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. 2025 Sep 1;52(5):323–329. doi: 10.1188/25.ONF.323-329

Association Between the CEP72 Genotype and Chemotherapy-Induced Peripheral Neuropathy Severity in Young Adults Receiving Vincristine or Paclitaxel

Robert Knoerl 1,✉, Emanuele Mazzola 1, Maria F Pazyra-Murphy 1, Lindsay Frazier 1, Roy Freeman 1, Marilyn J Hammer 1, Ann S LaCasce 1, Jennifer Ligibel 1, Marlise R Luskin 1, Donna L Berry 1, Rosalind A Segal 1
PMCID: PMC12377867  PMID: 40849922

Abstract

OBJECTIVES

To determine the relationship between chemotherapy-induced peripheral neuropathy (CIPN) severity and centrosomal protein 72 (CEP72) genotype in young adults receiving paclitaxel or vincristine.

SAMPLE & SETTING

50 young adults aged 21–39 years who were expected to receive a cumulative dose of at least 7 mg vincristine or 700 mg/m2 paclitaxel for the treatment of cancer were recruited from Dana-Farber Cancer Institute.

METHODS & VARIABLES

Participants completed a CIPN assessment tool and provided a blood sample before the first infusion. Participants completed the assessment tool at two additional time points. DNA was genotyped for CEP72 rs924607. CIPN scores were compared between those with the TT versus the CC or CT genotype over time using linear mixed-effects models.

RESULTS

Young adults receiving vincristine with the TT CEP72 genotype experienced higher CIPN severity by the final time point, but the differences were not statistically significant (p > 0.05).

IMPLICATIONS FOR NURSING

Future work to validate biomarkers like CEP72 may allow clinicians to identify patients who may benefit from altered chemotherapy dosages relative to CIPN risk.

Keywords: young adult, neoplasms, genotype, CEP72, chemotherapy-induced peripheral neuropathy

The development of chemotherapy-induced peripheral neuropathy (CIPN) (i.e., numbness, tingling, or pain in the hands or feet) during neurotoxic chemotherapy negatively affects chemotherapy dosing and physical function (Timmins et al., 2021). Adolescents and young adults (AYAs) aged 15–39 years frequently receive taxanes (e.g., paclitaxel for breast cancer) or vinca alkaloids (e.g., vincristine for leukemia) for the treatment of cancer. Preliminary data suggest that AYAs may experience higher rates of moderate to severe CIPN than older adults during neurotoxic chemotherapy treatment (Knoerl et al., 2022).

Because little evidence supports most treatments for CIPN prevention or management, the American Society of Clinical Oncology recommends that clinicians assess the appropriateness of neurotoxic chemotherapy dose reduction or delay for patients experiencing severe CIPN (Loprinzi et al., 2020). Inherited allelic variation of pharmacogenes associated with CIPN may be useful in identifying AYAs who may benefit from reduced neurotoxic chemotherapy dosages. In particular, investigation into the predictive value of single-nucleotide polymorphisms within the promoter region (i.e., rs924607) of centrosomal protein 72 (CEP72) (Whirl-Carrillo et al., 2021), a gene that encodes proteins essential for microtubule formation (Diouf et al., 2015), is warranted because a key pathophysiologic mechanism of both vincristine- and paclitaxel-induced neuropathy is microtubule interference (Fukuda et al., 2017). A case-control study (adult patients aged 17–76 years) (Stock et al., 2017) and a genome-wide association study (children aged 0.1–23.8 years) (Diouf et al., 2015) have shown that individuals with the TT (homozygous for the minor allele) CEP72 rs924607 genotype with acute lymphoblastic leukemia receiving vincristine experience increased CIPN in comparison to those with the CC (homozygous for the major allele) or CT (heterozygous) CEP72 genotype. Individuals expressing the CC or CT CEP72 genotype may experience less severe CIPN because microtubule function is preserved. A limitation of these studies was that CIPN severity was measured using the National Cancer Institute Common Terminology Criteria for Adverse Events (CTCAE), a measure with floor effects and low correlations with patient-reported CIPN measures (Lavoie Smith et al., 2013). In addition, fewer data are available about the association between CEP72 genotype and paclitaxel-induced peripheral neuropathy. One prospective study found no significant relationship between CEP72 status and patient- or clinician-reported neuropathy among 424 women with epithelial ovarian cancer receiving paclitaxel and carboplatin (Park et al., 2017).

