Skip to content

Not yet independently audited

This page was written from verified sources but has not yet passed the independent citation audit. Treat its claims as provisional.

Chemotherapy and toxic neuropathy

TL;DR — CIPN is a family of agent-specific toxic neuropathies. Across 31 studies/4,179 patients, neuropathy prevalence was 68.1% in month 1, 60.0% at 3 months and 30.0% at ≥6 months (Seretny 2014, PMID 25261162). A 2026 synthesis of 197 studies/72,794 chemotherapy recipients put chronic CIPN (persisting ≥3 months after chemotherapy) at 44.5% overall and 40.4% at ≥24 months, with very low certainty (D'Souza 2026, PMID 42713463). No preventive drug is established; ASCO supports dose modification when functionally significant and duloxetine for established painful CIPN, with limited benefit (Loprinzi 2020, PMID 32663120). Survivorship care must address numbness, balance, falls and work as well as pain.

Agent specificity

Platinums injure DRG neurons; taxanes and vinca alkaloids disrupt microtubules/axonal transport; proteasome inhibitors alter proteostasis and mitochondria (Staff 2017, PMID 28486769). Similar distal symptoms do not prove identical biology.

Exposure Dominant clinical clue Biological emphasis Time-course caution
Oxaliplatin Acute cold-triggered paresthesia plus cumulative sensory loss Ion-channel dysfunction, DRG injury Acute symptoms do not equal chronic CIPN
Cisplatin/carboplatin Cumulative sensory neuronopathy DRG DNA/mitochondrial injury Coasting may continue after cessation
Paclitaxel/docetaxel Distal sensory symptoms, sometimes pain Microtubules, axonal transport, immune signaling Dose schedule changes risk
Vinca alkaloids Sensory-motor/autonomic features Microtubule disruption Weakness/constipation broaden safety scope
Bortezomib Painful distal neuropathy Proteostasis, mitochondria and small fibers Route and schedule matter
Thalidomide analogues Cumulative sensory neuropathy Axonal and antiangiogenic pathways May be poorly reversible

Mechanistic reviews converge on mitochondrial dysfunction, oxidative stress, neuroinflammation, altered ion channels, axonal transport failure and distal terminal degeneration, but the balance differs by agent (Bae 2021, PMID 34676514); (Zajączkowska 2019, PMID 30909387). A broad label is therefore useful for surveillance but too coarse for mechanism-based trials.

Time course

Pooled prevalence was 68.1% (57.7–78.4) in month 1, 60.0% (36.4–81.6) at three months and 30.0% (6.4–53.5) at ≥6 months (Seretny 2014, PMID 25261162). These include painless neuropathy.

A much larger 2026 meta-analysis gives a less reassuring late course. Across 197 studies from 36 countries (72,794 chemotherapy recipients, 26,258 with chronic CIPN, defined as persisting ≥3 months after completion of chemotherapy), pooled prevalence was 44.50% (95% CI 40.77–48.25; I²=99%): 54.37% (48.24–60.45) at 3–12 months, 37.12% (30.15–44.26) at 12–24 months and 40.36% (34.72–46.08) at ≥24 months after chemotherapy. By regimen, platinum (61.12%, 43.08–78.37) and taxane (57.22%, 49.99–64.35) recipients were among the highest (D'Souza 2026, PMID 42713463).

The two syntheses should stand side by side rather than be averaged. Seretny pooled 31 studies at three time points; D'Souza pooled a far larger and more heterogeneous set, counted only neuropathy persisting ≥3 months after completion, and graded its own estimate very low certainty, with small-study asymmetry. Neither isolates painful CIPN. What the newer data add is that prevalence shows no further decline after the first year (37.12% at 12–24 months versus 40.36% at ≥24 months, overlapping intervals), so the older ~30% at ≥6 months should not be read as a point on a continuing downward curve.

Phenotype

Distal numbness, tingling, burning, vibration/proprioception loss and balance impairment predominate. Oxaliplatin acute cold-triggered symptoms differ from chronic cumulative neuropathy (Colvin 2019, PMID 31008843).

Assessment

Record baseline neuropathy, diabetes, alcohol and prior neurotoxins; combine patient report, examination and treatment-specific grading (Hershman 2014, PMID 24733808). Clinician grades alone under-detect burden.

