Introduction Chemotherapy-induced nausea and vomiting (CINV) is a common and debilitating adverse effect of breast cancer chemotherapy. The incidence of CINV in the first cycle of chemotherapy is essential, as it sets the tone for anticipatory CINV and the overall patients' treatment experience. We aimed to investigate the risk factors of first cycle CINV in breast cancer patients and to develop a classification and regression tree (CART) model to predict its occurrence. Methods This is a cross-sectional study that nested in a prospective cohort. One hundred and thirty-seven female breast cancer patients receiving highly emetogenic chemotherapy were included. We used the Common Toxicity Criteria for Adverse Events (CTCAE) version 4.0 to assess patient-reported nausea and vomiting in the first chemotherapy cycle. The proportional difference of CINV between sociodemographic and clinicopathologic variables was analyzed using chi-square, and the strength and direction of the relationship with CINV were analyzed using bivariable logistic regression analysis. Multivariable logistic regression and CART analysis included variables with a p-value <0.250. Results The incidence of first-cycle CINV was 43.1%. The chi-square test revealed a significant association between insurance status and CINV (p<0.001) and between the stage at diagnosis and CINV (p<0.001). Underweight to normal body mass index (BMI) patients are significantly associated with an increased risk of first-cycle CINV (OR =2.17, 95% CI 1.03-4.56, p =0.041). In hierarchical order, three variables (stage at diagnosis, BMI, and age) were included in the CART model, which significantly influenced the probability of first cycle CINV. With an accuracy of 61.3%, the CART model had a sensitivity of 28.8%, a specificity of 85.9%, a positive predictive value of 60.7%, a negative predictive value of 61.5%, and an area under curve (AUC) of 0.602.  Conclusion Breast cancer patients with an underweight to normal BMI have a higher risk of developing first-cycle CINV. Our CART model was better at identifying patients who would not develop CINV than those who would. The CART model may provide a simple and effective way to individualize patient care for first-cycle CINV.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10469922PMC
http://dx.doi.org/10.7759/cureus.44438DOI Listing

Publication Analysis

Top Keywords

breast cancer
16
nausea vomiting
12
chemotherapy-induced nausea
8
classification regression
8
regression tree
8
tree cart
8
cancer patients
8
logistic regression
8
cinv
6
vomiting patients
4

Similar Publications

Insights into NEK2 inhibitors as antitumor agents: From mechanisms to potential therapeutics.

Eur J Med Chem

January 2025

Department of Respiratory and Critical Care Medicine, Targeted Tracer Research and Development Laboratory, Institute of Respiratory Healthand, Department of Frontiers Science Center for Disease-related Molecular Network, Core Facilities, West China Hospital, Sichuan University, Chengdu, 610041, Sichuan, China. Electronic address:

NEK2, a serine/threonine protein kinase, is integral to mitotic events such as centrosome duplication and separation, microtubule stabilization, spindle assembly checkpoint, and kinetochore attachment. However, NEK2 overexpression leads to centrosome amplification and chromosomal instability, which are significantly associated with various malignancies, including liver, breast, and non-small cell lung cancer. This overexpression could facilitate tumor development and confer resistance to therapy by promoting aberrant cell division and centrosome amplification.

View Article and Find Full Text PDF

Analysis of circulating cell-free nuclear and mitochondrial DNA in plasma of Mexican patients with breast cancer.

Gac Med Mex

January 2025

División de Medicina Molecular, Centro de Investigación Biomédica de Occidente, Instituto Mexicano del Seguro Social, Guadalajara.

Background: The usefulness of circulating free DNA (cfDNA), nuclear DNA (nDNA) and mitochondrial DNA (mtDNA) as potential biomarkers in cancer remains controversial.

Objective: To determine the concentration of cfDNA and plasma nDNA and mtDNA levels in breast cancer (BC) patients.

Material And Methods: This study included a total of 86 women (69 patients with BC and 17 women as a control group).

View Article and Find Full Text PDF

MTHFD2 promotes breast cancer cell proliferation through IFRD1 RNA m6A methylation-mediated HDAC3/p53/mTOR pathway.

Neoplasma

December 2024

Department of Pathology and Forensic Medicine, College of Basic Medical Sciences, Dalian Medical University, Dalian, China.

MTHFD2 is highly overexpressed in breast cancer tissues, indicating that it might be used as a target in breast cancer treatment. This study aims to determine the role of MTHFD2 in breast cancer cell proliferation and the molecular pathways involved. In order to investigate MTHFD2 gene expression and its downstream pathways in breast cancer, we started our inquiry with a bioinformatics analysis.

View Article and Find Full Text PDF

Triple-negative breast cancer (TNBC) is a highly aggressive subtype of breast malignancy. Although some patients benefit from immune checkpoint therapy, current treatment methods rely mainly on chemotherapy. It is imperative to develop predictors of efficacy and identify individuals who will be sensitive to particular treatment regimens.

View Article and Find Full Text PDF

Background: CT thorax, abdomen and pelvis (CT-TAP) remains the standard in the identification of metastatic disease in patients with newly diagnosed breast cancer. In patients with proven micro and macro axillary nodal metastasis, the optimal radiological technique remains controversial. A consensus on which patients with axillary nodal disease should receive radiological staging for distant disease and how this should be performed is not currently available.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!