Erfolgreich durch internationale Zusammenarbeit

Oncology

Cite as: Archiv EuroMedica. 2026. 16; 4. DOI 10.35630/2026/16/Iss.4.21

Received 08 July 2026;
Accepted 11 August 2026;
Published 14 August 2026

CHEMOTHERAPY-INDUCED NAUSEA AND VOMITING: RISK STRATIFICATION, CURRENT MANAGEMENT, AND ADJUNCTIVE THERAPIES - NARRATIVE REVIEW

Filip Chodań¹ , Dagmara Laufer¹ ,
Olga Klimczak¹ , Estera Sośniecka¹ ,
Adam Miler¹ , Krystian Domeracki¹

¹ Faculty of Medicine, Medical University of Silesia, Katowice, Poland

download article (pdf)

  filip.ch3@wp.pl

ABSTRACT

Background

Chemotherapy induced nausea and vomiting remain among the most common adverse effects of anticancer treatment, affecting up to 80% of patients. Despite effective antiemetic prophylaxis, complete symptom control is not consistently achieved, particularly for nausea and delayed CINV. These symptoms impair quality of life and may negatively affect treatment adherence.

Aim

This narrative review aims to present the risk factors for CINV and discuss current preventive and therapeutic strategies, with particular emphasis on pharmacological optimization and adjunctive approaches.

Materials and Methods

A narrative literature review was conducted using PubMed and Google Scholar. The primary search included English language publications on CINV published between 20 April 2016 and 20 April 2026. Earlier key publications were included when they provided relevant information on pathogenesis, risk factors, or therapeutic strategies. A total of 46 publications were included.

Results

The risk of CINV is influenced by patient related and treatment related factors, supporting individualized risk assessment and preventive strategies. Current guidelines recommend antiemetic regimens according to the emetogenic potential of chemotherapy. Studies of reduced dose olanzapine and alternative agents such as mirtazapine suggest that selected strategies may improve tolerability in specific patient groups. Dietary and non-pharmacological interventions have also been evaluated, but their results remain inconsistent.

Conclusions

Management of CINV should combine assessment of individual risk with guideline based pharmacological prophylaxis. Selected dose modifications, alternative agents, and adjunctive interventions may be considered in appropriate patients, but further comparative studies are required before these approaches can be routinely recommended.

Keywords: chemotherapy-induced nausea and vomiting, pathogenesis, risk factors, guidelines, treatment optimization, non-pharmacological management

INTRODUCTION

Chemotherapy remains one of the most widely used modalities in the treatment of malignant neoplasms. Despite advances and supportive care chemotherapy-induced nausea and vomiting (CINV) continues to affect up to 80% of patients. The majority of patients undergoing chemotherapy experience adverse effects, the most prevalent of which is fatigue, followed by nausea and vomiting, as well as pain [1]. CINV contributes to a deterioration in patients’ quality of life, reduced nutritional intake, and an increased risk of malnutrition, which may lead to metabolic and fluid - electrolyte imbalances, impaired immune function and wound healing, and, in severe cases, esophageal rupture [1]. CINV is classified into six subtypes: acute, delayed, breakthrough, anticipatory, refractory, and extended delayed [2,3]. Acute symptoms occur within the first 24 hours after chemotherapy, while delayed CINV develops between 24 and 120 hours and may persist for several days. Breakthrough CINV refers to nausea and vomiting occurring within five days after chemotherapy despite the use of prophylactic antiemetic therapy and requiring rescue treatment [4,5].

Anticipatory CINV is triggered by previous negative experiences with anticancer treatment, occurring prior to the next cycle of chemotherapy [6]. Refractory CINV occurs despite adherence to guideline-recommended antiemetic prophylaxis and appropriate management of breakthrough episodes in previous treatment cycles [4]. Recently, extended delayed CINV - defined as symptoms occurring more than 120 hours after chemotherapy administration - has also been recognized [7]. The pathophysiology of CINV involves complex interactions between the gastrointestinal tract and the central and autonomic nervous systems. These mechanisms are summarized in Figure 1. In clinical practice, vomiting and nausea are often treated as concomitant conditions; however, the pathomechanism underlying nausea is not entirely identical to that of vomiting and remains less well understood [8]. Acute CINV is associated with the peripheral pathway, whereas delayed CINV is associated with the central pathway [9]. The peripheral pathway is linked to the gastrointestinal tract and the receptors located within it, including serotonin type 3 (5-HT3) and type 4 (5-HT4) receptors, dopamine (D2) receptors, and enterochromaffin cells that release serotonin and substance P [10]. The signal is transmitted via afferent vagus nerve fibers to the VC with the 5-HT3 receptor serving as the primary mediator [9]. The central pathway involves direct stimulation of the NTC in response to signals from the CTZ, the vestibular apparatus, or cortical centers [11]. As shown in Figure 1 the CTZ is located outside the blood-brain barrier; its chemoreceptors are activated by emetogenic substances such as cytostatics and other medications [9,12]. The main mediator of the central pathway is the substance P that binds to the NK-1 receptor [8].