Circulating axonal markers have not yet earned a place. In 30 patients receiving CapeOX plus bevacizumab, plasma phosphorylated neurofilament-heavy chain rose modestly by the final sample but was not associated with the onset, severity or persistence of CTCAE-graded CIPN (ρ=0.12, P=0.56 at onset; ρ=−0.02, P=0.93 at the final sample); the authors attribute this to a mismatch between dorsal-root-ganglion injury and an axon-oriented marker, and note that only CTCAE grading was used and that follow-up sampling was restricted to patients who developed CIPN (Motoo 2026, PMID 42873277).

Assessment must separate sensory loss, positive symptoms, neuropathic pain, motor impairment and autonomic dysfunction. The outcome most relevant to oncologic decisions is often function—buttoning, gait, falls or treatment completion—not pain intensity alone. Baseline measurement is essential because pre-existing diabetic, hereditary or compressive neuropathy changes attribution.

Domain Minimum longitudinal measure Why it matters
Symptoms Patient-reported numbness, tingling, pain, cold sensitivity Detects burden missed by clinician grade
Signs Vibration, pin, reflexes, strength, gait Localizes and tracks neurologic deficit
Function Dexterity, balance, walking and falls Links toxicity to survivorship
Exposure Agent, schedule, cumulative dose and changes Enables dose–toxicity analysis
Cancer outcome Delivered dose and treatment completion Prevents neuroprotection claims from ignoring efficacy

Prevention

ASCO found no routine preventive drug (Loprinzi 2020, PMID 32663120). Cryotherapy has a taxane-specific signal but heterogeneous protocols (Tai 2024, PMID 38955817); goshajinkigan is not established (Kuriyama 2018, PMID 29280005). An open-label randomized phase II trial (65 patients receiving carboplatin–paclitaxel, 80.0% with lung cancer) has since reported grade ≥2 CIPN within four courses in 28.1% (9/32) with goshajinkigan versus 51.5% (17/33) of controls (protocol-specified unstratified log-rank P=.013; HR 0.34, 90% CI 0.16–0.72), but the stratified analysis was attenuated (HR 0.48, 90% CI 0.22–1.02; P=.101), and the authors describe a phase II signal needing a double-blind, placebo-controlled phase III trial (Tanaka 2026, PMID 42750137). “Not established” therefore stands.

Targeted PubMed searches on 2026-08-30 and 2026-09-30 identified ongoing confirmatory prevention research rather than a new established standard. PROSPER is a randomized, double-blind phase III protocol testing lecithinized superoxide dismutase during mFOLFOX6; it reports design and endpoints, not efficacy results (Yamazaki 2026, PMID 42583153). The dated evidence gap is therefore a lack of completed confirmatory evidence sufficient to replace the ASCO conclusion, not an absence of prevention trials.

POLAR used each participant's untreated hand as control during taxane therapy. Grade ≥2 sensory CIPN occurred in 29% of cooled versus 50% of control hands (absolute difference 21.15%, 95% CI 5.98–35.55) and 24% of compressed versus 38% of control hands (difference 14.29%, 2.02–27.24) (Michel 2025, PMID 40048176). The within-person design strengthens local comparison but cannot show whole-body functional benefit, and 21/122 randomized participants withdrew.

This creates a genuine guideline lag/replication question. ASCO's 2020 conclusion of no established preventive intervention predates POLAR; a single-center, hand-level taxane trial does not automatically justify a universal recommendation across agents, limbs or cooling/compression protocols.

CryoPac, a between-person randomized trial of frozen gloves and socks during every taxane infusion versus usual care, did not meet its primary endpoint. Of 268 randomized, 217 were analyzed (123 cryotherapy, 94 usual care); CIPN at end of treatment (Total Neuropathy Score ≥2) occurred in 74% (91/123) versus 84% (79/94), P=.071, and CTCAE grade ≥2 CIPN did not differ (P=.2). Cryotherapy reduced patient-reported hand tingling and numbness, foot numbness and difficulty manipulating small objects on QLQ-CIPN20 subscales and reduced monofilament-detected tactile disturbance; it did not change dose modifications, and compliance was 67% (Lendorf 2026, PMID 42838271). Two cautions travel with the result: 51 of 268 randomized participants were excluded from analysis and the analyzed groups are unequal after 1:1 randomization (123 versus 94), which implies more exclusions from usual care, although the abstract does not give per-arm randomized numbers; and the subscale benefits are secondary endpoints. The trial's registry record (NCT05928429) still read “recruiting”, last updated 2023-07-03, when re-fetched on 2026-10-21. The full text was not accessible (subscription), so these figures are from the abstract. POLAR (positive, within-person, hand-level) and CryoPac (null primary, between-person, whole-limb TNS) therefore answer different questions; neither shows durable functional prevention.