The purpose of this secondary analysis was to explore the association between CEP72 genotype and patient-reported CIPN severity in AYAs receiving vincristine or paclitaxel. It was hypothesized that AYAs with the high-risk CEP72 genotype (i.e., TT at rs924607) would report worse CIPN severity in comparison to AYAs with the CC or CT CEP72 genotype as neurotoxic chemotherapy dose increased.

Methods

Design, Sample, and Setting

This analysis was a secondary aim of a single-arm prospective clinical study that measured CIPN severity among AYAs receiving vincristine or paclitaxel at three time points during treatment (Knoerl et al., 2024). This aim was guided by the theory of unpleasant symptoms (Lenz et al., 1997); it investigated the association between CEP72 genotype (e.g., a physiologic influencing factor) and patient-reported CIPN severity (e.g., a symptom) in AYAs receiving vincristine or paclitaxel. To summarize the eligibility criteria, researchers recruited AYAs aged 15–39 years who were expected to receive a cumulative dose of at least 7 mg vincristine for the treatment of hematologic malignancies or a cumulative dose of at least 700 mg/m2 paclitaxel for the treatment of breast cancer from Dana-Farber Cancer Institute in Boston, Massachusetts. Participants were excluded from participation if they planned to receive other neurotoxic agents besides paclitaxel or vincristine or had neuropathy from other causes. Verbal consent was obtained from all participants for all procedures associated with the primary and secondary aims of the study because of the COVID-19 pandemic. The study was regulated by the Dana-Farber/Harvard Cancer Center Office for Human Research Studies (19-862).

Measures

CIPN severity was measured using the subscales of the European Organisation for Research and Treatment of Cancer (EORTC) Quality-of-Life Questionnaire–CIPN 20-Item (QLQ-CIPN20) measure. The sensory subscale focuses on sensations like numbness, tingling, or pain in the hands or feet, and the motor subscale focuses on deficits like peripheral weakness or cramping. Each subscale is scored from 0 to 100, with higher scores indicating worse CIPN severity (Postma et al., 2005). The EORTC QLQ-CIPN20 has demonstrated strong reliability and validity (Lavoie Smith et al., 2013) and was recommended by the National Cancer Institute Clinical Trials Planning Meeting for Prevention and Treatment of CIPN to quantify CIPN in research (Dorsey et al., 2019). The authors obtained permission from the EORTC to use the QLQ-CIPN20 in this study. In addition to CIPN, participants self-reported demographic information at baseline, and study staff abstracted cancer treatment–related information at the end of the study.

To quantify CEP72 genotypes, genomic DNA was purified from frozen whole blood samples (less than 1 ml per sample) according to protocol. Samples were sequenced for the CEP72 promoter region (rs924607) according to protocol. Two probes (VIC phosphoramidite dye for allele C sequence and fluorescein amidite dye for allele T sequence) were used to detect the specific alleles of CEP72 rs924607. A mixture of sequence-specific primers, a genotyping master mix, and deoxyribonuclease-free water was used to amplify DNA following a quantitative polymerase chain reaction protocol of 10 minutes at 95°C (polymerase activation), 40 cycles of 15 seconds at 95°C, and 40 cycles of 1 minute at 60°C. For each assay, two no-template controls (deoxyribonuclease-free water) were used to detect DNA contamination.

Procedures

Enrolled participants completed the EORTC QLQ-CIPN20 and provided a blood sample between the time of consent and the first paclitaxel or vincristine infusion (T1). Participants completed the EORTC QLQ-CIPN20 at two additional time points during vincristine (T2: 3–5 mg; T3: 7–9 mg) or paclitaxel (T2: 350–450 mg/m2; T3: 700–900 mg/m2) treatment.