Despite the availability of guideline based antiemetic prophylaxis, chemotherapy induced nausea and vomiting remain inadequately controlled in a substantial proportion of patients, particularly during the delayed phase. Current recommendations are primarily based on the emetogenic potential of anticancer treatment, whereas individual patient related risk factors are not always incorporated into routine preventive strategies. In addition, evidence concerning dose optimization, alternative pharmacological agents, and adjunctive interventions remains heterogeneous and has not been consistently integrated into clinical practice. A focused synthesis linking individual risk stratification with current pharmacological and supportive management is therefore needed.

AIM

The aim of this narrative review is to evaluate the risk factors for chemotherapy induced nausea and vomiting and to summarize current preventive and therapeutic strategies, with particular attention to individualized risk assessment, optimization of antiemetic pharmacotherapy, and adjunctive interventions.

Research objectives

The objectives of this review are to identify patient related and treatment related risk factors for chemotherapy induced nausea and vomiting, describe current risk stratification approaches, summarize guideline recommended antiemetic regimens according to emetogenic risk and symptom phase, evaluate evidence concerning dose modifications and alternative pharmacological agents, and assess the potential role and limitations of selected dietary and nonpharmacological interventions.

MATERIALS AND METHODS

This study was designed as a narrative review. A literature search was conducted using the PubMed and Google Scholar databases. The primary search covered publications on chemotherapy induced nausea and vomiting published between 20 April 2016 and 20 April 2026. Earlier key publications were included additionally when they provided important information on pathogenesis, risk factors, or therapeutic strategies. The search strategy incorporated combinations of the following keywords: chemotherapy induced nausea and vomiting, pathogenesis, risk factors, prevention, guidelines, novel drugs, and non-pharmacological management.

Inclusion criteria were as follows:

1. Publications in English.
2. Randomized controlled trials, observational studies, meta analyses, systematic reviews, and narrative reviews related to CINV.
3. Studies addressing the pathogenesis, risk factors, prevention, and management of CINV, including pharmacological and adjunctive approaches.

Exclusion criteria were as follows:

1. Publications not directly related to CINV.
2. Conference abstracts and case reports.
3. Duplicate publications based on the same study population or dataset.

After assessment of their relevance to the topic of the review, 46 sources were included in the final analysis. The review was not conducted according to a formal systematic review protocol.

RESULTS

Risk factors and stratification

The risk of chemotherapy-induced nausea and vomiting (CINV) is determined by both patient-related factors and the characteristics of the administered anticancer therapy. Patient-related risk factors for CINV include poor performance status, younger age ( <60 years), female sex, low or no alcohol consumption, receipt of the first cycle of chemotherapy, and insufficient sleep prior to treatment (less than 7 hours). Additional factors include a history of hyperemesis gravidarum, motion sickness, prior CINV, anxiety, and electrolyte imbalances such as dehydration, hyperkalemia, hypocalcemia, and hyponatremia. Furthermore clinical conditions including ascites, bowel obstruction and the use of certain medications such as opioids and antibiotics, may further increase the risk. Factors with less consistently established significance include the anticipation of CINV and the use of selective serotonin reuptake inhibitors (SSRIs), such as fluoxetine and paroxetine [2–4]. Genetic determinants play a significant role in interindividual variability in susceptibility to CINV. These encompass genes involved in blood–brain barrier permeability (e.g., ABCB1), serotonin receptors genes targeted by 5-HT3 receptor antagonists (e.g., HTR3B, HTR3C, HTR3D), and genes involved in the metabolism of these agents (e.g., CYP2D6, ALDH2). Polymorphisms within these genes have been linked to an increased risk of CINV [13,14]. Emerging evidence suggests that chemotherapy-induced alterations in the gut microbiota may also play a significant role in the pathophysiology of CINV. These changes include a decrease in the number of commensal bacteria, such as Lactobacillus, Bifidobacterium, and Bacteroides, and an increase in the number of pathogenic bacteria, such as Clostridium cluster XI, Escherichia coli, and Staphylococcus spp., which may disrupt gut–brain axis signaling and contribute to symptom development [13].

As summarized in Table 1 anticancer agents are classified into four categories according to their emetogenic potential, These include agents with high (>90% incidence of vomiting), moderate (30–90%), low (10–30%), and minimal (<10%) risk of emesis.

Based on clinical factors, including patient characteristics, treatment-related variables, and a history of previous symptoms, several predictive models for CINV risk have been developed. Typically, these models integrate variables such as prior CINV episodes , age, sex, and the type of anticancer treatment using statistical methods, including logistic regression and risk scoring systems, to estimate individual risk [16].

