Cite this DOI
10.46243/jst.2026.v11.i05.pp01-19 · Cause-Specific Cox and Fine-Gray Regression in Competing Risks: A Reproducible Synthetic Prostate Cancer Illustration
APA (7th edition)
Bashir Ahmed Younis, A., & Omer Ahmed Mohmmed, A. (2026). Cause-Specific Cox and Fine-Gray Regression in Competing Risks: A Reproducible Synthetic Prostate Cancer Illustration. *Journal of Science & Technology*, *11*(05), 1. https://doi.org/10.46243/jst.2026.v11.i05.pp01-19
⬇ text Italics are shown as *asterisks* in plain text — the journal or book title and the volume.
BibTeX
@article{bashirahmedyounis2026causespecific,
author = {Bashir Ahmed Younis, Abubaker and Omer Ahmed Mohmmed, Altaiyb},
title = {{Cause-Specific Cox and Fine-Gray Regression in Competing Risks: A Reproducible Synthetic Prostate Cancer Illustration}},
journal = {Journal of Science \& Technology},
year = {2026},
month = {may},
volume = {11},
number = {05},
pages = {1},
publisher = {Longman Publishers},
issn = {2456-5660},
doi = {10.46243/jst.2026.v11.i05.pp01-19},
url = {https://doi.org/10.46243/jst.2026.v11.i05.pp01-19},
language = {en},
abstract = {Background: Competing mortality complicates estimation and interpretation of prostate cancer-specific death. Cause-specific Cox and Fine-Gray models answer related but different questions and should be selected according to the target estimand. Objective: To demonstrate, using a fully reproducible fixed synthetic dataset, how cause-specific and subdistribution hazard estimands differ in risk-set construction, regression interpretation, and relation to cumulative incidence. Methods: A single fixed dataset of 500 synthetic observations was generated using seed 123. Covariates, treatment indicators, follow-up time sampled from 1-60 months, and event status sampled with probabilities 0.20 for prostate cancer death, 0.20 for other-cause death, and 0.60 for censoring were mutually independent; therefore, no covariate or treatment effects were encoded. Multivariable cause-specific Cox and Fine-Gray models included 15 regression parameters. Cumulative incidence functions, proportionality diagnostics, event-per-parameter calculations, an exploratory other-cause Cox model, and comparison with the naive Kaplan-Meier complement were examined. Results: Within this single realization, the fitted hormonal-therapy estimates were below unity in both models (CSHR 0.568, 95\% CI 0.381-0.849; SHR 0.605, 95\% CI 0.405-0.903). Stage III versus stage I had estimates in the same direction and of comparable magnitude (CSHR 2.227, 95\% CI 1.045-4.746; SHR 2.006, 95\% CI 0.948-4.245), and the difference in p-value thresholds was not interpreted as model disagreement. Global proportionality tests were not significant for the primary cause-specific Cox (p = 0.605) or Fine-Gray (p = 0.550) model. At 60 months, the naive Kaplan-Meier complement exceeded the cumulative incidence estimate by 12.2 percentage points, although only seven observations remained at risk.}
}RIS (EndNote, Zotero, Mendeley)
TY - JOUR TI - Cause-Specific Cox and Fine-Gray Regression in Competing Risks: A Reproducible Synthetic Prostate Cancer Illustration AU - Bashir Ahmed Younis, Abubaker AU - Omer Ahmed Mohmmed, Altaiyb JO - Journal of Science & Technology PY - 2026 DA - 2026/05/22/ VL - 11 IS - 05 SP - 1 PB - Longman Publishers SN - 2456-5660 LA - en AB - Background: Competing mortality complicates estimation and interpretation of prostate cancer-specific death. Cause-specific Cox and Fine-Gray models answer related but different questions and should be selected according to the target estimand. Objective: To demonstrate, using a fully reproducible fixed synthetic dataset, how cause-specific and subdistribution hazard estimands differ in risk-set construction, regression interpretation, and relation to cumulative incidence. Methods: A single fixed dataset of 500 synthetic observations was generated using seed 123. Covariates, treatment indicators, follow-up time sampled from 1-60 months, and event status sampled with probabilities 0.20 for prostate cancer death, 0.20 for other-cause death, and 0.60 for censoring were mutually independent; therefore, no covariate or treatment effects were encoded. Multivariable cause-specific Cox and Fine-Gray models included 15 regression parameters. Cumulative incidence functions, proportionality diagnostics, event-per-parameter calculations, an exploratory other-cause Cox model, and comparison with the naive Kaplan-Meier complement were examined. Results: Within this single realization, the fitted hormonal-therapy estimates were below unity in both models (CSHR 0.568, 95% CI 0.381-0.849; SHR 0.605, 95% CI 0.405-0.903). Stage III versus stage I had estimates in the same direction and of comparable magnitude (CSHR 2.227, 95% CI 1.045-4.746; SHR 2.006, 95% CI 0.948-4.245), and the difference in p-value thresholds was not interpreted as model disagreement. Global proportionality tests were not significant for the primary cause-specific Cox (p = 0.605) or Fine-Gray (p = 0.550) model. At 60 months, the naive Kaplan-Meier complement exceeded the cumulative incidence estimate by 12.2 percentage points, although only seven observations remained at risk. DO - 10.46243/jst.2026.v11.i05.pp01-19 UR - https://doi.org/10.46243/jst.2026.v11.i05.pp01-19 ER -
CSL-JSON
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} ⬇ .json What citeproc and reference managers read; the DOI system hands it out for Accept: application/vnd.citationstyles.csl+json, and so does this registry's resolver.
From the record as registered (version 2) — the record and its history. Programs: https://registry.smartscholars.in/api.php?action=cite&doi=10.46243%2Fjst.2026.v11.i05.pp01-19 gives all four in one JSON answer.
