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Trials recruiting now, the landmark trials, the trials held by this cancer's subtypes, the key papers and what they mean, the latest literature, and the milestones year by year.
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The 48 most recent of 116 papers; see them all →
Veterinary paste is dosed for animals by weight, and 'one squirt' is not a human dose. Liver injury of this severity can be fatal and this patient was fortunate to present in time.
For men with low- or intermediate-risk prostate cancer, protons and modern IMRT give the same excellent quality of life and cancer control, so the choice can rest on access, cost and convenience rather than on an expected sparing of bowel or bladder. The result removes prostate cancer from the list of adult indications where a proton advantage was assumed but untested.
One technology page on OnCo cites this paper by its DOI; this record gives the citation a page of its own so a reader can follow it without leaving OnCo. Read the abstract above alongside the citing page listed under Related; the record was created automatically from the Europe PMC entry and its figures have not been checked by hand.
This series is the standard reference for US cancer numbers and the source of most headlines about cancer in younger adults. The gap between falling mortality and rising incidence is the argument for both continued treatment advances and stronger prevention and screening.
This is the paper Europe PMC returns for registry id NCT03748641 with the most citations, so it is the natural first reading for anyone following the MAGNITUDE trial. Read the abstract above alongside the trial page and the registry entry; the record was linked automatically and its figures have not been checked by hand.
This is the paper Europe PMC returns for registry id NCT03732820 with the most citations, so it is the natural first reading for anyone following the PROpel trial. Read the abstract above alongside the trial page and the registry entry; the record was linked automatically and its figures have not been checked by hand.
Long-term data support active surveillance as a safe choice for low and much intermediate-risk disease, while the lower metastasis rate with treatment informs the discussion for men with longer life expectancy.
This edition supplied two widely quoted signals: the first population-level evidence of HPV vaccination preventing cervical cancer in the United States, and the warning that reduced PSA screening was shifting prostate cancer towards later diagnosis.
Query for this cancer: (TITLE:"Prostate cancer" OR ABSTRACT:"Prostate cancer" OR TITLE:"Prostatic acinar adenocarcinoma" OR ABSTRACT:"Prostatic acinar adenocarcinoma" OR TITLE:"Acinar adenocarcinoma of the prostate" OR ABSTRACT:"Acinar adenocarcinoma of the prostate" OR TITLE:"Adenocarcinoma of the prostate" OR ABSTRACT:"Adenocarcinoma of the prostate" OR TITLE:"Prostate carcinoma" OR ABSTRACT:"Prostate carcinoma" OR TITLE:"Carcinoma of the prostate" OR ABSTRACT:"Carcinoma of the prostate") AND (treatment OR therapy OR trial OR survival OR diagnosis). Results are unfiltered search hits about Prostate cancer, not a curated reading list.
Huggins and Hodges castrated men with metastatic prostate cancer, or gave them oestrogen, and the disease regressed; androgen injection made it worse. The first demonstration that a human cancer depends on a circulating hormone, and the origin of systemic cancer therapy. Huggins shared the 1966 Nobel Prize for it.
Stamey measured the antigen in 2,200 samples from 699 patients: it tracked tumour volume, fell to undetectable after prostatectomy with a half-life of 2.2 days, and detected recurrence. The same paper warned that it is raised in benign prostatic hyperplasia and is not specific.
Catalona screened 1,653 healthy men over 50 and biopsied those at or above 4.0 micrograms per litre. Rectal examination alone would have missed 12 of the 37 cancers. Testing spread through primary care over the following decade with no randomised evidence that it saved lives.
Visakorpi found androgen receptor gene amplification in 7 of 23 tumours recurring on androgen deprivation and in none of the pre-treatment samples from the same men. Chen showed in 2004 that receptor overexpression alone is necessary and sufficient to convert sensitive disease to resistant, and turns antagonists into agonists.
In the same year as the amplification finding, ligand-binding-domain mutations that let progesterone, oestrogen and the antiandrogen itself switch the receptor on are found in 5 of 10 androgen-independent cancers, the second of the five routes out of castration.
An immunohistochemical survey shows PSMA is detectable in prostatic epithelium, duodenal mucosa and some renal tubules and almost nowhere else, while falling in dedifferentiated disease, predicting both the treatment and its limits.
TAX 327 gave median survival of 18.9 months with three-weekly docetaxel against 16.5 with mitoxantrone, and improved pain and quality of life; SWOG 9916 reported 17.5 against 15.6 months in the same issue. The end of therapeutic nihilism in castration-resistant disease.
A modest rise in androgen receptor expression, with no mutation, is shown to be necessary and sufficient for antiandrogen resistance and to turn antagonists into agonists, which is the argument that produced abiraterone and enzalutamide.
Tomlins found TMPRSS2 fused to ERG or ETV1 in 23 of 29 prostate tumours, putting a growth gene under the control of the hormone the prostate lives in. The first recurrent rearrangement described in a common solid cancer, and still without a drug twenty years later.
Attard's phase 1 of abiraterone in 21 men resistant to multiple hormonal therapies produced prostate-specific antigen falls of at least 50 percent in 12 of them, lasting up to at least 578 days. The disease was renamed from hormone-refractory to castration-resistant on the strength of results like this.
ERSPC found a 20 percent reduction in prostate cancer mortality, at 1,410 men screened and 48 extra cancers treated per death prevented. PLCO found no difference, with control-group screening at 52 percent by year six. Welch and Albertsen counted 1,305,600 extra United States diagnoses and 1,004,800 definitive treatments since 1986.
TROPIC gave cabazitaxel after docetaxel: 15.1 against 12.7 months, with grade 3 or higher neutropenia in 82 percent. Prostate cancer became a sequencing problem rather than a single-treatment disease.