Current management

Current treatment standards for CINV are based on guidelines from international organizations such as the American Society of Clinical Oncology (ASCO) and the Multinational Association of Supportive Care in Cancer/European Society of Medical Oncology (MASCC/ESMO). Currently, medical management is based on the use of 5-HT3 receptor antagonists (5-HT3 RAs), NK-1 receptor antagonists (NK-1 RAs), and corticosteroids—almost exclusively dexamethasone (DEX)—often in 3- or 4-drug combination regimens that include olanzapine (OLZ) [17,18].

A summary of recommended regimens according to emetogenic risk and CINV phase is presented in Table 2. When using chemotherapy with a high emetogenic potential, the following 4-drug regimen for the prophylaxis of acute CINV is recommended: NK1 RA + 5HT-3 RA + DEX + OLZ [17,19,20]. Recommendations for delayed-onset prophylaxis are less conclusive and vary depending on the chemotherapy regimen used: those involving anthracyclines and cyclophosphamide (AC) and those without them (Non-AC). In AC regimens, the use of olanzapine is recommended, whereas in Non-AC regimens, it is combined with dexamethasone [17,20]. When using cytostatic agents with moderate emetogenic potential, the 5-HT3 RA + DEX regimen is recommended during the acute phase, while for delayed nausea, the use of DEX or no routine prophylaxis is considered [17]. When dealing with chemotherapeutic agents carrying minimal risk, guidelines suggest refraining from routine antiemetic prophylaxis unless the patient has previously reported episodes of CINV. In patients who have experienced breakthrough CINV, guidelines recommend adding olanzapine to the standard regimen if it was not included in the initial prophylaxis [19,20]. Common side effects of antiemetic medications include headaches, constipation, and fatigue; in addition, dexamethasone, which is used in numerous treatment regimens, may cause insomnia, dyspepsia, agitation, and hyperglycemia particularly with prolonged use [21,22].

Optimization of antiemetic pharmacotherapy

Olanzapine is an atypical antipsychotic that acts as an antagonist at several receptors, including D2, 5-HT2c and 5-HT3. Despite its efficacy in preventing CINV symptoms, olanzapine at doses of 5 and 10 mg is associated with adverse effects such as daytime drowsiness, which may limit treatment tolerance. A phase III RCT (randomised clinical trial) compared the efficacy of a reduced (2.5 mg) and standard dose of olanzapine (10 mg) in the prophylaxis of CINV. The study included patients with solid tumours who had not previously received chemotherapy and were receiving treatment with a high emetogenic potential – doxorubicin and cyclophosphamide or cisplatin. No significant differences in treatment efficacy were observed between the study group receiving a 3-drug regimen (a 5-HT3 antagonist, dexamethasone and an NK1 antagonist) in combination with a reduced dose of olanzapine, and the control group receiving the same 3-drug regimen and a standard dose of olanzapine. However, significant differences were observed in the incidence of olanzapine-related adverse effects throughout the treatment period – as many as 90% of patients in the control group reported daytime sleepiness compared to 65% of patients in the study group [23]. Mirtazapine is an antidepressant. It acts as an antagonist at histamine and serotonin receptors, with minimal anticholinergic effects. Compared with olanzapine, mirtazapine may be associated with less severe sedation, while retaining an appetite stimulating effect [24,25]. The efficacy of mirtazapine in the secondary prevention of CINV was assessed in a phase III RCT. The study included women with breast cancer who had a history of delayed CINV and were undergoing highly emetogenic chemotherapy with epirubicin, cyclophosphamide or cisplatin. The addition of 15 mg of mirtazapine to standard antiemetic therapy was associated with a significantly higher response rate in the delayed phase compared to placebo – 78.3% vs 49%. A higher response rate was also observed in the group receiving mirtazapine in an analysis covering all phases of CINV. However, the use of mirtazapine was associated with a higher incidence of adverse effects such as drowsiness and weight gain compared to placebo – 17.4% vs 4.1%. Other adverse effects, including anorexia, fatigue and dyspepsia, occurred with similar frequency in both groups [24]. A. Maleki et al. conducted a phase III RCT designed to compare the therapeutic efficacy of olanzapine and mirtazapine in women with breast cancer receiving highly emetogenic chemotherapy based on doxorubicin and cyclophosphamide. No significant differences in the efficacy of CINV control were observed across all phases between mirtazapine (15 mg) and olanzapine (10 mg), when used in combination with standard antiemetic therapy. However, differences were observed in the adverse event profile regarding the severity of drowsiness. Drowsiness was more common in the olanzapine group, both in mild form (46.7% vs 26.7%) and in more severe form, which did not occur in the mirtazapine group. These results suggest that mirtazapine may potentially serve as an alternative to olanzapine, particularly in patients with limited tolerance to sedation [25]. The PantoCIN trial (a phase II RCT) evaluated the effect of pantoprazole on the control of CINV in patients receiving chemotherapy with moderate and high emetogenic potential. All patients received standard antiemetic prophylaxis. A higher proportion of patients were free from symptoms of delayed CINV in the pantoprazole group compared with the placebo group – 51.4% vs 39.3% [26]. Thalidomide was previously used to treat persistent nausea and vomiting in pregnant women; however, due to its documented teratogenic effects, it was withdrawn from this indication. Currently, due to its immunomodulatory and anti-angiogenic properties, it is used in oncology. The CLOG1302 trial (a phase III RCT) evaluated the efficacy of thalidomide as an adjunct to CINV prophylaxis in patients receiving chemotherapy with a high emetogenic potential. Thalidomide, administered twice daily at a dose of 100 mg in combination with standard antiemetic therapy, was associated with a higher delayed and overall response rate compared with placebo (76.9% vs 61.7% and 66.1% vs 53.3%). However, use of the drug was associated with a higher incidence of adverse effects, including sedation, dry mouth, dizziness and constipation [27].

