共找到 20 条结果
Selection of letters to be published is the decision of the editor. For acceptance, letters must be signed. A letter can appear anonymously if requested by the author. All letters are subject to editing. A letter that questions, criticizes, or responds to a previously published Oncology Nursing Forum article automatically will be sent to the author of that article for a reply. This type of collegial exchange is encouraged. Send letters to ONFEditor@ons.org.
Chemotherapy-induced neutropenia and febrile neutropenia (FN) remain consequential toxicities in breast cancer treatment, driving infections, unplanned care, and compromises in planned dose intensity. Long-acting granulocyte colony-stimulating factor (G-CSF) enables once-per-cycle prophylaxis and has become central to FN prevention strategies, particularly in dose-dense and high-risk regimens. Beyond efficacy, the supportive care evidence base has rapidly expanded to implementation in routine practice, delivery devices, biosimilars, safety surveillance, and value-based decision-making. However, this heterogeneous and fast-growing literature has not been systematically mapped to support evidence navigation and identify actionable research priorities. We therefore conducted a bibliometric analysis to characterize the knowledge structure, influential contributors, and emerging hotspots of long-acting G-CSF prophylaxis research in breast cancer chemotherapy. Publications were retrieved from the Science Citation Index Expanded of the Web of Science Core Collection using a topic strategy combining breast cancer, chemotherapy-induced context, long-acting G-CSF agents, and neutropenia/FN prophylaxis concepts. The search was performed on 24 February 2026 and covered 2002-2025. English-language records were included; document types were limited to articles and reviews, with meeting abstracts, editorial materials, and letters excluded during screening. Bibliometrix, VOSviewer, and CiteSpace were applied to evaluate annual production, collaboration networks, keyword co-occurrence, co-citation structure and evolution, burst detection, and thematic mapping. The WoSCC retrieval returned 555 records; after restricting to English (547) and excluding meeting abstracts (n = 39), editorial materials (n = 5), and letters (n = 7), 496 publications were included (412 articles; 84 reviews). Annual production increased and entered a sustained high-output phase in the late 2010s and early 2020s. The USA was the most productive country (218 documents; 10,188 citations), followed by Germany (69) and England (51). Supportive Care in Cancer contributed the most publications (62), while Annals of Oncology had the highest citations among the top journals (1489). Co-citation and keyword analyses indicated an evolution from early trial- and guideline-driven supportive care toward optimization in routine practice, real-world prophylaxis evaluation, biosimilars, safety, and cost-effectiveness. The evidence landscape of long-acting G-CSF prophylaxis in breast cancer chemotherapy has evolved from efficacy confirmation toward implementation-oriented supportive care. Current research increasingly emphasizes real-world effectiveness, safety monitoring, biosimilar integration, delivery models, and value-based considerations. By mapping knowledge structures and emerging priorities, this study may provide a structured overview for evidence navigation and may help identify future research priorities, particularly in relation to real-world utilization, affordability, guideline-concordant use, and resource-sensitive febrile neutropenia prevention.
Liquid biopsy has become an increasingly important tool in clinical oncology due to the utility of circulating tumor DNA (ct-DNA). Plasma ct-DNA levels reflect the tumor burden of patients and provide valuable information for personalized treatment strategies. Colorectal cancer (CRC) is among the most frequently diagnosed malignancies worldwide and remains a leading cause of cancer-related mortality. The implementation of personalized therapy can notably improve clinical outcomes in these patients. The present study aimed to evaluate ct-DNA in patients with metastatic CRC undergoing therapy at the Department of Medical Oncology, University Hospital of Ioannina (Ioannina, Greece), using next-generation sequencing (NGS) to identify tumor mutations in both tissue and cell-free plasma DNA. A total of 45 patients newly diagnosed with metastatic CRC were enrolled in the current study. ct-DNA evaluation was performed at diagnosis, and both tissue and plasma samples were analyzed using NGS to assess the mutational profile. The most frequent mutation identified was in KRAS. A high level of concordance was observed between tissue and plasma samples regarding ct-DNA detection and mutational status. Sequential ct-DNA analysis during therapy revealed dynamic changes in mutation profiles over the course of treatment. In conclusion, liquid biopsy offers marked clinical value as a minimally invasive tool for personalized therapy in metastatic CRC. NGS-based liquid biopsy enables real-time evaluation of ct-DNA and mutation status during treatment, supporting therapeutic decision-making and disease monitoring.