Statistical Analysis

Prior results suggested that about 16% of participants would express the TT CEP72 rs924607 genotype (Diouf et al., 2015). Assuming a similar prevalence, researchers estimated that about 8 of 50 participants would express the TT CEP72 genotype. With this sample configuration, the study had 80% power (one-sided significance level of 0.05) to detect an effect size of 0.98 in EORTC QLQ-CIPN20 sensory and motor subscale score changes between participants with the TT versus the CC or CT CEP72 genotype. Assuming an SD of 22 for the EORTC QLQ-CIPN20 sensory subscale score and 19.9 for the EORTC QLQ-CIPN20 motor subscale score (Lavoie Smith et al., 2013), researchers estimated that the EORTC QLQ-CIPN20 sensory subscale scores would be 21.8 units higher in participants with the TT CEP72 genotype, and EORTC QLQ-CIPN20 motor subscale scores would be 19.4 units higher in participants with the TT CEP72 genotype.

R, version 4.0, was used to conduct the analyses. The frequency of CEP72 genotype at T1 was described. EORTC QLQ-CIPN20 sensory and motor subscale scores were modeled using linear mixed-effects models (i.e., accounting for the repeated measurements on each patient) with genotype and time as covariates and including an interaction term addressing the effect of genotype over time. The same analyses were repeated among participants receiving paclitaxel and vincristine.

Results

Sample Characteristics

The demographic characteristics have been previously reported (Knoerl et al., 2024). Overall, participants in this secondary analysis (N = 50) were aged a median of 35 years (range = 21–39) and were mainly White (n = 40), female (n = 44), and diagnosed with breast cancer (n = 39) or lymphoma (n = 9). At T3, the median cumulative paclitaxel (n = 39) or vincristine (n = 11) dose received was 700 mg/m2 and 8 mg, respectively.

Association Between CEP72 Genotype and CIPN Severity

Overall, 10 participants had the TT CEP72 rs924607 genotype, 19 had the CC genotype, and 21 had the CT genotype. Among the entire sample (see Figure 1), there were no statistically significant differences in sensory (p = 0.83) or motor (p = 0.8) EORTC QLQ-CIPN20 subscale scores between participants with the CC or CT and the TT CEP72 genotype over time (p = 0.95). For participants receiving vincristine, a greater proportion of participants with the TT CEP72 genotype (n = 3) experienced worse sensory (p = 0.09) and motor (p = 0.3) CIPN severity from T1 to T3 compared to participants with the CC or CT genotype (n = 8), but these differences were not statistically significant. For participants receiving paclitaxel, a greater proportion of participants with the CC or CT CEP72 genotype (n = 32) experienced worse sensory (p = 0.48) and motor (p = 0.66) CIPN severity from T1 to T3 compared to participants with the TT genotype (n = 7), but these differences were not statistically significant (see Table 1).

FIGURE 1.

FIGURE 1

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Mean EORTC QLQ-CIPN20 Sensory and Motor Subscale Scores by CEP72 Genotype (N = 50)

CEP72—centrosomal protein 72; CIPN—chemotherapy-induced peripheral neuropathy; EORTC QLQ-CIPN20—European Organisation for Research and Treatment of Cancer Quality-of-Life Questionnaire–Chemotherapy-Induced Peripheral Neuropathy 20-Item; T—time point

Note. EORTC QLQ-CIPN20 subscales are scored from 0 to 100, with higher scores indicating worse sensory or motor CIPN severity.

Note. CEP72 genotypes are as follows: CC is homozygous for the major allele, CT is heterozygous (n = 40 for CC/CT), and TT is homozygous for the minor allele (n = 10 for TT).

TABLE 1.