A 2026 network meta-analysis of 25 RCTs (1,625 patients) found that no glutathione-related agent reduced all-grade CIPN versus placebo; N-acetylcysteine (OR 0.19, 95% CrI 0.05–0.63), glutathione (0.34, 0.13–0.79) and vitamin E (0.33, 0.11–0.91) were associated with less grade 3/4 CIPN, but these associations were not retained when analysis was restricted to double-blind studies, and the authors call them preliminary (Geum 2026, PMID 42876024).

Pain treatment

Duloxetine has the strongest CIPN-specific evidence from a 231-person randomized crossover trial (Smith 2013, PMID 23549581). Systematic review describes benefit as modest and the comparable trial base as small (Chow 2023, PMID 36194493).

A three-arm double-blind trial in Iran (141 randomized; duloxetine to 60 mg/day, venlafaxine to 75 mg/day, or placebo; registered IRCT20240314061286N1) found no between-group difference in pain at its week-6 primary endpoint (P=0.59). A between-group difference appeared at week 12 (P=0.03), attributed post hoc to duloxetine versus placebo; venlafaxine improved within-group but did not separate from placebo (Shahini 2026, PMID 42866777). This does not displace the duloxetine evidence above, but it is another trial in which the prespecified primary endpoint was missed and benefit emerged only at a secondary time point.

Rehabilitation

Exercise meta-analysis suggests benefit but interventions and measures vary (Guo 2023, PMID 35149899). Gait, balance, dexterity, footwear and work adaptations matter even without analgesia (Zhang 2021, PMID 34607709).

In a secondary analysis of a phase III exercise trial (N=355), a six-week walking/resistance program changed hot/cold symptoms by −0.46 points versus control (P=0.045) and numbness/tingling by −0.42 points (P=0.061) on 0–10 scales (Kleckner 2018, PMID 29243164). The small effects, secondary endpoint status and predominantly female breast-cancer sample limit claims of established analgesic efficacy, but support testing function-focused programs.

Patient experience and survivorship

A qualitative synthesis pooled five US studies/88 participants and identified four themes: CIPN as an unclear experience, a risk deprioritized against cancer, impaired quality of life, and a persistent feature of survivorship (Tanay 2017, PMID 26786536). A later 15-interview study found difficulty processing risk information, dependence on trust during treatment decisions, barriers to symptom reporting and challenges self-managing symptoms (Tanay 2019, PMID 30790382).

These studies do not estimate prevalence. They show why surveillance can fail: patients may normalize symptoms, fear dose reduction, or receive information when cancer-related cognitive load is high. Prospective trials should measure comprehension, time-to-report and concordance between patient report and clinician grading.

Benefit–harm controversy

CIPN prevention is inseparable from cancer control. A neuroprotective intervention must not reduce chemotherapy delivery or tumor efficacy; conversely, preserving planned dose at the cost of irreversible neurologic disability is not automatically patient-centered. Trials should report both delivered relative dose intensity and long-term neurologic function.

Dose modification

Delay, reduction, substitution or cessation balances expected cancer control against neurologic injury. Analgesia must not mask progressive toxicity (Loprinzi 2020, PMID 32663120).

In an Australian multisite cross-sectional study of 901 people assessed a median 12 months after neurotoxic treatment, 37% had clinical grade ≥2 CIPN and 31% had required dose modification because of CIPN; female sex was associated with dose-limiting CIPN (OR 1.7, 95% CI 1.2–2.5), while patient-reported neuropathy after treatment was associated with older age and diabetes (Li 2026, PMID 42814908; abstract only, full text not accessible).

For oxaliplatin, planned limitation of exposure has the most direct cancer-outcome evidence. A meta-analysis of 24 studies (15 randomized, 9 retrospective; 30,395 patients) found reduced oxaliplatin exposure was not associated with worse disease-free survival in adjuvant colorectal cancer (HR 1.06, 95% CI 0.97–1.17) or with worse progression-free or overall survival in metastatic colorectal or gastroesophageal cancer, while it reduced grade 2 (OR 0.46, 0.25–0.84) and grade ≥3 CIPN (OR 0.34, 0.21–0.57) (Schwengber 2026, PMID 42801795). Absence of a statistically significant survival difference is not proof of equivalence, and the pooled set mixes randomized and retrospective designs; neither neuropathic pain nor long-term neuropathy was a reported endpoint.