Use of Zingiber officinale in the management of CINV

In recent years, there has been increasing interest in complementary approaches, including dietary strategies and plant-derived compounds. Among these, ginger (Zingiber officinale) is one of the most extensively studied agents, demonstrating potential anti-nausea and antiemetic effects alongside a favorable safety profile. Its activity is attributed to bioactive constituents such as shogaols and gingerols. Preclinical evidence indicates that these effects may be mediated through modulation of serotonergic pathways via inhibition of 5-HT3 receptors, as well as interactions with NK-1 and cholinergic receptors and effects on gastrointestinal motility [28–31]. A randomized controlled trial demonstrated that ginger supplementation significantly reduced the severity of acute nausea on the first day of chemotherapy compared with placebo, with the greatest benefit observed at doses of 0.5 g and 1.0 g [32]. Another RCT reported a reduction in delayed nausea accompanied by improvements in nutritional status and fatigue [33]. Oral administration of 6-gingerol (10 mg) was associated with higher response rates in both the acute and delayed phases (88% vs. 58% and 77% vs. 32%, respectively), as well as improved appetite [34]. In patients with gynecological malignancies, supplementation reduced the severity of acute nausea without a measurable effect on delayed symptoms [35]. However, several randomized trials did not demonstrate a consistent benefit of ginger in controlling CINV in either phase [36,37].

Other adjunctive therapies

The largest body of data concerns acupoint stimulation methods. A meta-analysis including 58 RCTs, demonstrated, that acupoint stimulation (acupoint patch) was the most effective non-pharmacological intervention for alleviating the delayed CINV, while acupuncture showed the greatest benefit in improving overall performance status, as assessed by the Karnofsky scale [38]. Auriculotherapy has shown a potential benefit in reducing nausea and vomiting in the late phase, particularly in breakthrough CINV, with no significant effect on the acute phase [39]. Acupressure, particularly at the P6 point in a limited way, can reduce the severity of nausea, with no significant effect on vomiting [40]. Acupuncture may improve the control of acute and delayed vomiting, but no clear benefit has been demonstrated for nausea [41]. Aromatherapy may be associated with a reduction in symptom severity, particularly when peppermint oil is used [42]. Data on music therapy are limited, but indicate a potential effect in reducing the anticipatory component [43]. Dietary interventions favour the control of CINV symptoms, particularly with an adequate supply of energy and protein and dietary patterns similar to the Mediterranean diet [44].

DISCUSSION

The development of predictive models reflects the growing interest in a more personalized approach to CINV prevention. By integrating patient and treatment related variables, these models may enable more accurate risk stratification than approaches based solely on chemotherapy emetogenicity [16]. Future refinement may include the incorporation of emerging risk determinants, such as pharmacogenetic and microbiome-related factors. Further studies are required to determine their clinical utility and to establish whether personalized risk assessment translates into improved patient outcomes [13,14]. Contemporary guideline-based regimens have markedly reduced the incidence of vomiting. However, complete control of nausea, particularly during the delayed phase, remains insufficient, with delayed nausea affecting up to 60% of patients despite prophylaxis. Furthermore, adherence to guideline-recommended antiemetic therapy in routine clinical practice remains suboptimal, which may further compromise symptom control and contribute to treatment modifications, including dose reductions or premature discontinuation of chemotherapy. Anticipatory CINV, affecting approximately 20–30% of patients during subsequent chemotherapy cycles, represents an additional challenge and underscores the importance of effective prophylaxis from the first cycle of treatment [45,46]. Recent studies suggest that optimization of antiemetic pharmacotherapy should focus not only on maximizing efficacy but also on improving treatment tolerability. This is illustrated by studies evaluating reduced-dose olanzapine, which may decrease sedation while maintaining antiemetic efficacy, as well as investigations of alternative agents, such as mirtazapine, pantoprazole, and thalidomide [23–27]. Although these findings are encouraging, most evidence is derived from individual randomized studies performed in selected patient populations, highlighting the need for larger comparative trials before these approaches can be routinely recommended. Complementary interventions, including ginger supplementation, acupuncture-related techniques, dietary interventions, and other non-pharmacological approaches, have shown encouraging but inconsistent results. The available data remains heterogeneous in terms of study quality, intervention protocols, and outcome measures [32,33,36,39–41,43,44]. Although current evidence does not support their routine use as standalone interventions, selected complementary approaches may provide additional benefit in appropriately selected patients and may be considered according to individual clinical circumstances and patient preferences.