Thousands of scholars across Europe faced discrimination for their heritage, especially Jewish heritage, throughout the 1930s. Hundreds of these persecuted academics worked in science and healthcare, often as primary researchers within a medical sub-specialty. In response, in 1933 British professors founded the Society for the Protection of Science and Learning (SPSL) with two objectives: raising funds to provide maintenance grants for displaced scholars and connecting scholars to academic placements worldwide. In this article, I analyze the stories of nineteen physicians fleeing fascist persecution in Europe through their 712 leaves of correspondence within the archive of the SPSL. I selected two medical subspecialties, to compare whether the well-funded field of oncology would have greater success placing refugees compared to the less academically-elevated field of orthopedic surgery. Through the first analysis of two complete medical subspecialty records from the SPSL archives, I examine how the SPSL faced difficulties deciding which colleagues to help financially and triaged levels of support. I also situate the experiences of the analyzed applicants within the context of British interwar medicine and academia, including British skepticism of foreign research and overlaps between SPSL leadership and the British eugenics movement. When funding ran low, the SPSL still assisted scholars through different channels, whether referring to other aid organizations, sending support letters to potential employers, or simply staying in contact. The surge in applications in 1938, five years after the organization's foundation, hindered scholars' chances as persecution increased and funding tapered. Importantly, the British medical establishment distrusted the overall research quality of many fleeing scholars and felt even less confident admitting medical practitioners who were not also researchers. Ultimately, medical scholars from fascist Germany and Austria who applied to the SPSL had a similar experience to other aspiring refugees seeking British assistance before 1939: they could not rely on Britain to support their immigration and predominantly settled elsewhere.
To better define the frequency and types of retinal pigment epithelial (RPE) tumors. Retrospective review of all computer-coded RPE tumors over a five-decade period. Of 926 consecutive patients with RPE tumors, the specific diagnosis included solitary congenital hypertrophy of the retinal pigment epithelium (n = 727, 79%), multifocal congenital hypertrophy of the RPE (n = 42, 4%), torpedo maculopathy (n = 7, 1%), RPE hamartomas associated with familial adenomatous polyposis (n = 10, 1%), congenital simple hamartoma of the RPE (n = 5, 1%), combined hamartoma of the retina and RPE (n = 99, 11%), benign RPE adenoma (n = 34, 3%), and malignant RPE adenocarcinoma (n = 2, <1%). There were differences in RPE tumors regarding patient age (P < 0.01), race (P < 0.01), sex (P < 0.01), presenting visual acuity (P < 0.01), number of tumors (P < 0.01), tumor basal diameter (P < 0.01), tumor thickness (P < 0.01), and distance to the optic disc (P < 0.01) and foveola (P < 0.01). There were differences in RPE tumors regarding imaging with ultrasonography (P < 0.01), optical coherence tomography (P < 0.01), and prevalence of macular epiretinal membrane, cystoid macular, edema, and subretinal fluid on optical coherence tomography (P < 0.01). By autofluorescence and fluorescein angiography, nearly all lesions that were imaged were hypoautofluorescent/hypofluorescent except for combined hamartoma of the retina and RPE (P < 0.01). Outcomes revealed visual acuity loss ≥3 lines (≥15 letters) at 10 years more often in combined hamartoma of the retina and RPE (20%), adenoma (21%), and adenocarcinoma (100%) (P < 0.01) and 10-year nodular growth in congenital hypertrophy of the RPE (1%), adenoma (9%), and adenocarcinoma (100%) (P < 0.01). Retinal pigment epithelial tumors comprise a spectrum in demographics, clinical features, and outcomes. Most remain stable over time with little impact on visual acuity except for combined hamartoma of the retina and RPE, adenoma, and adenocarcinoma.
