PTEN‐PI3K pathway alterations in advanced prostate cancer and clinical implications

Background Despite significant advances in molecular characterization and therapeutic targeting of advanced prostate cancer, it remains the second most common cause of cancer death in men in the United States. The PI3K (Phosphatidylinositol 3‐kinase)/AKT (AKT serine/threonine kinase)/mTOR (mammalian...

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Vydané v:	The Prostate Ročník 82; číslo S1; s. S60 - S72
Hlavný autor:	Choudhury, Atish D.
Médium:	Journal Article
Jazyk:	English
Vydavateľské údaje:	United States Wiley Subscription Services, Inc 01.08.2022
Predmet:	1-Phosphatidylinositol 3-kinase AKT AKT protein Biomarkers capivasertib Cell migration Cell proliferation Cell survival Clinical trials Humans Immune checkpoint inhibitors ipatasertib Kinases LY3023414 Male mTOR Phosphatidylinositol 3-Kinases - metabolism PI3K PIK3CA Poly(ADP-ribose) Polymerase Inhibitors - therapeutic use Prostate cancer Prostatic Neoplasms - drug therapy Protein-serine/threonine kinase Proto-Oncogene Proteins c-akt - metabolism PTEN PTEN Phosphohydrolase - metabolism PTEN protein Rapamycin Ribose samotolisib Signal Transduction Tensin Therapeutic targets TOR protein TOR Serine-Threonine Kinases - metabolism Tumor suppressor genes Tumors prostate cancer samotolisib LY3023414 PI3K PIK3CA ipatasertib PTEN mTOR capivasertib AKT
ISSN:	0270-4137, 1097-0045, 1097-0045
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Abstract	Background Despite significant advances in molecular characterization and therapeutic targeting of advanced prostate cancer, it remains the second most common cause of cancer death in men in the United States. The PI3K (Phosphatidylinositol 3‐kinase)/AKT (AKT serine/threonine kinase)/mTOR (mammalian target of rapamycin) signaling pathway is commonly altered in prostate cancer, most frequently through loss of the PTEN (Phosphatase and Tensin Homolog) tumor suppressor, and is critical for cancer cell proliferation, migration, and survival. Methods This study summarizes signaling through the PTEN/PI3K pathway, alterations in pathway components commonly seen in advanced prostate cancer, and results of clinical trials of pathway inhibitors reported to date with a focus on more recently reported studies. It also reviews rationale for combination approaches currently under study, including with taxanes, immune checkpoint inhibitors and poly (ADP‐ribose) polymerase inhibitors, and discusses future directions in biomarker testing and therapeutic targeting of this pathway. Results Clinical trials studying pharmacologic inhibitors of PI3K, AKT or mTOR kinases have demonstrated modest activity of specific agents, with several trials of pathway inhibitors currently in progress. A key challenge is the importance of PI3K/AKT/mTOR signaling in noncancerous tissues, leading to predictable but often severe toxicities at therapeutic doses. Results Further advances in selective pharmacologic inhibition of the PI3K/AKT/mTOR pathway in tumors, development of rational combinations, and appropriate biomarker selection to identify the appropriate tumor‐ and patient‐specific vulnerabilities will be required to optimize clinical benefit from therapeutic targeting of this pathway.