Limitations

This narrative review has several limitations. The literature search was limited to PubMed and Google Scholar, and the review was not conducted using a formal systematic review methodology. The included publications differed in study design, patient populations, antiemetic regimens, intervention protocols, and outcome measures. These differences limit direct comparison of the findings and prevent firm conclusions regarding the relative effectiveness of the reviewed pharmacological and adjunctive approaches.

CONCLUSIONS

Chemotherapy-induced nausea and vomiting remain a significant challenge in supportive oncology despite substantial advances in evidence-based antiemetic prophylaxis. Although current management has markedly improved the prevention of vomiting, delayed nausea continues to represent an important unmet clinical need. Future progress is likely to depend on more individualized approaches integrating validated risk assessment with optimized pharmacological prophylaxis and appropriately selected supportive interventions. Further high-quality prospective studies are needed to strengthen the evidence base and define the optimal implementation of these strategies in routine clinical practice.

DISCLOSURE

Author Contributions

Conceptualization: Dagmara Laufer, Filip Chodań. Methodology: Filip Chodań, Adam Miler, Olga Klimczak. Formal analysis: Filip Chodań, Estera Sośniecka. Investigation and data collection: Olga Klimczak, Dagmara Laufer, Adam Miler, Estera Sośniecka. Writing, original draft preparation: Olga Klimczak, Filip Chodań, Dagmara Laufer, Krystian Domeracki. Writing, review and editing: Dagmara Laufer, Estera Sośniecka, Filip Chodań, Adam Miler. Supervision: Filip Chodań.

All authors read and approved the final version of the manuscript.

Funding

This research received no external funding.

Conflict of Interest

The authors declare no conflicts of interest.

Use of Artificial Intelligence

Artificial intelligence tools, including ChatGPT and other OpenAI systems, were used for language refinement and structural improvement. All content generated with the assistance of artificial intelligence was reviewed and verified by the authors.

