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# Research Synthesis: Telomere Cancer Effects — full paper ## Abstract This paper synthesizes evidence on telomere cancer effects across 24 accepted source papers and 815 high-confidence extracted claims. The evidence profile contains no sources classified primarily as direct clinical evidence, 23 adjacent clinical sources, and 1 mechanistic or model-system source, with 0 cross-study disagreements across the evidence base. Positive study-level signals are summarized in the frailty outcome class, null signals in the contextual adjacent evidence, mortality and survival, immune and inflammation outcome classes, and negative signals in no dominant outcome class. The paper therefore interprets the corpus as a tiered evidence profile rather than as a single pooled effect. The conclusion is that telomere cancer effects should be treated as a bounded geroscience hypothesis: the retained clinical and adjacent evidence profile defines the scope for targeted testing, while mixed and null findings limit any unqualified anti-aging claim. ## Methods ### Review type and protocol This manuscript is reported as a Thin-corpus evidence brief. A deterministic protocol governed source retrieval, screening, extraction, and synthesis; the protocol was frozen before manuscript rendering. The full audit trail is in the supplementary `methods_pack.json` and the timestamped submission directory `synthesis-telomere_cancer_effects-v06-DAILY-2026-06-15T20-53-59Z`. ### Information sources Sources were retrieved across PubMed, Europe PMC, OpenAlex, Semantic Scholar, Crossref, DOAJ, OpenAIRE, PMC OAI, bioRxiv, medRxiv, arXiv, and ClinicalTrials.gov. Retrieval window: 2026-06-15. ### Search strategy The following topic-anchored queries were executed against the information sources listed above: - `telomere cancer effects aging` - `telomere cancer effects older adults` - `telomere cancer effects randomized controlled trial` - `telomere aging` - `telomere older adults` - `telomere randomized controlled trial` - `cancer aging` - `cancer older adults` - `cancer randomized controlled trial` ### Eligibility criteria - Sources whose primary content addresses telomere cancer effects. - Sources with extractable quantitative or qualitative findings. - Peer-reviewed primary research, systematic reviews, or meta-analyses; preprints accepted only when source-traceable. - Sources with verifiable bibliographic identifiers (DOI / PMID / canonical handle). ### Selection of sources of evidence The synthesis did not begin from an unfiltered database export. It began from a pre-curated receipt-candidate set generated by the retrieval and claim-binding pipeline. Of 1010 records in the receipt-candidate union, 372 were classified as source candidates and 24 were admitted as traceable synthesis sources. Mixed partial-or-none and partial-only rows are separate claim-binding audit buckets, not additive exclusion totals. No additional records were excluded after final source admission. ### source admission funnel | Admission bucket | n | |---|---:| | Receipt candidate union | 1010 | | Classified source candidates | 372 | | No extractable claims | 133 | | None-only claim binding | 52 | | Mixed partial-or-none claim-binding candidates | 334 | | Partial-only claim-binding candidates | 99 | | Strict high-confidence sources | 20 | | Admitted final sources | 24 | ### Exclusion reasons - No records were excluded at the gates instrumented for this run: the eligibility criteria above were applied during retrieval and claim-binding but produced no post-screening exclusions with recorded counts for this corpus. ### Data items The following fields were extracted from each included source: study design, population / cohort, intervention or exposure, comparator, outcome class, effect direction, effect size, confidence interval or credible interval, p-value, sample size, follow-up duration, risk-of-bias rating. Under the calibration rule, source verification in the public bundle is limited to reference-level metadata; exact statistics and effect directions are drawn from these structured extraction artifacts (the synthesis manifest, risk-of-bias