Mean EORTC QLQ-CIPN20 Sensory and Motor Subscale Scores by CEP72 Genotype for Young Adults Receiving Paclitaxel or Vincristine (N = 50)

Measure Paclitaxel Treated Vincristine Treated
CC or CT (N = 32) TT (N = 7) CC or CT (N = 8) TT (N = 3)
X̄ SD X̄ SD X̄ SD X̄ SD
EORTC QLQ-CIPN20 Sensory Subscale
T1 2.66 9.37 2.12 4.2 1.39 2.76 – –
T2 10.88 15.31 4.32a 4.92 6.02 11.36 8.64 5.66
T3 7.99 11.29 3.7 4.78 5.09 5.92 16.05 14.97
EORTC QLQ-CIPN20 Motor Subscale
T1 2.49 9.64 – – 4.17 6.68 1.39 2.41
T2 9.97 20.75 1.39a 2.15 11.01 16.92 9.52 9.52
T3 6.68 12.16 1.79 3.28 9.33 10.7 15.68 12.26
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a

N = 6

CEP72—centrosomal protein 72; CIPN—chemotherapy-induced peripheral neuropathy; EORTC QLQ-CIPN20—European Organisation for Research and Treatment of Cancer Quality-of-Life Questionnaire–Chemotherapy-Induced Peripheral Neuropathy 20-Item; T—time point

Note. EORTC QLQ-CIPN20 subscales are scored from 0 to 100, with higher scores indicating worse sensory or motor CIPN severity. Dashes indicate scores of 0.

Note. T1 occurred at the first paclitaxel or vincristine infusion. For participants receiving vincristine, T2 occurred at 3–5 mg, and T3 occurred at 7–9 mg. For participants receiving paclitaxel, T2 occurred at 350–450 mg/m2, and T3 occurred at 700–900 mg/m2.

Note. CEP72 genotypes are as follows: CC is homozygous for the major allele, CT is heterozygous, and TT is homozygous for the minor allele.

Discussion

The results indicated that young adults with the TT CEP72 rs924607 genotype receiving vincristine to treat hematologic malignancies experienced higher sensory and/or motor CIPN severity compared to young adults with the CC or CT genotype over time, although the differences were not statistically significant. The trends observed are consistent with previous studies conducted in larger samples of participants receiving vincristine (Diouf et al., 2015; Stock et al., 2017). For example, results from a meta-analysis found that participants (n = 696) with the TT CEP72 genotype had a higher risk of developing vincristine-induced peripheral neuropathy compared to participants (n = 399) with the CC or CT genotype (odds ratio = 2.15) (Klumpers et al., 2022). Additional data suggest that women with the TT CEP72 genotype receiving vincristine for the treatment of aggressive B-cell lymphoma experienced significantly worse CIPN than women with the CC or CT genotype (p = 0.016) (Christofyllakis et al., 2024). Despite the small sample, the results of the current study build on the existing literature by providing data surrounding the relationship between the CEP72 genotype and patient-reported vincristine-induced peripheral neuropathy, whereas previous studies mainly used the CTCAE to quantify vincristine-induced peripheral neuropathy.

Consistent with prior reports, the TT CEP72 genotype was not predictive of worse CIPN severity among young adults receiving paclitaxel. In particular, prior data demonstrate no association between CIPN severity (measured using the EORTC QLQ–Ovarian Cancer module and the CTCAE) and CEP72 genotype among women receiving paclitaxel and carboplatin for the treatment of ovarian cancer (N = 454) (Park et al., 2017). It is unclear why findings from the current study and in the literature indicate that the TT CEP72 genotype leads to higher CIPN risk among patients receiving vincristine but not paclitaxel, despite both being microtubule-targeting chemotherapy agents (Fukuda et al., 2017). Prior reports (Park et al., 2017; Tamburin et al., 2019) have identified several potential barriers to the identification of genetic predictors of CIPN, including the lack of a gold standard CIPN assessment tool and small sample sizes. Alternatively, the literature suggests that a cluster of single-nucleotide polymorphisms may be associated with the development of taxane-induced neuropathy (Lustberg et al., 2023).

