The Effect of Age on Prostate Cancer Survival

Abstract

It is not clear to what extent the age of diagnosis and the attained age impact on cancer mortality rates in men with newly diagnosed prostate cancer. We estimated annual prostate cancer mortality rates and 20-year survival rates according to the age of diagnosis, race, grade and time since diagnosis using data from the Surveillance, Epidemiology and End-Results (SEER) program. We identified 116,796 prostate cancer patients diagnosed between 1992 and 1997 and followed them for 20 years. There were 21,896 deaths from prostate cancer. We calculated actuarial survival rates and annual prostate cancer mortality rates by age of diagnosis and by tumor grade. The risk of a man dying of prostate cancer was 17% for men diagnosed before age 70 and was 21% for those diagnosed after age 70. The mean annual prostate cancer mortality rate calculated over the 20-year period post-diagnosis was 1.5%. The annual rate increased from 0.9% for those diagnosed below age 60 to 2.1% for those diagnosed above age 70. For men with Gleason score ≥ 7 prostate cancer, the annual prostate cancer mortality rate peaked 2–3 years after diagnosis and then declined. For men diagnosed with Gleason score ≤ 6 prostate cancer, the annual prostate cancer mortality rate continued to rise 20 years after diagnosis and peaked after age 85. This suggests that high-grade prostate cancers are aggressive from the outset, but that low-grade prostate cancers may enter a state of dormancy and reactivate as the patient ages.

Hospital outcomes and costs for prostate cancer patients with comorbid heart failure by age group: An analysis of the US Nationwide Inpatient Sample

“…Among the comorbidities that have been found to be particularly relevant is HF, as it has been associated with both an increased risk of cancer and cancer‐related mortality 17 . It is known that PC incidence and mortality increases with age; one study found that the annual probability of PC‐related mortality rises continuously with attained age, from 0.5% at age 50% to 2.0% at age 90 18 . While age has been studied as a significant contributor to higher mortality rates in PC patients, there has been no study that has specifically examined the impact of comorbidities in the context of PC patient age.…”

Identification of age‐ and immune‐related gene signatures for clinical outcome prediction in lung adenocarcinoma

“…Age has been associated with survival in many cancer types 38–44 . A recent systematic review of pan‐cancer prognostic clinicopathological factors associated with survival outcomes found that advanced patient age (135 studies) and higher pathological stage (133 studies) were common features associated with death from cancer, including LUAD 45 .…”

“…Age has been associated with survival in many cancer types. 38 , 39 , 40 , 41 , 42 , 43 , 44 A recent systematic review of pan‐cancer prognostic clinicopathological factors associated with survival outcomes found that advanced patient age (135 studies) and higher pathological stage (133 studies) were common features associated with death from cancer, including LUAD. 45 Previous studies have shown that aging and cancer are characterized by a series of partially overlapping “hallmarks” including genomic instability, epigenetic alterations, and chronic inflammation.…”

Androgen Metabolism and Response in Prostate Cancer Anti-Androgen Therapy Resistance

“…Although early-stage low-grade prostate cancer can be cured with surgery or radiation therapy, most patients have progressed to CSPC by the time they are admitted to the hospital. ADT therapy can promote tumor dormancy, prolong the survival of patients, and improve the quality of life, but it can rarely cure prostate cancer, and most tumors will recur [ 110 , 111 ]. Tumor resistance to ADT is cumulative: with the change of lineage, some tumor cells will eventually lose AR expression and develop into small cell carcinoma; this type of tumor is called neuroendocrine prostate cancer (NEPC), and this type of cancer cells express neuroendocrine markers, mostly induced by treatment, and a small part is primary, and does not respond to ARSI et al [ 112 ].…”