AbstractList	Despite significant advances in molecular characterization and therapeutic targeting of advanced prostate cancer, it remains the second most common cause of cancer death in men in the United States. The PI3K (Phosphatidylinositol 3-kinase)/AKT (AKT serine/threonine kinase)/mTOR (mammalian target of rapamycin) signaling pathway is commonly altered in prostate cancer, most frequently through loss of the PTEN (Phosphatase and Tensin Homolog) tumor suppressor, and is critical for cancer cell proliferation, migration, and survival. This study summarizes signaling through the PTEN/PI3K pathway, alterations in pathway components commonly seen in advanced prostate cancer, and results of clinical trials of pathway inhibitors reported to date with a focus on more recently reported studies. It also reviews rationale for combination approaches currently under study, including with taxanes, immune checkpoint inhibitors and poly (ADP-ribose) polymerase inhibitors, and discusses future directions in biomarker testing and therapeutic targeting of this pathway. Clinical trials studying pharmacologic inhibitors of PI3K, AKT or mTOR kinases have demonstrated modest activity of specific agents, with several trials of pathway inhibitors currently in progress. A key challenge is the importance of PI3K/AKT/mTOR signaling in noncancerous tissues, leading to predictable but often severe toxicities at therapeutic doses. Further advances in selective pharmacologic inhibition of the PI3K/AKT/mTOR pathway in tumors, development of rational combinations, and appropriate biomarker selection to identify the appropriate tumor- and patient-specific vulnerabilities will be required to optimize clinical benefit from therapeutic targeting of this pathway. Despite significant advances in molecular characterization and therapeutic targeting of advanced prostate cancer, it remains the second most common cause of cancer death in men in the United States. The PI3K (Phosphatidylinositol 3-kinase)/AKT (AKT serine/threonine kinase)/mTOR (mammalian target of rapamycin) signaling pathway is commonly altered in prostate cancer, most frequently through loss of the PTEN (Phosphatase and Tensin Homolog) tumor suppressor, and is critical for cancer cell proliferation, migration, and survival.BACKGROUNDDespite significant advances in molecular characterization and therapeutic targeting of advanced prostate cancer, it remains the second most common cause of cancer death in men in the United States. The PI3K (Phosphatidylinositol 3-kinase)/AKT (AKT serine/threonine kinase)/mTOR (mammalian target of rapamycin) signaling pathway is commonly altered in prostate cancer, most frequently through loss of the PTEN (Phosphatase and Tensin Homolog) tumor suppressor, and is critical for cancer cell proliferation, migration, and survival.This study summarizes signaling through the PTEN/PI3K pathway, alterations in pathway components commonly seen in advanced prostate cancer, and results of clinical trials of pathway inhibitors reported to date with a focus on more recently reported studies. It also reviews rationale for combination approaches currently under study, including with taxanes, immune checkpoint inhibitors and poly (ADP-ribose) polymerase inhibitors, and discusses future directions in biomarker testing and therapeutic targeting of this pathway.METHODSThis study summarizes signaling through the PTEN/PI3K pathway, alterations in pathway components commonly seen in advanced prostate cancer, and results of clinical trials of pathway inhibitors reported to date with a focus on more recently reported studies. It also reviews rationale for combination approaches currently under study, including with taxanes, immune checkpoint inhibitors and poly (ADP-ribose) polymerase inhibitors, and discusses future directions in biomarker testing and therapeutic targeting of this pathway.Clinical trials studying pharmacologic inhibitors of PI3K, AKT or mTOR kinases have demonstrated modest activity of specific agents, with several trials of pathway inhibitors currently in progress. A key challenge is the importance of PI3K/AKT/mTOR signaling in noncancerous tissues, leading to predictable but often severe toxicities at therapeutic doses.RESULTSClinical trials studying pharmacologic inhibitors of PI3K, AKT or mTOR kinases have demonstrated modest activity of specific agents, with several trials of pathway inhibitors currently in progress. A key challenge is the importance of PI3K/AKT/mTOR signaling in noncancerous tissues, leading to predictable but often severe toxicities at therapeutic doses.Further advances in selective pharmacologic inhibition of the PI3K/AKT/mTOR pathway in tumors, development of rational combinations, and appropriate biomarker selection to identify the appropriate tumor- and patient-specific vulnerabilities will be required to optimize clinical benefit from therapeutic targeting of this pathway.RESULTSFurther advances in selective pharmacologic inhibition of the PI3K/AKT/mTOR pathway in tumors, development of rational combinations, and appropriate biomarker selection to identify the appropriate tumor- and patient-specific vulnerabilities will be required to