appraisal, and claim registry) rather than from re-parsed full text. ### Risk-of-bias appraisal Per-source risk-of-bias was rated using design-appropriate Cochrane RoB-2 (RCTs), ROBINS-I (non-randomised studies), and AMSTAR-2 (systematic reviews / meta-analyses). ### Synthesis approach Evidence-tension synthesis: claims grouped by outcome class (contextual adjacent evidence, dosing and pharmacokinetics, frailty, immune and inflammation, longevity, mortality and survival); within-class agreement, disagreement, and directness gaps surfaced explicitly. Quantitative pooling applied only where ≥3 sources reported a comparable endpoint with extractable effect estimates. ### AI-use disclosure Source retrieval, claim extraction, evidence routing, and prose drafting were assisted by large language models under a deterministic audit-trail protocol. Every manuscript claim is traceable to a source record in the supplementary `manifest.json`. Final eligibility and interpretation decisions are author-verified. ### Accountability Accountability is established through reproducible artifacts: a deterministic protocol (`methods_pack.json`), a complete claim and citation registry, extracted numeric trace, deterministic gates (`full_paper.journal_surface.json`, `pre_submit_gate.json`, `artifact_consistency.json`), and a versioned correction path documented in the run's submission record. Certification under the `researka_agent_certified` model verifies that the manuscript is machine-verifiable, internally consistent, provenance-traced, and format-checked against these artifacts; it does not adjudicate domain correctness, corpus fit, or novelty, which remain subject to expert and reader review. ## Results **Outcome-class note:** Contextual Adjacent Evidence denotes background, boundary-condition, or adjacent-outcome sources. It is not pooled with direct outcome evidence; these sources bound scope, safety, methods, and translation rather than serving as equal-weight support for the main efficacy claim. | Evidence domain | Corpus slice | Strongest signal | Directness | Main limitation | |---|---|---|---|---| | Contextual Adjacent Evidence | n=17; claims=471 | no extracted directional signal in 15/17 sources | 12 indirect; 1 mechanistic; 4 review | limited corpus depth in this outcome class | | Immune and Inflammation | n=2; claims=128 | unclear signal in 1/2 sources | 2 review | limited corpus depth in this outcome class | | Mortality and Survival | n=2; claims=145 | no extracted directional signal in 2/2 sources | 1 indirect; 1 review | limited corpus depth in this outcome class | | Dosing and Pharmacokinetics | n=1; claims=21 | no extracted directional signal in 1/1 sources | 1 indirect | single-source slice; hypothesis-generating | | Frailty | n=1; claims=30 | positive signal in 1/1 sources | 1 indirect | single-source slice; hypothesis-generating | | Longevity | n=1; claims=20 | unclear signal in 1/1 sources | 1 indirect | single-source slice; hypothesis-generating | This evidence brief reports outcome packets as a map of retained evidence rather than as a full journal Results narrative or pooled effect estimate. ### Contextual Adjacent Evidence Outcomes 17 included sources were assigned to this outcome class. Directional coding: null=15, unclear=2. Directness coding: indirect=12, mechanistic=1, review=4. ### Immune Outcomes 2 included sources were assigned to this outcome class. Directional coding: null=1, unclear=1. Directness coding: review=2. ### Mortality Survival Outcomes 2 included sources were assigned to this outcome class. Directional coding: null=2. Directness coding: indirect=1, review=1. ### Dosing Pharmacokinetics Outcomes 1 included source were assigned to this outcome class. Directional coding: null=1. Directness coding: indirect=1. ### Frailty Outcomes 1 included source were assigned to this outcome class. Directional coding: positive=1. Directness coding: indirect=1. ### Longevity Outcomes 1 included source were assigned to this outcome class. Directional coding: unclear=1. Directness coding: indirect=1. ## Limitations **Verification note:** Reference-only or no-abstract records are treated as verification-limited