Profiling 218 tumours on three platforms identifies NCOA2 as an oncogene in 11% and shows that counting copy-number changes separates high- from low-risk disease beyond Gleason score.
Proof that castration-resistant disease is still AR-driven.
AURKA and MYCN are co-amplified in 40% of neuroendocrine prostate cancers against 5% of adenocarcinomas, and Aurora kinase inhibition switches off the neuroendocrine programme in models.
The United States task force issued a grade D recommendation against prostate-specific antigen screening at any age; it moved men aged 55 to 69 to grade C in 2018. In the same year AFFIRM reported enzalutamide after chemotherapy, 18.4 against 13.6 months, with a prostate-specific antigen response rate of 54 percent against 2 percent.
Exome sequencing of 112 tumours makes SPOP the commonest point mutation in prostate cancer and shows SPOP-mutant tumours never carry an ETS fusion; rapid-autopsy sequencing of 50 lethal cancers adds CHD1 deletion, FOXA1 mutation and the chromatin genes that partner the androgen receptor.
Among 2,019 men, carriers present at higher grade and stage and live 8.6 years from diagnosis against 15.7 for non-carriers, which is why a carrier's localised disease is treated rather than watched.
Antonarakis found AR-V7, an androgen receptor lacking the part the drugs bind, in circulating tumour cells: a zero percent prostate-specific antigen response rate to enzalutamide and abiraterone in the men who carried it, against 53 and 68 percent in those who did not.
The Prostate Cancer Foundation working committee publishes the six categories that separate incidental neuroendocrine staining from small cell carcinoma, which is what makes treatment-emergent neuroendocrine disease countable at all.
TCGA put 74 percent of 333 primary tumours into seven subtypes and found DNA repair inactivation in 19 percent; the Stand Up To Cancer cohort sequenced 150 metastatic biopsies and found BRCA2, BRCA1 and ATM aberrations in 19.3 percent; TOPARP-A treated 50 unselected men with olaparib and 14 of the 16 with DNA repair defects responded. Gundem showed metastases seed other metastases.
Pritchard found presumed deleterious germline DNA repair mutations in 11.8 percent of 692 men with metastatic prostate cancer, BRCA2 in 5.3 percent, with no relation to family history or age at diagnosis. The argument for testing every man with metastatic disease rather than selecting by family history.
Methylation separates neuroendocrine from castration-resistant adenocarcinoma far more sharply than mutations do, in a pattern fitting divergent clonal evolution from a common ancestor rather than a late mutational event.
Mu and Ku showed that losing TP53 and RB1 lets a prostate cancer cell switch on SOX2 and stop needing the androgen receptor, reversibly in the laboratory. PROMIS showed multiparametric magnetic resonance imaging is 93 percent sensitive for clinically significant cancer against 48 percent for standard biopsy, and could spare a quarter of men a biopsy.
Above a 2% tumour fraction, plasma reproduces every somatic mutation found in a matched metastatic biopsy, which is the number that makes a liquid biopsy reportable in this disease; in the same year BRCA2 reversion is identified as the mechanism of PARP inhibitor resistance.
SPCG-4 at 29 years: surgery cut prostate cancer death by 45 percent in clinically detected disease and added a mean 2.9 years of life. PIVOT at 19.5 years, in a largely screen-detected population, found no significant difference. Dess showed that once treatment and access are equal, the excess prostate cancer mortality in Black men largely disappears while the excess other-cause mortality does not.
Deep whole genomes of 101 metastases find the AR upstream enhancer amplified in 81% of men, invisible to exome panels; reanalysis of 1,013 exomes finds 97 driver genes, 70 of them new, most below 3%.
Microsatellite instability-high or mismatch repair deficient disease is found in 3.1% of 1,033 men, with durable checkpoint inhibitor responses in 6 of 11 treated; gallium-68 PSMA-11 PET is shown prospectively to localise recurrence in 75% of 635 men with a rising PSA. RB1 alteration emerges as the only genomic marker independently predicting shorter survival in castration-resistant disease.
In 302 randomised men, PSMA PET-CT is 27% more accurate than CT with bone scan, changes management twice as often and delivers less than half the radiation.
KEYNOTE-199 gave objective response rates of 5 and 3 percent with pembrolizumab and PD-L1 predicted nothing, consistent with a median tumour mutational burden of 2.6 mutations per megabase. TRANSFORMER found identical progression-free survival for high-dose testosterone and enzalutamide and a difference of 8.6 months in progression-free survival through crossover depending on which came first.
Circulating tumour DNA is detectable in 94% of 3,334 men with advanced prostate cancer and agrees with tissue on BRCA mutations 93% of the time; in parallel, clonal haematopoiesis is shown to account for almost half the somatic repair-gene variants found in plasma, most often in ATM.
Cell-free DNA methylation separates neuroendocrine from castration-resistant adenocarcinoma with near-perfect discrimination in two small cohorts; a 2,069-man single-centre series shows tumour genomes differ by self-reported race after adjusting for clinical factors, with more 8q gain in tumours from Black men and an association between community income and 8q gain.
TRITON3 randomised 405 men and found imaging-based progression-free survival of 11.2 against 6.4 months in the BRCA subgroup, and a hazard ratio of 0.95 in the ATM subgroup: no effect. 4,855 men were screened to randomise 405.
ProBio's study completion is listed for December 2026, PSMAddition for 11 February 2027, CAPItello-281 for 31 March 2027, TALAPRO-3 for 28 August 2027, PROTEUS for 13 October 2028, PEACE III for December 2028, PSMA-DC for 3 October 2031, and STAMPEDE2, with 3,360 men planned, for March 2032.