Limitations

The results of this secondary analysis are limited in that the sample size was likely smaller than necessary to detect statistically significant associations between CIPN severity and CEP72 genotype among participants receiving paclitaxel or vincristine. In addition, the potential impacts of confounders, such as age, sex, race and ethnicity, and comorbidities, were not accounted for in any of the analyses. Finally, the findings have low external generalizability because the sample consisted mainly of individuals with similar age (young adults), race (White), and sex (female) from one institution.

Implications for Nursing

Nurse scientists may use these findings to inform future research exploring inherited genetic variation of paclitaxel- or vincristine-induced peripheral neuropathy. In particular, because the results suggest that single-nucleotide polymorphisms within the promoter region of CEP72 may have different effects on vincristine-versus paclitaxel-induced peripheral neuropathy, future studies should also assess the impact of genomic biomarkers on CIPN caused by distinct neurotoxic agents and not pool the results across neurotoxic agents. In addition, the identification of such biomarkers will decrease the required sample size in future CIPN prevention clinical trials because nurse scientists will be able to recruit patients more likely to develop CIPN (Gewandter et al., 2018). Clinically, results of future research to explore genotype-based dosing of paclitaxel- or vincristine-induced peripheral neuropathy may allow nurses to identify AYAs who may benefit from reduced vincristine or paclitaxel dosages or require additional supportive care during treatment.

Conclusion

Using patient-reported CIPN measures, this secondary analysis indicated that young adults with the TT CEP72 rs924607 genotype receiving vincristine, but not those receiving paclitaxel, experienced a trend toward greater sensory and/or motor CIPN over time than young adults with the CC or CT CEP72 genotype. As well as additional studies to validate CEP72 genotype as a predictor of vincristine-induced peripheral neuropathy, further work is needed long term to optimize clinical workflows to support pharmacogenomics testing to be able to use clinically relevant biomarkers for CIPN risk stratification in practice.

KNOWLEDGE TRANSLATION.

  • ■ This is among the first studies to evaluate the impact of the centrosomal protein 72 (CEP72) genotype on the development of vincristine-induced peripheral neuropathy using patient-reported chemotherapy-induced peripheral neuropathy (CIPN) measures.

  • ■ Preliminary evidence suggests that young adults with the TT CEP72 rs924607 genotype receiving vincristine report worse sensory and motor CIPN than young adults with the CC or CT CEP72 genotype.

  • ■ Consistent with prior reports, the TT CEP72 genotype was not predictive of worse CIPN severity in young adults receiving paclitaxel.

QUESTION GUIDE FOR A JOURNAL CLUB.

Journal clubs can help to increase and translate findings to clinical practice, education, administration, and research. Use the following questions to start discussion at your next journal club meeting. Then, take time to recap the discussion and make plans to proceed with suggested strategies.

  1. How can biomarkers help manage chemotherapy-induced peripheral neuropathy severity in people receiving vincristine?

  2. What other symptoms would be helpful to manage using biomarkers?

  3. Should people who have a particular biomarker that may indicate more severe toxicity from certain drugs receive those drugs?

Visit https://bit.ly/3C7ar0z for details on creating and participating in a journal club. Contact pubONF@ons.org for assistance or feedback. Photocopying of the article for discussion purposes is permitted.

Funding Statement

This research was funded, in part, by a National Institute of Nursing Research award (K23NR018689; principal investigator: Knoerl).

Footnotes

The authors gratefully acknowledge Erica Fox, MEd, RN, Barbara Halpenny, MA, MSW, LCSW, and Anna Tanasijevic, MPH, for their assistance with participant screening and recruitment, data collection, and/or study management.

This research was funded, in part, by a National Institute of Nursing Research award (K23NR018689; principal investigator: Knoerl).

Knoerl, Frazier, Freeman, Ligibel, Luskin, Berry, and Segal contributed to the conceptualization and design. Knoerl, Pazyra-Murphy, Ligibel, and Luskin completed the data collection. Mazzola provided statistical support. Freeman and LaCasce provided the analysis. Knoerl, Frazier, Freeman, Hammer, LaCasce, Ligibel, Luskin, Berry, and Segal contributed to the manuscript preparation.

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