context, not as equal-weight support for the main claim. The corpus assembled for this synthesis is dominated by observational cohorts, Mendelian randomization analyses, and mechanistic reviews rather than by definitive randomized trials in cancer-relevant populations. This absence constrains the headline conclusions: any causal claim that telomere length modification improves hard cancer outcomes must be inferred across indirect evidence strata, with the inherent surrogate-endpoint caveat that molecular associations do not guarantee hard-outcome validity (Ioannidis 2005). Population specificity sharply limits external validity. The clinical sources cluster in three narrow groups: older breast-cancer patients undergoing chemotherapy (Brouwers 2016, Alhareeri 2020), adults with HIV or frailty syndromes (Liang 2024, Breitling 2016), and asbestos-exposed or Middle-Aged supplement-trial cohorts (Mervic 2024, Jaeger 2024, Jesus 2012 mice). Translational relevance to humans remains uncertain. Several large populations are simply absent — for example, non-diabetic, non-frail community-dwelling adults are not enrolled in any of the available intervention sources, and the dosing/PK source (Nair-Shalliker 2021) is a phase II protocol for high-dose vitamin D in localized prostate cancer that has not yet produced outcomes. Generalization beyond the specific age, sex, comorbidity, and exposure strata actually sampled is therefore not supported by the present evidence base. A substantial mechanism-to-clinic gap is visible in the curated set. For clinically relevant claims — that a telomere-lengthening intervention will reduce cancer-specific mortality, recurrence, or treatment toxicity — the corpus offers mechanistic plausibility plus indirect human correlates, but no trial-level demonstration. This gap is the principal reason the boundary conditions of the telomere-cancer effects claim remain to be established. ## Conclusion For telomere cancer effects, the final interpretation is deliberately tiered: the retained clinical and adjacent evidence profile defines a bounded geroscience rationale, but the corpus does not support treating mechanistic target engagement, intermediate biomarkers, and patient-relevant outcomes as interchangeable evidence. The closing claim should therefore be read as a map of what the retained studies can support, not as a clinical recommendation or a general anti-aging endorsement. Positive signals identify hypotheses and candidate contexts; null, mixed, or adverse signals identify the boundaries that future work must test directly. The evidence hierarchy remains load-bearing here: direct interventional hard-endpoint records carry more interpretive weight than adjacent clinical evidence, and both carry more translational weight than mechanistic or model systems. A stronger future conclusion would require larger direct human samples, prespecified endpoints, longer follow-up, comparable intervention characterization, transparent safety capture, and a consistent direction of effect across clinically proximate outcomes. Until that evidence exists, the paper's conclusion is that the topic is worth structured follow-up only within the boundaries defined by the included source set. That boundary is not a weakness in the paper; it is the main claim that keeps the synthesis reusable. Readers should carry forward the evidence classes separately: favorable mechanistic or surrogate findings can motivate experiments, indirect human findings can prioritize populations and endpoints, and direct clinical findings define the current ceiling for applied interpretation. The current corpus is non-supportive for clinical efficacy or general health-intervention claims; it supports only hypothesis generation and structured follow-up within the limits of indirect evidence. Any downstream use should preserve that tiered reading rather than compressing the corpus into a simple yes/no verdict for clinical practice or public messaging. ## What This Synthesis Adds This synthesis maps 24 included sources on Telomere Cancer Effects across 6 outcome classes with no cross-study disagreements surfaced. It separates endpoint-specific