Trial matrix

Failure mode Required correction
Pool all drugs Agent-specific strata
No baseline exam Pretreatment phenotype
Clinician grade only Patient report plus objective measure
Acute endpoint ≥6-month follow-up
Pain/numbness combined Separate domains
Completers only Count dose reduction/cessation

Evidence interpretation map

The table makes the evidence role and inferential boundary explicit; it is not a replacement for the full reports.

PMID Year Evidence role What it cannot establish alone
25261162 2014 Time-stratified prevalence meta-analysis Painful-CIPN prevalence specifically
42713463 2026 Chronic-CIPN (≥3 months after completion) prevalence meta-analysis, 197 studies Painful-CIPN prevalence; a precise estimate (I²=99%, very low certainty)
42750137 2026 Open-label randomized phase II goshajinkigan prevention trial Blinded, confirmed preventive efficacy
23549581 2013 Duloxetine randomized crossover trial Prevention or disease modification
40048176 2025 Cooling/compression randomized hand-level trial Universal prevention across agents/limbs
42838271 2026 CryoPac between-person cryotherapy RCT; primary endpoint not met Absence of benefit (unequal analyzed groups; 67% compliance; end-of-treatment endpoint)
42876024 2026 Glutathione/booster network meta-analysis Any preventive effect under double-blind conditions
42801795 2026 Reduced-oxaliplatin-exposure meta-analysis Survival equivalence; effect on painful or long-term CIPN
42814908 2026 901-person cross-sectional CIPN risk-factor study Causal or prospective prediction
42873277 2026 Exploratory pNF-H biomarker cohort (n=30) That axonal markers are uninformative for other agents or outcomes
42866777 2026 Duloxetine/venlafaxine/placebo RCT; primary endpoint not met Confirmed week-12 benefit (secondary, post hoc)
29243164 2018 Exercise RCT secondary analysis Definitive CIPN treatment efficacy
26786536 2017 Qualitative thematic synthesis Theme prevalence or causal burden

Minimum reporting controls

Domain Required report
Case definition Possible, probable or definite neuropathic pain
Etiology Lesion/disease and diagnostic evidence
Distribution Focal, length-dependent, dermatomal, at-level or below-level
Baseline phenotype Negative and positive sensory signs
Comparator Placebo/sham, active care or natural history
Exposure Dose, duration, adherence and co-interventions
Benefit Mean change plus ≥30% and ≥50% responders where applicable
Function Sleep, mobility, participation and patient global change
Harm Adverse events, withdrawals and serious events
Durability Follow-up after treatment and attrition
Subgroups Prespecified interaction test, not within-group significance
Missingness Denominator and imputation method

Reporting cautions

  • Do not infer lesion presence from a symptom descriptor.
  • Do not convert a group-average association into an individual diagnostic rule.
  • Do not treat statistical significance as clinically important benefit.
  • Do not compare NNTs without checking outcome threshold, duration and population.
  • Do not interpret an inactive or completed registry record as proof of efficacy.
  • Do not merge painful and painless neuropathy outcomes.
  • Do not omit adverse-event withdrawals from responder interpretation.
  • Do not call a post hoc subgroup predictive without an interaction test.
  • Do not generalize a focal peripheral result to central neuropathic pain.
  • State when evidence is short-term, indirect or restricted to a selected cohort.

Open questions

  • OQ-1: Which baseline phenotype predicts persistence?
  • OQ-2: Can agent-specific biomarkers guide cumulative dose?
  • OQ-3: Does standardized cryotherapy prevent durable neuropathy?
  • OQ-4: Which rehabilitation program reduces falls?