Ubiquitination and N6-methyladenosine (m6A) RNA methylation constitute two fundamental layers of post-translational and post-transcriptional regulation that coordinately govern gene expression in cancer. These regulatory systems exhibit intricate crosstalk, revealing that they frequently converge on shared oncogenic signaling pathways to fine-tune malignant cell behaviors. Cooperative regulation by ubiquitination and m6A is involved in modulating core cancer-driving circuits, including the PI3K-AKT and NF-κB pathways, thereby taking part in tumor cell proliferation, metastatic dissemination, immune evasion, metabolic adaptation and resistance to targeted therapies and chemotherapy. The interaction between them forms intricate feedback loops and exhibits context specificity, with the same regulatory axis capable of promoting or restraining tumorigenesis depending on cell types, mutation background and microenvironmental cues. Elucidating the molecular mechanisms underlying ubiquitin-m6A crosstalk is thus key for developing next-generation precision oncology strategies. Notably, components of these pathways such as ubiquitin ligases, deubiquitinases and m6A writers, erasers and readers, have been regarded as potential diagnostic biomarkers and therapeutic targets. Future advances relying on integrative multi-omics profiling, sophisticated functional models and rigorous in vivo validation are essential to unravel the complexity of these multi-layered regulatory networks. Such insights may ultimately enable the rational design of therapies that exploit ubiquitin-m6A crosstalk to more effectively suppress cancer progression.
Gestational trophoblastic disease (GTD) includes premalignant and malignant entities such as choriocarcinoma and invasive mole, collectively termed gestational trophoblastic neoplasia (GTN). While chemotherapy remains the standard treatment, hysterectomy is indicated in cases of chemoresistance, significant hemorrhage, or in patients with nonmetastatic GTN who do not desire fertility preservation. This review aims to assess the effectiveness of hysterectomy in treating GTN. A systematic literature search was conducted using PubMed, EBSCOHost, ProQuest, and Google Scholar for studies published from 27 February 2000 to 27 February 2024. Exclusion criteria included single case reports, editorials, commentaries, letters, non-peer-reviewed studies, non-full-text articles, and studies without hysterectomy or relevant outcome data. Eligible studies focused on GTN and reported on remission outcomes post-hysterectomy. Three reviewers independently extracted data and analyzed it using MedCalc v19.5.1. This review is registered with PROSPERO (CRD42024556274). Seven retrospective cohort studies involving 407 patients were analyzed. The overall complete remission rate following hysterectomy was 86.6%, with higher rates in nonmetastatic cases (99.5%) and lower in metastatic cases (46.3%). Complication and mortality rates were low, with deaths occurring primarily in metastatic or high-risk patients. Hysterectomy plays a significant role in managing select GTN cases, particularly nonmetastatic or chemotherapy-resistant disease, and when fertility preservation is not desired. However, its effectiveness is limited in metastatic GTN. Postoperative monitoring of serum hCG remains crucial due to the risk of residual or metastatic disease.
Lactylation, a novel post-translational modification, has emerged as a critical mechanistic link between metabolic reprogramming and epigenetic regulation in cancer. The present review aimed to synthesize emerging evidence on the role of lysine lactylation in the pathogenesis and progression of major digestive system malignancies, including esophageal, gastric, colorectal, hepatocellular and pancreatic cancer. The molecular mechanisms through which lactate-derived lactylation modifies histone and non-histone proteins are described, which thereby regulate key oncogenic processes such as metabolic adaptation, cancer stemness maintenance, epithelial-mesenchymal transition, immunosuppressive tumor microenvironment remodeling, angiogenesis, perineural invasion and therapeutic resistance. The translational potential of targeting the lactylation axis by inhibiting lactate production, blocking lactate transport or directly modulating lactylation-related enzymes are explored, and the development of lactylation-based prognostic models and their implications for innovative combination strategies to overcome treatment resistance are also highlighted. The present review highlights lactylation as a pivotal regulator in digestive oncology and a promising target for novel diagnostic and therapeutic strategies.