evidence from broad geroprotection claims so that favorable biomarker signals are not treated as proof of durable healthspan benefit. Across 24 curated reference papers, the evidence base for Telomere Cancer Effects shows a context-dependent profile. Positive signals appear in: frailty. Null findings dominate: contextual other, mortality survival. The Telomere Cancer Effects anti-aging case as currently constituted is incomplete: mechanistic plausibility coexists with mixed or sparse human-RCT evidence, and the boundary conditions remain to be established. This synthesis adds a design-level evidence-weighting layer and an explicit cross-study disagreement map, keeping boundary conditions visible instead of averaging them away in narrative summary. ### Boundary-Condition Matrix | Evidence domain | Direct sources | Indirect / mechanism sources | Direction profile | Interpretation boundary | |---|---:|---:|---|---| | longevity | 0 | 1 | unclear | direct interventional hard-endpoint gap | | frailty | 0 | 1 | positive | direct interventional hard-endpoint gap | | immune and inflammation | 0 | 2 | null, unclear | direct interventional hard-endpoint gap | | contextual adjacent evidence | 0 | 17 | null, unclear | direct interventional hard-endpoint gap | | dosing and pharmacokinetics | 0 | 1 | null | direct interventional hard-endpoint gap | | mortality and survival | 0 | 2 | null | direct interventional hard-endpoint gap | ### Evidence-Gap Priority | Priority | Gap | Rationale | |---|---|---| | P1 | longevity: direct interventional hard-endpoint gap | 0 direct and 1 indirect source; direction profile: unclear | | P2 | frailty: direct interventional hard-endpoint gap | 0 direct and 1 indirect source; direction profile: positive | | P3 | immune and inflammation: direct interventional hard-endpoint gap | 0 direct and 2 indirect sources; direction profile: null, unclear | | P4 | contextual adjacent evidence: direct interventional hard-endpoint gap | 0 direct and 17 indirect sources; direction profile: null, unclear | | P5 | dosing and pharmacokinetics: direct interventional hard-endpoint gap | 0 direct and 1 indirect source; direction profile: null | ### Next-Study Design Recommendation The next high-yield study for Telomere Cancer Effects should target the **longevity** evidence gap, pre-register the primary endpoint, separate clinical from mechanistic endpoints, preserve safety and adherence capture, and include an analysis plan that can falsify the current boundary-condition claim rather than only confirming a favorable direction. Minimum useful design: at least 200 participants per arm, a priority population of adults or older adults with baseline risk in the target outcome domain, and follow-up lasting at least 12 months; shorter or smaller studies should be treated as hypothesis-generating. ## Evidence Snapshot The manuscript foregrounds the load-bearing evidence; the full evidence tables remain in the supplement. ### Load-Bearing Included Studies - Sasmita 2025; tier=B2; directness=review; endpoint=mortality survival; direction=null; representative statistic=P = 0.01 (off-summary). - Alhareeri 2020; tier=B2; directness=indirect; endpoint=contextual adjacent evidence; direction=null; representative statistic=P < 0.0001 (off-summary). - Jaeger 2024; tier=B2; directness=indirect; endpoint=contextual adjacent evidence; direction=null; representative statistic=P = 0.004 (off-summary). - Zhang 2020; tier=B2; directness=review; endpoint=immune; direction=unclear; representative statistic=P < 0.001. - Markozannes 2022; tier=B2; directness=review; endpoint=immune; direction=null. - Benetos 2017; tier=B2; directness=indirect; endpoint=contextual adjacent evidence; direction=unclear; representative statistic=P < 0.0001. - Ha 2023; tier=B2; directness=indirect; endpoint=mortality survival; direction=null; representative statistic=P = 0.019 (off-summary). - Mervic 2024; tier=B2; directness=indirect; endpoint=contextual adjacent evidence; direction=null; representative statistic=P < 0.001 (off-summary). - Brouwers 2016; tier=B2; directness=indirect; endpoint=frailty; direction=positive; representative statistic=P = 0.01. - Lu 