References

  1. Seretny M, Currie GL, Sena ES, et al.. Incidence, prevalence, and predictors of chemotherapy-induced peripheral neuropathy: A systematic review and meta-analysis. Pain. 2014;155:2461-2470. PMID 25261162
  2. Loprinzi CL, Lacchetti C, Bleeker J, et al.. Prevention and Management of Chemotherapy-Induced Peripheral Neuropathy in Survivors of Adult Cancers: ASCO Guideline Update. J Clin Oncol. 2020;38:3325-3348. PMID 32663120
  3. Staff NP, Grisold A, Grisold W, et al.. Chemotherapy-induced peripheral neuropathy: A current review. Ann Neurol. 2017;81:772-781. PMID 28486769
  4. Colvin LA. Chemotherapy-induced peripheral neuropathy: where are we now? Pain. 2019;160 Suppl 1:S1-S10. PMID 31008843
  5. Hershman DL, Lacchetti C, Dworkin RH, et al.. Prevention and management of chemotherapy-induced peripheral neuropathy in survivors of adult cancers: American Society of Clinical Oncology clinical practice guideline. J Clin Oncol. 2014;32:1941-67. PMID 24733808
  6. Tai HY, Lin LY, Huang TW, et al.. Efficacy of cryotherapy in the prevention of chemotherapy-induced peripheral neuropathy: A systematic review and meta-analysis. Support Care Cancer. 2024;32:482. PMID 38955817
  7. Kuriyama A, Endo K. Goshajinkigan for prevention of chemotherapy-induced peripheral neuropathy: a systematic review and meta-analysis. Support Care Cancer. 2018;26:1051-1059. PMID 29280005
  8. Smith EM, Pang H, Cirrincione C, et al.. Effect of duloxetine on pain, function, and quality of life among patients with chemotherapy-induced painful peripheral neuropathy: a randomized clinical trial. JAMA. 2013;309:1359-67. PMID 23549581
  9. Chow R, Novosel M, So OW, et al.. Duloxetine for prevention and treatment of chemotherapy-induced peripheral neuropathy (CIPN): systematic review and meta-analysis. BMJ Support Palliat Care. 2023;13:27-34. PMID 36194493
  10. Guo S, Han W, Wang P, et al.. Effects of exercise on chemotherapy-induced peripheral neuropathy in cancer patients: a systematic review and meta-analysis. J Cancer Surviv. 2023;17:318-331. PMID 35149899
  11. Zhang S. Chemotherapy-induced peripheral neuropathy and rehabilitation: A review. Semin Oncol. 2021;48:193-207. PMID 34607709
  12. Andersen NE, Boehmerle W, Huehnchen P, et al.. Neurofilament light chain as a biomarker of chemotherapy-induced peripheral neuropathy. Trends Pharmacol Sci. 2024;45:872-879. PMID 39242335
  13. Zajączkowska R, Kocot-Kępska M, Leppert W, et al.. Mechanisms of Chemotherapy-Induced Peripheral Neuropathy. Int J Mol Sci. 2019;20. PMID 30909387
  14. Starobova H, Vetter I. Pathophysiology of Chemotherapy-Induced Peripheral Neuropathy. Front Mol Neurosci. 2017;10:174. PMID 28620280
  15. D'Souza RS, Alvarez GAM, Dombovy-Johnson M, et al.. Evidence-Based Treatment of Pain in Chemotherapy-Induced Peripheral Neuropathy. Curr Pain Headache Rep. 2023;27:99-116. PMID 37058254
  16. Lyman GH, Greenlee H, Bohlke K, et al.. Integrative Therapies During and After Breast Cancer Treatment: ASCO Endorsement of the SIO Clinical Practice Guideline. J Clin Oncol. 2018;36:2647-2655. PMID 29889605
  17. Harris SR, Schmitz KH, Campbell KL, et al.. Clinical practice guidelines for breast cancer rehabilitation: syntheses of guideline recommendations and qualitative appraisals. Cancer. 2012;118:2312-24. PMID 22488705
  18. Farquhar-Smith P. Chemotherapy-induced neuropathic pain. Curr Opin Support Palliat Care. 2011;5:1-7. PMID 21192267
  19. Strand N, Wie C, Peck J, et al.. Small Fiber Neuropathy. Curr Pain Headache Rep. 2022;26:429-438. PMID 35384587
  20. Knezevic NN, Jovanovic F, Candido KD, et al.. Oral pharmacotherapeutics for the management of peripheral neuropathic pain conditions - a review of clinical trials. Expert Opin Pharmacother. 2020;21:2231-2248. PMID 32772737
  21. Finnerup NB, Attal N, Haroutounian S, et al.. Pharmacotherapy for neuropathic pain in adults: a systematic review and meta-analysis. Lancet Neurol. 2015;14:162-73. PMID 25575710