REFERENCES

1. Rao KV, Faso A. Chemotherapy-Induced Nausea and Vomiting: Optimizing Prevention and Management. Am Health Drug Benefits. 2012 Jul;5(4):232–40.
2. Lavanya D, Prasanna V, Firdous A, Thakur S. A systemic review on chemotherapy induced nausea and vomiting- risk and clinical management with alternative therapies. Cancer Treat Res Commun. 2025 Jan 1;44:100938. https://doi.org/10.1016/j.ctarc.2025.100938
3. Majem M, de las Peñas R, Virizuela JA, Cabezón-Gutiérrez L, Cruz P, Lopez-Castro R, et al. SEOM Clinical Guideline update for the prevention of chemotherapy-induced nausea and vomiting (2021). Clin Transl Oncol. 2022;24(4):712–23. https://doi.org/10.1007/s12094-022-02802-1
4. Marx W, Kiss N, McCarthy AL, McKavanagh D, Isenring L. Chemotherapy-Induced Nausea and Vomiting: A Narrative Review to Inform Dietetics Practice. J Acad Nutr Diet. 2016 May;116(5):819–27. https://doi.org/10.1016/j.jand.2015.10.020
5. Navari RM, Aapro M. Antiemetic Prophylaxis for Chemotherapy-Induced Nausea and Vomiting. N Engl J Med. 2016 Apr 7;374(14):1356–67. https://doi.org/10.1056/NEJMra1515442
6. Razvi Y, Chan S, McFarlane T, McKenzie E, Zaki P, DeAngelis C, et al. ASCO, NCCN, MASCC/ESMO: a comparison of antiemetic guidelines for the treatment of chemotherapy-induced nausea and vomiting in adult patients. Support Care Cancer Off J Multinatl Assoc Support Care Cancer. 2019 Jan;27(1):87–95. https://doi.org/10.1007/s00520-018-4464-y
7. Chow R, Yin LB, Baqri W, Huang R, Boldt G, Younus J, et al. Prevalence and predictors of long-delayed (> 120 h) chemotherapy-induced nausea and vomiting (CINV)-a systematic review and individual patient data meta-analysis. Support Care Cancer Off J Multinatl Assoc Support Care Cancer. 2023 Aug 3;31(8):505. https://doi.org/10.1007/s00520-023-07978-y
8. Aapro M. CINV: still troubling patients after all these years. Support Care Cancer. 2018 Mar 1;26(1):5–9. https://doi.org/10.1007/s00520-018-4131-3
9. Gupta K, Walton R, Kataria SP. Chemotherapy-Induced Nausea and Vomiting: Pathogenesis, Recommendations, and New Trends. Cancer Treat Res Commun. 2021 Jan 1;26:100278. https://doi.org/10.1016/j.ctarc.2020.100278
10. Zhong W, Shahbaz O, Teskey G, Beever A, Kachour N, Venketaraman V, et al. Mechanisms of Nausea and Vomiting: Current Knowledge and Recent Advances in Intracellular Emetic Signaling Systems. Int J Mol Sci. 2021 May 28;22(11). https://doi.org/10.3390/ijms22115797
11. Singh P, Kuo B. Central Aspects of Nausea and Vomiting in GI Disorders. Curr Treat Options Gastroenterol. 2016 Dec 1;14(4):444–51. https://doi.org/10.1007/s11938-016-0107-x
12. MacDougall MR, Sharma S. Physiology, Chemoreceptor Trigger Zone. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2026 [cited 2026 Apr 20]. Available from: http://www.ncbi.nlm.nih.gov/books/NBK537133/
13. Crowder SL, Hoogland AI, Welniak TL, LaFranchise EA, Carpenter KM, Li D, et al. Metagenomics and Chemotherapy-Induced Nausea: A Roadmap for Future Research. Cancer. 2022 Feb 1;128(3):461–70. https://doi.org/10.1002/cncr.33892
14. Yeo W, Mo FKH, Huang J, Yeo HL, Ko WH, Li LV, et al. Personalized Prophylactic Antiemetic Regimens for Control of Chemotherapy-Induced Nausea and Vomiting by Pharmacogenetic Analysis of Three Receptor Genes: HTR3A, HTR3B, TACR1. JCO Precis Oncol. 2025 Apr;(9):e2400858. https://doi.org/10.1200/PO-24-00858
15. Jordan K, Chan A, Gralla RJ, Jahn F, Rapoport B, Ruhlmann CH, et al. Emetic risk classification and evaluation of the emetogenicity of antineoplastic agents—updated MASCC/ESMO consensus recommendation. Support Care Cancer. 2024;32(1):53. https://doi.org/10.1007/s00520-023-08220-5
16. Wang Y, Zheng R, Wu Y, Liu T, Hao L, Liu J, et al. Risk prediction model for chemotherapy-induced nausea and vomiting in cancer patients: a systematic review. Int J Nurs Stud. 2025 Aug 1;168:105094. https://doi.org/10.1016/j.ijnurstu.2025.105094
17. Kennedy SKF, Goodall S, Lee SF, DeAngelis C, Jocko A, Charbonneau F, et al. 2020 ASCO, 2023 NCCN, 2023 MASCC/ESMO, and 2019 CCO: a comparison of antiemetic guidelines for the treatment of chemotherapy-induced nausea and vomiting in cancer patients. Support Care Cancer. 2024 Apr 10;32(5):280. https://doi.org/10.1007/s00520-024-08462-x