optimize clinical benefit from therapeutic targeting of this pathway. Background Despite significant advances in molecular characterization and therapeutic targeting of advanced prostate cancer, it remains the second most common cause of cancer death in men in the United States. The PI3K (Phosphatidylinositol 3‐kinase)/AKT (AKT serine/threonine kinase)/mTOR (mammalian target of rapamycin) signaling pathway is commonly altered in prostate cancer, most frequently through loss of the PTEN (Phosphatase and Tensin Homolog) tumor suppressor, and is critical for cancer cell proliferation, migration, and survival. Methods This study summarizes signaling through the PTEN/PI3K pathway, alterations in pathway components commonly seen in advanced prostate cancer, and results of clinical trials of pathway inhibitors reported to date with a focus on more recently reported studies. It also reviews rationale for combination approaches currently under study, including with taxanes, immune checkpoint inhibitors and poly (ADP‐ribose) polymerase inhibitors, and discusses future directions in biomarker testing and therapeutic targeting of this pathway. Results Clinical trials studying pharmacologic inhibitors of PI3K, AKT or mTOR kinases have demonstrated modest activity of specific agents, with several trials of pathway inhibitors currently in progress. A key challenge is the importance of PI3K/AKT/mTOR signaling in noncancerous tissues, leading to predictable but often severe toxicities at therapeutic doses. Results Further advances in selective pharmacologic inhibition of the PI3K/AKT/mTOR pathway in tumors, development of rational combinations, and appropriate biomarker selection to identify the appropriate tumor‐ and patient‐specific vulnerabilities will be required to optimize clinical benefit from therapeutic targeting of this pathway. BackgroundDespite significant advances in molecular characterization and therapeutic targeting of advanced prostate cancer, it remains the second most common cause of cancer death in men in the United States. The PI3K (Phosphatidylinositol 3‐kinase)/AKT (AKT serine/threonine kinase)/mTOR (mammalian target of rapamycin) signaling pathway is commonly altered in prostate cancer, most frequently through loss of the PTEN (Phosphatase and Tensin Homolog) tumor suppressor, and is critical for cancer cell proliferation, migration, and survival.MethodsThis study summarizes signaling through the PTEN/PI3K pathway, alterations in pathway components commonly seen in advanced prostate cancer, and results of clinical trials of pathway inhibitors reported to date with a focus on more recently reported studies. It also reviews rationale for combination approaches currently under study, including with taxanes, immune checkpoint inhibitors and poly (ADP‐ribose) polymerase inhibitors, and discusses future directions in biomarker testing and therapeutic targeting of this pathway.ResultsClinical trials studying pharmacologic inhibitors of PI3K, AKT or mTOR kinases have demonstrated modest activity of specific agents, with several trials of pathway inhibitors currently in progress. A key challenge is the importance of PI3K/AKT/mTOR signaling in noncancerous tissues, leading to predictable but often severe toxicities at therapeutic doses.ResultsFurther advances in selective pharmacologic inhibition of the PI3K/AKT/mTOR pathway in tumors, development of rational combinations, and appropriate biomarker selection to identify the appropriate tumor‐ and patient‐specific vulnerabilities will be required to optimize clinical benefit from therapeutic targeting of this pathway.
Author	Choudhury, Atish D.
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BackLink	https://www.ncbi.nlm.nih.gov/pubmed/35657152$$D View this record in MEDLINE/PubMed
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Snippet	Background Despite significant advances in molecular characterization and therapeutic targeting of advanced prostate cancer, it remains the second most common... Despite significant advances in molecular characterization and therapeutic targeting of advanced prostate cancer, it remains the second most common cause of... BackgroundDespite significant advances in molecular characterization and therapeutic targeting of advanced prostate cancer, it remains the second most common...
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SubjectTerms	1-Phosphatidylinositol 3-kinase AKT AKT protein Biomarkers capivasertib Cell migration Cell proliferation Cell survival Clinical trials Humans Immune checkpoint inhibitors ipatasertib Kinases LY3023414 Male mTOR Phosphatidylinositol 3-Kinases - metabolism PI3K PIK3CA Poly(ADP-ribose) Polymerase Inhibitors - therapeutic use Prostate cancer Prostatic Neoplasms - drug therapy Protein-serine/threonine kinase Proto-Oncogene Proteins c-akt - metabolism PTEN PTEN Phosphohydrolase - metabolism PTEN protein Rapamycin Ribose samotolisib Signal Transduction Tensin Therapeutic targets TOR protein TOR Serine-Threonine Kinases - metabolism Tumor suppressor genes Tumors
Title	PTEN‐PI3K pathway alterations in advanced prostate cancer and clinical implications
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