  22. Derry S, Bell RF, Straube S, et al.. Pregabalin for neuropathic pain in adults. Cochrane Database Syst Rev. 2019;1:CD007076. PMID 30673120
  23. Bäckryd E, Ghafouri N, Gerdle B, et al.. Rehabilitation interventions for neuropathic pain: a systematic review and meta-analysis of randomized controlled trials. J Rehabil Med. 2024;56:jrm40188. PMID 39101676
  24. Zhang YH, Hu HY, Xiong YC, et al.. Exercise for Neuropathic Pain: A Systematic Review and Expert Consensus. Front Med (Lausanne). 2021;8:756940. PMID 34901069
  25. Burgess J, Ferdousi M, Gosal D, et al.. Chemotherapy-Induced Peripheral Neuropathy: Epidemiology, Pathomechanisms and Treatment. Oncol Ther. 2021;9:385-450. PMID 34655433
  26. Bae EH, Greenwald MK, Schwartz AG. Chemotherapy-Induced Peripheral Neuropathy: Mechanisms and Therapeutic Avenues. Neurotherapeutics. 2021;18:2384-2396. PMID 34676514
  27. Kleckner IR, Kamen C, Gewandter JS, et al. Effects of exercise during chemotherapy on chemotherapy-induced peripheral neuropathy: a multicenter, randomized controlled trial. Support Care Cancer. 2018;26:1019-1028. PMID 29243164
  28. Michel LL, Schwarz D, Romar P, et al. Efficacy of Hand Cooling and Compression in Preventing Taxane-Induced Neuropathy: The POLAR Randomized Clinical Trial. JAMA Oncol. 2025;11:408-415. PMID 40048176
  29. Schneider BP, Hershman DL, Loprinzi C. Symptoms: Chemotherapy-Induced Peripheral Neuropathy. Adv Exp Med Biol. 2015;862:77-87. PMID 26059930
  30. Tanay MAL, Armes J, Ream E. The experience of chemotherapy-induced peripheral neuropathy in adult cancer patients: a qualitative thematic synthesis. Eur J Cancer Care (Engl). 2017;26. PMID 26786536
  31. Tanay MA, Armes J. Lived experiences and support needs of women who developed chemotherapy-induced peripheral neuropathy following treatment for breast and ovarian cancer. Eur J Cancer Care (Engl). 2019;28:e13011. PMID 30790382
  32. Yamazaki K, Kato T, Yamada T, et al. PROSPER: a phase III trial of lecithinized superoxide dismutase to prevent oxaliplatin-induced peripheral neuropathy in patients with colorectal cancer. ESMO Gastrointest Oncol. 2026;13:100353. PMID 42583153
  33. D'Souza RS, Whitfield S, Hussain N, et al. Prevalence and Study-Level Predictors of Chronic Chemotherapy-Induced Peripheral Neuropathy: A Systematic Review and Meta-Analysis. J Pain Res. 2026;19:643363. PMID 42713463
  34. Tanaka T, Makimoto G, Nakamura N, et al. Preventive effect of goshajinkigan on paclitaxel-induced peripheral neuropathy: an open-label, randomized phase II study (OLCSG2101). Oncologist. 2026;31(10):oyag352. PMID 42750137
  35. Lendorf ME, Bille MB, Krog SM, et al. Efficacy of Cryotherapy in Preventing Taxane-Induced Neuropathy: The CryoPac Randomised Controlled Trial. Ann Oncol. 2026. doi:10.1016/j.annonc.2026.09.014. PMID 42838271
  36. Geum MJ, Jeon J, Moon J, et al. Evidence on Glutathione and Boosters for Prevention of Chemotherapy-Induced Neuropathy: A Systematic Review and Network Meta-Analysis. Basic Clin Pharmacol Toxicol. 2026;139:e70319. PMID 42876024
  37. Shahini N, Lashkarbolouk N, Khaki S, et al. Evaluation of the efficacy of duloxetine and venlafaxine in chemotherapy-induced neuropathy in cancer patients: a double-blind multicenter randomized clinical trial. Ann Med Surg (Lond). 2026;88:6262-6271. PMID 42866777
  38. Li T, Timmins HC, Horvath LG, et al. Multifactorial Contributors to Dose Limiting and Post-Treatment Neurologic Toxicity During Chemotherapy Treatment. Neurology. 2026;107:e218599. PMID 42814908
  39. Schwengber WK, Jamal F, da Silva LFL, et al. Reduced oxaliplatin exposure in gastrointestinal cancers: A systematic review and meta-analysis. Cancer Treat Rev. 2026;150:103215. PMID 42801795
  40. Motoo Y, Shinozaki K, Miura M, et al. Longitudinal plasma phosphorylated neurofilament-heavy chain levels in oxaliplatin-induced peripheral neuropathy: a prospective multi-institutional exploratory study. Cancer Chemother Pharmacol. 2026;96. PMID 42873277