 kostenfrei https://doaj.org/toc/1176-9351 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_374 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_2704 GBV_ILN_2707 GBV_ILN_2890 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 21 2022
allfieldsSound	10.1177/11769351221087046 doi (DE-627)DOAJ078152372 (DE-599)DOAJb9b02e5b8c0d4ac6b5846a38e93b77de DE-627 ger DE-627 rakwb eng RC254-282 Wensheng Zhang verfasserin aut Deciphering the Increased Prevalence of TP53 Mutations in Metastatic Prostate Cancer 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The prevalence of TP53 mutations in advanced prostate cancers (PCa) is 3 to 5 times of the quantity in primary PCa. By an integrative analysis of the Cancer Genome Atlas and Catalogue of Somatic Mutations in Cancer data, we revealed the supporting evidence for 2 complementary hypotheses: H 1 - TP53 abnormalities promote metastasis or therapy-resistance of PCa cells, and H 2 —part of TP53 mutations in PCa metastases occur after the diagnosis of original cancers. The plausibility of these hypotheses can explain the increased prevalence of TP53 mutations in PCa metastases. With H 1 and H 2 as the general assumptions, we developed mathematical models to decipher the change of the percentage frequency (prevalence) of TP53 mutations from primary tumors to metastases. The following results were obtained. Compared to TP53-normal patients, TP53-mutated patients had poorer biochemical relapse-free survival, higher Gleason scores, and more advanced t-stages ( P < .01). Single-nucleotide variants in metastases more frequently occurred on G bases of the coding sequence than those in primary cancers ( P = .03). The profile of TP53 hotspot mutations was significantly different between primary and metastatic PCa as demonstrated in a set of statistical tests ( P < .05). By the derived formulae, we estimated that about 40% TP53 mutation records collected from metastases occurred after the diagnosis of the original cancers. Our study provided significant insight into PCa progression. The proposed models can also be applied to decipher the prevalence of mutations on TP53 (or other driver genes) in other cancer types. Neoplasms. Tumors. Oncology. Including cancer and carcinogens Yan Dong verfasserin aut Oliver Sartor verfasserin aut Kun Zhang verfasserin aut In Cancer Informatics SAGE Publishing, 2005 21(2022) (DE-627)500019932 (DE-600)2202739-7 11769351 nnns volume:21 year:2022 https://doi.org/10.1177/11769351221087046 kostenfrei https://doaj.org/article/b9b02e5b8c0d4ac6b5846a38e93b77de kostenfrei https://doi.org/10.1177/11769351221087046 kostenfrei https://doaj.org/toc/1176-9351 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_374 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_2704 GBV_ILN_2707 GBV_ILN_2890 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 21 2022
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callnumber-first	R - Medicine
author	Wensheng Zhang
spellingShingle	Wensheng Zhang misc RC254-282 misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens Deciphering the Increased Prevalence of TP53 Mutations in Metastatic Prostate Cancer
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topic_title	RC254-282 Deciphering the Increased Prevalence of TP53 Mutations in Metastatic Prostate Cancer
topic	misc RC254-282 misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens
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title	Deciphering the Increased Prevalence of TP53 Mutations in Metastatic Prostate Cancer
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title_full	Deciphering the Increased Prevalence of TP53 Mutations in Metastatic Prostate Cancer
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title_sort	deciphering the increased prevalence of tp53 mutations in metastatic prostate cancer
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title_auth	Deciphering the Increased Prevalence of TP53 Mutations in Metastatic Prostate Cancer
abstract	The prevalence of TP53 mutations in advanced prostate cancers (PCa) is 3 to 5 times of the quantity in primary PCa. By an integrative analysis of the Cancer Genome Atlas and Catalogue of Somatic Mutations in Cancer data, we revealed the supporting evidence for 2 complementary hypotheses: H 1 - TP53 abnormalities promote metastasis or therapy-resistance of PCa cells, and H 2 —part of TP53 mutations in PCa metastases occur after the diagnosis of original cancers. The plausibility of these hypotheses can explain the increased prevalence of TP53 mutations in PCa metastases. With H 1 and H 2 as the general assumptions, we developed mathematical models to decipher the change of the percentage frequency (prevalence) of TP53 mutations from primary tumors to metastases. The following results were obtained. Compared to TP53-normal patients, TP53-mutated patients had poorer biochemical relapse-free survival, higher Gleason scores, and more advanced t-stages ( P < .01). Single-nucleotide variants in metastases more frequently occurred on G bases of the coding sequence than those in primary cancers ( P = .03). The profile of TP53 hotspot mutations was significantly different between primary and metastatic PCa as demonstrated in a set of statistical tests ( P < .05). By the derived formulae, we estimated that about 40% TP53 mutation records collected from metastases occurred after the diagnosis of the original cancers. Our study provided significant insight into PCa progression. The proposed models can also be applied to decipher the prevalence of mutations on TP53 (or other driver genes) in other cancer types.