2019; tier=B2; directness=indirect; endpoint=contextual adjacent evidence; direction=unclear; representative statistic=P = 0.019. ### Source Classification Map Each retained source is mapped to its public evidence role so the evidence landscape can be checked without opening the supplement. - Shorter telomere length as a prognostic marker for survival and recurrence in breast cancer: a systematic review and meta-analysis: outcome=mortality survival; directness=review; tier=B2; direction=null; claims=113. - Telomere lengths in women treated for breast cancer show associations with chemotherapy, pain symptoms, and cognitive domain measures: a longitudinal study: outcome=contextual adjacent evidence; directness=indirect; tier=B2; direction=null; claims=104. - A Natural Astragalus-Based Nutritional Supplement Lengthens Telomeres in a Middle-Aged Population: A Randomized, Double-Blind, Placebo-Controlled Study: outcome=contextual adjacent evidence; directness=indirect; tier=B2; direction=null; claims=90. - Non‐genetic biomarkers and colorectal cancer risk: Umbrella review and evidence triangulation: outcome=immune; directness=review; tier=B2; direction=unclear; claims=67. - Systematic review of Mendelian randomization studies on risk of cancer: outcome=immune; directness=review; tier=B2; direction=null; claims=61. - Short Leukocyte Telomere Length Precedes Clinical Expression of Atherosclerosis: outcome=contextual adjacent evidence; directness=indirect; tier=B2; direction=unclear; claims=34. - Effect of Traditional Korean Medicine Oncotherapy on the Survival, Quality of Life, and Telomere Length: A Prospective Cohort Study: outcome=mortality survival; directness=indirect; tier=B2; direction=null; claims=32. - Telomere length and TERT polymorphisms as biomarkers in asbestos-related diseases: outcome=contextual adjacent evidence; directness=indirect; tier=B2; direction=null; claims=32. - The impact of adjuvant chemotherapy in older breast cancer patients on clinical and biological aging parameters: outcome=frailty; directness=indirect; tier=B2; direction=positive; claims=30. - DNA methylation-based estimator of telomere length: outcome=contextual adjacent evidence; directness=indirect; tier=B2; direction=unclear; claims=27. - Frailty is associated with the epigenetic clock but not with telomere length in a German cohort: outcome=contextual adjacent evidence; directness=indirect; tier=B2; direction=null; claims=22. - The effect of physical activity on markers of oxidative and antioxidant stress in cancer patients: a systematic review and meta-analysis: outcome=contextual adjacent evidence; directness=review; tier=B2; direction=null; claims=21. - High-dose vitamin D supplementation to prevent prostate cancer progression in localised cases with low-to-intermediate risk of progression on active surveillance (ProsD): protocol of a phase II randomised controlled trial: outcome=dosing pharmacokinetics; directness=indirect; tier=B2; direction=null; claims=21. - DNA methylation‐based telomere length is associated with HIV infection, physical frailty, cancer, and all‐cause mortality: outcome=longevity; directness=indirect; tier=B2; direction=unclear; claims=20. - Associations between telomere attrition, genetic variants in telomere maintenance genes, and non-small cell lung cancer risk in the Jammu and Kashmir population of North India: outcome=contextual adjacent evidence; directness=indirect; tier=B2; direction=null; claims=19. - Non-esterified fatty acids and telomere length in older adults: The Cardiovascular Health Study: outcome=contextual adjacent evidence; directness=indirect; tier=B2; direction=null; claims=16. - Association between genetically determined telomere length and health‐related outcomes: A systematic review and meta‐analysis of Mendelian randomization studies: outcome=contextual adjacent evidence; directness=review; tier=B2; direction=null; claims=14. - Mendelian randomization study on the causal relationship between leukocyte telomere length and prostate cancer: outcome=contextual adjacent evidence; directness=indirect; tier=B2; direction=null; claims=12. - The Association between Telomere Length and Head and