18. Filetti M, Lombardi P, Giusti R, Falcone R, Scotte F, Giannarelli D, et al. Efficacy and safety of antiemetic regimens for highly emetogenic chemotherapy-induced nausea and vomiting: A systematic review and network meta-analysis. Cancer Treat Rev. 2023 Apr 1;115:102512. https://doi.org/10.1016/j.ctrv.2023.102512
19. Hesketh PJ, Kris MG, Basch E, Bohlke K, Barbour SY, Clark-Snow RA, et al. Antiemetics: ASCO Guideline Update. J Clin Oncol. 2020;38(24):2782–2797. https://doi.org/10.1200/JCO.20.01296
20. Herrstedt J, Clark-Snow R, Ruhlmann CH, Molassiotis A, Olver I, Rapoport BL, et al. 2023 MASCC and ESMO guideline update for the prevention of chemotherapy- and radiotherapy-induced nausea and vomiting. ESMO Open. 2024;9(2):102195. https://doi.org/10.1016/j.esmoop.2023.102195
21. Gu YL, Xie J ming, Ren J, Cao H, Wei J rong, Chen C, et al. Dexamethasone-sparing regimen is an effective and safe alternative in overall antiemetic protection. Medicine (Baltimore). 2019 Sep 27;98(39):e17364. https://doi.org/10.1097/MD.0000000000017364
22. Patel P, Robinson PD, Wahib N, Cheung P, Wong T, Cabral S, et al. Interventions for the prevention of acute phase chemotherapy-induced nausea and vomiting in adult and pediatric patients: a systematic review and meta-analysis. Support Care Cancer Off J Multinatl Assoc Support Care Cancer. 2022 Nov;30(11):8855–69. https://doi.org/10.1007/s00520-022-07287-w
23. Bajpai J, Kapu V, Rath S, Kumar S, Sekar A, Patil P, et al. Low-dose versus standard-dose olanzapine with triple antiemetic therapy for prevention of highly emetogenic chemotherapy-induced nausea and vomiting in patients with solid tumours: a single-centre, open-label, non-inferiority, randomised, controlled, phase 3 trial. Lancet Oncol. 2024 Feb;25(2):246–54. https://doi.org/10.1016/S1470-2045(23)00628-9
24. Cao J, Ouyang Q, Wang S, Ragaz J, Wang X, Teng Y, et al. Mirtazapine, a dopamine receptor inhibitor, as a secondary prophylactic for delayed nausea and vomiting following highly emetogenic chemotherapy: an open label, randomized, multicenter phase III trial. Invest New Drugs. 2020 Apr;38(2):507–14. https://doi.org/10.1007/s10637-020-00903-8
25. Maleki A, Ghadiyani M, Salamzadeh J, Salari S, Banihashem S, Tavakoli-Ardakani M. Comparison of mirtazapine and olanzapine on nausea and vomiting following anthracycline-cyclophosphamide chemotherapy regimen in patients with breast cancer. Iran J Pharm Res. 2020;19(3):451–64. https://doi.org/10.22037/ijpr.2020.113955.14584
26. Wewala N, Kim Y, Sharples K, Benge S, Cartwright R, Tan A, et al. Proton pump inhibition to prevent delayed chemotherapy-induced nausea and vomiting in patients receiving adjuvant or neoadjuvant breast cancer chemotherapy: a phase II, randomised double-blind crossover trial (PantoCIN). Support Care Cancer Off J Multinatl Assoc Support Care Cancer. 2025 May 20;33(6):484. https://doi.org/10.1007/s00520-025-09528-0
27. Zhang L, Qu X, Teng Y, Shi J, Yu P, Sun T, et al. Efficacy of Thalidomide in Preventing Delayed Nausea and Vomiting Induced by Highly Emetogenic Chemotherapy: A Randomized, Multicenter, Double-Blind, Placebo-Controlled Phase III Trial (CLOG1302 study). J Clin Oncol. 2017 Nov;35(31):3558–65. https://doi.org/10.1200/JCO.2017.72.2538
28. Walstab J, Krüger D, Stark T, Hofmann T, Demir IE, Ceyhan GO, et al. Ginger and its pungent constituents non-competitively inhibit activation of human recombinant and native 5-HT3 receptors of enteric neurons. Neurogastroenterol Motil. 2013 May;25(5):439–47, e302. https://doi.org/10.1111/nmo.12107
29. Jin Z, Lee G, Kim S, Park CS, Park YS, Jin YH. Ginger and its pungent constituents non-competitively inhibit serotonin currents on visceral afferent neurons. Korean J Physiol Pharmacol Off J Korean Physiol Soc Korean Soc Pharmacol. 2014 Apr;18(2):149–53. https://doi.org/10.4196/kjpp.2014.18.2.149
30. Qian Q hui, Yue W, Chen W hui, Yang Z hong, Liu Z tao, Wang Y xia. Effect of gingerol on substance P and NK1 receptor expression in a vomiting model of mink. Chin Med J (Engl). 2010 Feb 20;123(4):478–84.
31. Pertz HH, Lehmann J, Roth-Ehrang R, Elz S. Effects of ginger constituents on the gastrointestinal tract: role of cholinergic M3 and serotonergic 5-HT3 and 5-HT4 receptors. Planta Med. 2011 Jul;77(10):973–8. https://doi.org/10.1055/s-0030-1270747