abstractGer	The prevalence of TP53 mutations in advanced prostate cancers (PCa) is 3 to 5 times of the quantity in primary PCa. By an integrative analysis of the Cancer Genome Atlas and Catalogue of Somatic Mutations in Cancer data, we revealed the supporting evidence for 2 complementary hypotheses: H 1 - TP53 abnormalities promote metastasis or therapy-resistance of PCa cells, and H 2 —part of TP53 mutations in PCa metastases occur after the diagnosis of original cancers. The plausibility of these hypotheses can explain the increased prevalence of TP53 mutations in PCa metastases. With H 1 and H 2 as the general assumptions, we developed mathematical models to decipher the change of the percentage frequency (prevalence) of TP53 mutations from primary tumors to metastases. The following results were obtained. Compared to TP53-normal patients, TP53-mutated patients had poorer biochemical relapse-free survival, higher Gleason scores, and more advanced t-stages ( P < .01). Single-nucleotide variants in metastases more frequently occurred on G bases of the coding sequence than those in primary cancers ( P = .03). The profile of TP53 hotspot mutations was significantly different between primary and metastatic PCa as demonstrated in a set of statistical tests ( P < .05). By the derived formulae, we estimated that about 40% TP53 mutation records collected from metastases occurred after the diagnosis of the original cancers. Our study provided significant insight into PCa progression. The proposed models can also be applied to decipher the prevalence of mutations on TP53 (or other driver genes) in other cancer types.
abstract_unstemmed	The prevalence of TP53 mutations in advanced prostate cancers (PCa) is 3 to 5 times of the quantity in primary PCa. By an integrative analysis of the Cancer Genome Atlas and Catalogue of Somatic Mutations in Cancer data, we revealed the supporting evidence for 2 complementary hypotheses: H 1 - TP53 abnormalities promote metastasis or therapy-resistance of PCa cells, and H 2 —part of TP53 mutations in PCa metastases occur after the diagnosis of original cancers. The plausibility of these hypotheses can explain the increased prevalence of TP53 mutations in PCa metastases. With H 1 and H 2 as the general assumptions, we developed mathematical models to decipher the change of the percentage frequency (prevalence) of TP53 mutations from primary tumors to metastases. The following results were obtained. Compared to TP53-normal patients, TP53-mutated patients had poorer biochemical relapse-free survival, higher Gleason scores, and more advanced t-stages ( P < .01). Single-nucleotide variants in metastases more frequently occurred on G bases of the coding sequence than those in primary cancers ( P = .03). The profile of TP53 hotspot mutations was significantly different between primary and metastatic PCa as demonstrated in a set of statistical tests ( P < .05). By the derived formulae, we estimated that about 40% TP53 mutation records collected from metastases occurred after the diagnosis of the original cancers. Our study provided significant insight into PCa progression. The proposed models can also be applied to decipher the prevalence of mutations on TP53 (or other driver genes) in other cancer types.
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title_short	Deciphering the Increased Prevalence of TP53 Mutations in Metastatic Prostate Cancer
url	https://doi.org/10.1177/11769351221087046 https://doaj.org/article/b9b02e5b8c0d4ac6b5846a38e93b77de https://doaj.org/toc/1176-9351
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up_date	2024-07-03T16:15:25.635Z
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The profile of TP53 hotspot mutations was significantly different between primary and metastatic PCa as demonstrated in a set of statistical tests ( P < .05). By the derived formulae, we estimated that about 40% TP53 mutation records collected from metastases occurred after the diagnosis of the original cancers. Our study provided significant insight into PCa progression. The proposed models can also be applied to decipher the prevalence of mutations on TP53 (or other driver genes) in other cancer types.</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">Neoplasms. Tumors. Oncology. 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Deciphering the Increased Prevalence of TP53 Mutations in Metastatic Prostate Cancer

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