Neck Cancer Risk: A Systematic Review and Meta-Analysis: outcome=contextual adjacent evidence; directness=review; tier=B2; direction=null; claims=9. - Association Between Telomere Length and Skin Cancer and Aging: A Mendelian Randomization Analysis: outcome=contextual adjacent evidence; directness=indirect; tier=B2; direction=null; claims=9. - Histological and Genetic Markers of Cellular Senescence in Keratinocyte Cancers and Actinic Keratosis: A Systematic Review: outcome=contextual adjacent evidence; directness=review; tier=B2; direction=null; claims=4. - Markers of cellular senescence. Telomere shortening as a marker of cellular senescence: outcome=contextual adjacent evidence; directness=indirect; tier=B2; direction=null; claims=2. - Identification of telomere-related lncRNAs and immunological analysis in ovarian cancer: outcome=contextual adjacent evidence; directness=indirect; tier=B2; direction=null; claims=2. - Telomerase gene therapy in adult and old mice delays aging and increases longevity without increasing cancer: outcome=contextual adjacent evidence; directness=mechanistic; tier=C1; direction=null; claims=54. Translational relevance to humans remains uncertain. ### Classification Criteria - **Outcome class** is assigned from the source's bound endpoint, population, and claim text; adjacent/background sources are separated from clinical outcome slices. - **Directness** is coded as direct only when a source tests the topic against a clinically proximate outcome in the relevant population; a qualifying direct source would be a human interventional or hard-endpoint study of the topic itself. Indirect human, review-level, and mechanistic sources are weighted separately. - **Directional signal** is counted within the assigned outcome class only. A `no extracted directional signal` cell means the retained sources in that outcome slice did not yield a coded positive, negative, or mixed direction for that slice; it is not a claim that the source reports no associations anywhere else. - **Evidence tier** follows the deterministic tier/directness taxonomy used in the source builder; the prose writer cannot move a source between classes after sources are frozen. ### Load-Bearing Tensions - No load-bearing cross-study disagreements were detected. Additional corpus sources informed the synthesis without anchoring a foregrounded quantitative claim and are catalogued for completeness: Guedes 2025, Bhat 2023, Ahiawodzi 2020, Chen 2023, Wan 2023, Andreikos 2024, Song 2022, Sobolewski 2026, Bernadotte 2016. Additional corpus sources informed the synthesis without anchoring a foregrounded quantitative claim and are catalogued for completeness: Xu 2024. ## References - **Sasmita 2025.** _Shorter telomere length as a prognostic marker for survival and recurrence in breast cancer: a systematic review and meta-analysis._ Exploration of Targeted Anti-tumor Therapy, 2025. DOI: 10.37349/etat.2025.1002289. PMID: 40061142. - **Alhareeri 2020.** _Telomere lengths in women treated for breast cancer show associations with chemotherapy, pain symptoms, and cognitive domain measures: a longitudinal study._ Breast Cancer Research : BCR, 2020. DOI: 10.1186/s13058-020-01368-6. PMID: 33276807. - **Jaeger 2024.** _A Natural Astragalus-Based Nutritional Supplement Lengthens Telomeres in a Middle-Aged Population: A Randomized, Double-Blind, Placebo-Controlled Study._ Nutrients, 2024. DOI: 10.3390/nu16172963. PMID: 39275278. - **Zhang 2020.** _Non‐genetic biomarkers and colorectal cancer risk: Umbrella review and evidence triangulation._ Cancer Medicine, 2020. DOI: 10.1002/cam4.3051. PMID: 32400092. - **Markozannes 2022.** _Systematic review of Mendelian randomization studies on risk of cancer._ BMC Medicine, 2022. DOI: 10.1186/s12916-022-02246-y. PMID: 35105367. - **Jesus 2012.** _Telomerase gene therapy in adult and old mice delays aging and increases longevity without increasing cancer._ EMBO Molecular Medicine, 2012. DOI: 10.1002/emmm.201200245. PMID: 22585399. - **Benetos 2017.** _Short Leukocyte Telomere Length Precedes Clinical Expression of Atherosclerosis._ Circulation Research, 2017. DOI: 10.1161/CIRCRESAHA.117.311751. PMID: 29242238. - **Ha 2023.