32. Ryan JL, Heckler CE, Roscoe JA, Dakhil SR, Kirshner J, Flynn PJ, et al. Ginger (Zingiber officinale) reduces acute chemotherapy-induced nausea: a URCC CCOP study of 576 patients. Support Care Cancer Off J Multinatl Assoc Support Care Cancer. 2012 Jul;20(7):1479–89. https://doi.org/10.1007/s00520-011-1236-3
33. Crichton M, Marshall S, Isenring E, Lohning A, McCarthy AL, Molassiotis A, et al. Effect of a Standardized Ginger Root Powder Regimen on Chemotherapy-Induced Nausea and Vomiting: A Multicenter, Double-Blind, Placebo-Controlled Randomized Trial. J Acad Nutr Diet. 2024 Mar;124(3):313-330.e6. https://doi.org/10.1016/j.jand.2023.09.003
34. Konmun J, Danwilai K, Ngamphaiboon N, Sripanidkulchai B, Sookprasert A, Subongkot S. A phase II randomized double-blind placebo-controlled study of 6-gingerol as an anti-emetic in solid tumor patients receiving moderately to highly emetogenic chemotherapy. Med Oncol. 2017 Apr;34(4):69. https://doi.org/10.1007/s12032-017-0931-4
35. Uthaipaisanwong A, Oranratanaphan S, Musigavong N. Effects of ginger adjunct to the standard prophylaxis on reducing carboplatin and paclitaxel-induced nausea vomiting: a randomized controlled study. Support Care Cancer. 2020 Aug;28(8):3831–8. https://doi.org/10.1007/s00520-019-05201-5
36. Bossi P, Cortinovis D, Fatigoni S, Cossu Rocca M, Fabi A, Seminara P, et al. A randomized, double-blind, placebo-controlled, multicenter study of a ginger extract in the management of chemotherapy-induced nausea and vomiting (CINV) in patients receiving high-dose cisplatin. Ann Oncol Off J Eur Soc Med Oncol. 2017 Oct 1;28(10):2547–51. https://doi.org/10.1093/annonc/mdx315
37. Li X, Qin Y, Liu W, Zhou XY, Li YN, Wang LY. Efficacy of Ginger in Ameliorating Acute and Delayed Chemotherapy-Induced Nausea and Vomiting Among Patients With Lung Cancer Receiving Cisplatin-Based Regimens: A Randomized Controlled Trial. Integr Cancer Ther. 2018 Sep;17(3):747–54. https://doi.org/10.1177/1534735417753541
38. Wang Y, Wang F, Hu F, Long F. Effect of non-pharmacological interventions on chemotherapy induced delayed nausea and vomiting for tumors: A systematic review and Bayesian network meta-analysis. Complement Ther Med. 2025 Mar 1;88:103124. https://doi.org/10.1016/j.ctim.2024.103124
39. Chen L, Wu X, Chen X, Zhou C. Efficacy of Auricular Acupressure in Prevention and Treatment of Chemotherapy-Induced Nausea and Vomiting in Patients with Cancer: A Systematic Review and Meta-Analysis. Evid-Based Complement Altern Med ECAM. 2021 Aug 3;2021:8868720. https://doi.org/10.1155/2021/8868720
40. Li K, Cai Y, Xie S, Zhou Y, Dong J, Zhu Q, et al. Evidence Summary for Nonpharmacological Management of Chemotherapy-Induced Nausea and Vomiting. BioMed Res Int. 2022;2022:4741193. https://doi.org/10.1155/2022/4741193
41. Yan Y, López-Alcalde J, Zhang L, Siebenhüner AR, Witt CM, Barth J. Acupuncture for the prevention of chemotherapy-induced nausea and vomiting in cancer patients: A systematic review and meta-analysis. Cancer Med. 2023 Jun;12(11):12504–17. https://doi.org/10.1002/cam4.5962
42. Toniolo J, Delaide V, Beloni P. Effectiveness of Inhaled Aromatherapy on Chemotherapy-Induced Nausea and Vomiting: A Systematic Review. J Altern Complement Med. 2021;27(12):1058–1069. https://doi.org/10.1089/acm.2021.0067
43. Wei TT, Tian X, Zhang FY, Qiang WM, Bai AL. Music interventions for chemotherapy-induced nausea and vomiting: a systematic review and meta-analysis. Support Care Cancer Off J Multinatl Assoc Support Care Cancer. 2020 Sep;28(9):4031–41. https://doi.org/10.1007/s00520-020-05409-w
44. Gala D, Wright HH, Zigori B, Marshall S, Crichton M. Dietary strategies for chemotherapy-induced nausea and vomiting: A systematic review. Clin Nutr. 2022 Oct 1;41(10):2147–55. https://doi.org/10.1016/j.clnu.2022.08.003
45. Jordan K, de Azambuja E, García del Barrio MÁ, Jahn F, Di Palma M, Scotté F, et al. Going beyond the 2023 MASCC and ESMO guideline update for the prevention of chemotherapy- and radiotherapy-induced nausea and vomiting. Eur J Cancer. 2025 Jun 3;222:115451. https://doi.org/10.1016/j.ejca.2025.115451
46. Cohen L, de Moor CA, Eisenberg P, Ming EE, Hu H. Chemotherapy-induced nausea and vomiting: incidence and impact on patient quality of life at community oncology settings. Support Care Cancer Off J Multinatl Assoc Support Care Cancer. 2007 May;15(5):497–503. https://doi.org/10.1007/s00520-006-0173-z

back