Introduction: People living with HIV are at increased risk of suicidal behaviors. It is critical to assess risk factors in resource-poor settings. Our study aimed to quantitatively assess the prevalence, pattern, and risk factors for suicidal behaviors among HIV-positive adults. Material and...

Background/Objectives: Thyroid cancer, predominantly papillary thyroid carcinoma (PTC), is diagnosed about three times more often in women than in men, yet in several cohorts male sex is associated with worse outcomes after diagnosis. We critically appraised this “female incidence–male outcome paradox” and evaluated non-coding RNA (ncRNA) as a candidate regulatory layer. Methods: We conducted a narrative review with documented search methods and an evidence table, complemented by an exploratory, covariate-adjusted analysis of CD274 and ACTA2 transcripts in The Cancer Genome Atlas thyroid carcinoma cohort (497 tumors; 58 normal samples). Results: Similar prevalence of subclinical PTC at autopsy in both sexes supports detection bias as the main driver of the female excess in incidence. Among diagnosed patients, male sex was associated with cancer-specific mortality in a large registry (adjusted HR 1.46, 95% CI 1.26–1.69) but not in several other cohorts; in a multicenter cohort, this association was confined to BRAF V600E-positive disease. In TCGA, ACTA2 was higher in male tumors after adjustment (fold difference 1.22, 95% CI 1.06–1.41), whereas lower CD274 in men was also present in normal thyroid. Sex-stratified androgen receptor–miR-146b correlations have been reported, but formal tests of sex-dependent effect modification are lacking. Conclusions: The paradox reflects detection-driven differences in incidence and a heterogeneous, mechanistically unresolved outcome association in men. The evidence supports sex-stratified studies with formal interaction testing, not sex-specific management.

Background/Objectives: Papillary thyroid carcinoma (PTC) shows a striking sex disparity: women are diagnosed roughly three times more often than men, yet male sex is an independent risk factor for recurrence, disease progression, and disease-specific mortality once PTC is established. This “female incidence–male mortality paradox” has hormonal, genetic, immunological, and clinical explanations, none individually sufficient, and clinical risk-stratification has only recently begun incorporating sex-relevant molecular variables. We synthesized this evidence and evaluated an underexplored regulatory layer, non-coding RNA, as a candidate mechanistic bridge across the pathways implicated. Methods: We conducted a structured narrative synthesis of epidemiological, hormonal, genetic, immunological, and clinical literature on sex differences in PTC (over 100 candidate papers), integrated with institutional pilot data (native-classification reanalysis of tumor-only clinical exome sequencing; 18 patients, 13 female, 5 male), an independent validation query of The Cancer Genome Atlas (TCGA) thyroid carcinoma (THCA) cohort (n = 564) for two immune- and stroma-related transcripts, and a targeted review of non-coding RNA literature intersecting the mechanisms identified. Results: Global age-standardized incidence in 2022 was 13.60 per 100,000 in women versus 4.60 per 100,000 in men, while mortality rates were far closer (0.53 vs. 0.35 per 100,000); this gap narrows toward parity for small, subclinical tumors, consistent with detection and surveillance bias. Independent of detection bias, male sex remained an adjusted predictor of mortality (HR 1.46–1.63), with the female survival advantage confined to age under 55 years and a marked sex-by-BRAF/TERT genotype interaction (HR 0.70 in BRAF-wild-type disease versus 2.74–3.51 in BRAF V600E-positive disease; HR 37.77 with BRAF/TERT co-alteration). Institutional and TCGA data were consistent with a more immunosuppressive, PD-L1-low, α-SMA-high male tumor phenotype. Literature review identified the lncRNA XIST, X-linked microRNAs, and an androgen receptor–miR-146b axis as mechanistically plausible, PTC-relevant non-coding RNA regulators of these same sex-differential pathways that have not yet been analyzed with patient sex as a stratifying variable. Conclusions: The paradox reflects superimposed detection bias and multiple converging, incompletely consistent biological mechanisms that disadvantage male patients once PTC is established. Non-coding RNA regulation of these pathways is mechanistically plausible but remains untested by sex, and represents a concrete, near-term research priority for sex-stratified PTC investigation.