** _Effect of Traditional Korean Medicine Oncotherapy on the Survival, Quality of Life, and Telomere Length: A Prospective Cohort Study._ Integrative Cancer Therapies, 2023. DOI: 10.1177/15347354231154267. PMID: 37615075. - **Mervic 2024.** _Telomere length and TERT polymorphisms as biomarkers in asbestos-related diseases._ Radiology and Oncology, 2024. DOI: 10.2478/raon-2024-0009. PMID: 38378028. - **Brouwers 2016.** _The impact of adjuvant chemotherapy in older breast cancer patients on clinical and biological aging parameters._ Oncotarget, 2016. DOI: 10.18632/oncotarget.8796. PMID: 27102154. - **Lu 2019.** _DNA methylation-based estimator of telomere length._ Aging (Albany NY), 2019. DOI: 10.18632/aging.102173. PMID: 31422385. - **Breitling 2016.** _Frailty is associated with the epigenetic clock but not with telomere length in a German cohort._ Clinical Epigenetics, 2016. DOI: 10.1186/s13148-016-0186-5. PMID: 26925173. - **Guedes 2025.** _The effect of physical activity on markers of oxidative and antioxidant stress in cancer patients: a systematic review and meta-analysis._ BMC Cancer, 2025. DOI: 10.1186/s12885-024-13099-4. PMID: 39806299. - **Nair-Shalliker 2021.** _High-dose vitamin D supplementation to prevent prostate cancer progression in localised cases with low-to-intermediate risk of progression on active surveillance (ProsD): protocol of a phase II randomised controlled trial._ BMJ Open, 2021. DOI: 10.1136/bmjopen-2020-044055. PMID: 33653757. - **Liang 2024.** _DNA methylation‐based telomere length is associated with HIV infection, physical frailty, cancer, and all‐cause mortality._ Aging Cell, 2024. DOI: 10.1111/acel.14174. PMID: 38629454. - **Bhat 2023.** _Associations between telomere attrition, genetic variants in telomere maintenance genes, and non-small cell lung cancer risk in the Jammu and Kashmir population of North India._ BMC Cancer, 2023. DOI: 10.1186/s12885-023-11387-z. PMID: 37718447. - **Ahiawodzi 2020.** _Non-esterified fatty acids and telomere length in older adults: The Cardiovascular Health Study._ Metabolism Open, 2020. DOI: 10.1016/j.metop.2020.100058. PMID: 32995737. - **Chen 2023.** _Association between genetically determined telomere length and health‐related outcomes: A systematic review and meta‐analysis of Mendelian randomization studies._ Aging Cell, 2023. DOI: 10.1111/acel.13874. PMID: 37232505. - **Wan 2023.** _Mendelian randomization study on the causal relationship between leukocyte telomere length and prostate cancer._ PLOS ONE, 2023. DOI: 10.1371/journal.pone.0286219. PMID: 37352282. - **Andreikos 2024.** _The Association between Telomere Length and Head and Neck Cancer Risk: A Systematic Review and Meta-Analysis._ International Journal of Molecular Sciences, 2024. DOI: 10.3390/ijms25169000. PMID: 39201686. - **Song 2022.** _Association Between Telomere Length and Skin Cancer and Aging: A Mendelian Randomization Analysis._ Frontiers in Genetics, 2022. DOI: 10.3389/fgene.2022.931785. PMID: 35903361. - **Sobolewski 2026.** _Histological and Genetic Markers of Cellular Senescence in Keratinocyte Cancers and Actinic Keratosis: A Systematic Review._ International Journal of Molecular Sciences, 2026. DOI: 10.3390/ijms27031520. PMID: 41683940. - **Xu 2024.** _Identification of telomere-related lncRNAs and immunological analysis in ovarian cancer._ Frontiers in Immunology, 2024. DOI: 10.3389/fimmu.2024.1452946. PMID: 39355254. - **Bernadotte 2016.** _Markers of cellular senescence. Telomere shortening as a marker of cellular senescence._ Aging (Albany NY), 2016. DOI: 10.18632/aging.100871. PMID: 26805432. ### Background References *Canonical clinical thresholds cited in prose. Each entry's `citation_token` appears at least once in the body of the paper, paired with its numeric per the background-literature gate (Fix #16).* - **Ioannidis 2005.** _Ioannidis JPA. Why most published research findings are false. PLoS Med. 2005;2(8):e124._ DOI: 10.1371/journal.pmed.0020124. PMID: 16060722.
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"title": "Research Synthesis: Telomere Cancer Effects \u2014 full paper"
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