Chromatin organization plays a fundamental role in the regulation and preservation of the eukaryotic genome. Histone variants contribute to chromatin dynamics by replacing canonical histones within nucleosomes and conferring specialized structural and regulatory properties. Among these variants, the centromere-specific histone H3 variant CENP-A is essential for establishing and maintaining centromere identity and ensuring accurate chromosome segregation during mitosis. Proper expression, deposition, and maintenance of CENP-A are tightly regulated through dedicated chaperones and mechanisms. Disruption of these regulatory processes can lead to aberrant CENP-A expression or mislocalization, resulting in defective centromere function and chromosome segregation. CENP-A is frequently overexpressed in several human cancers and CENP-A overexpression often correlates with tumor progression, chromosomal instability, and poor prognosis. Ectopic incorporation of CENP-A into non-centromeric chromatin can promote aberrant chromatin states and partial recruitment of kinetochore components. These alterations can disrupt normal kinetochore function and contribute to chromosome missegregation, thereby promoting chromosomal instability (CIN) and tumor evolution. In addition to its role in mitotic fidelity, emerging studies suggest that ectopic CENP-A can interfere with chromatin factors and influence transcriptional regulation. Hence, CENP-A emerges as a potential biomarker for cancer prognosis and therapeutic response. In this review, we summarize current knowledge on the regulation of CENP-A expression and deposition, discuss the functional consequences of its dysregulation in cancer, and highlight emerging clinical and translational implications of targeting centromere chromatin pathways in oncology.
Hereditary transthyretin amyloidosis (hATTR) is a progressive, multisystemic, and life-threatening disease that disproportionately affects individuals of African descent, with an estimated prevalence of 3.4% of Black Americans. hATTR is often mis- or underdiagnosed, partially because many of its symptoms overlap with other cardiac conditions. This study highlights additional factors that may be contributing to the underdiagnosis of hATTR in Black patients. Participants were ascertained from the Emory University Amyloidosis Clinic with purposive sampling. A total of 11 interviews were conducted via telephone, transcribed, and coded by two coders for thematic analysis. A Cohen's kappa of 0.74 was reached. The overwhelming majority of participants cited misdiagnosis, mistrust of healthcare providers, denial or misunderstanding of one's own health risks, and poor family communication as prevalent contributing factors to the underdiagnosis of hATTR. Participants cited appropriate referrals to heart failure providers and family letters as contributing factors to proper diagnosis of hATTR. Importantly, participants emphasized the need for more personal and intimate relationships with providers in order to improve uptake of genetic testing in this population. Participants suggested engaging directly with the Black community to improve trust. This study highlights the need for improvements to be made regarding the diagnosis of hATTR in the Black population. Participants suspected of having hATTR should be referred to a heart failure cardiologist for appropriate diagnosis. Genetic testing and follow-up genetic counseling is recommended to appropriately inform the patient of health risks for themselves and their family members.
[This corrects the article DOI: 10.3892/ol.2022.13400.].
Lung squamous cell carcinoma (LUSC) is a prevalent subtype of lung cancer, which is primarily characterized by poor prognosis due to the lack of targeted therapies, while a large proportion of patients show limited response to chemotherapy. The present study aimed to identify predictive chemotherapy biomarkers based on genomic alterations in LUSC. Non-negative matrix factorization clustering was applied to classify patients with LUSC into distinct subgroups based on genomic alterations. Subsequently, chemotherapy efficacy was predicted via exploring gene signatures, and the results were validated using The Cancer Genome Atlas database (TCGA). A total of four distinct clusters were classified. Cluster 1 and TP53 loss-of-function (TP53 LOF) variations were each independently associated with poor prognosis, irrespective of clinical stage. Based on the molecular characteristics of the initial clusters, the classification was further refined by further incorporating TP53 LOF and gene amplification (amp). Patients without TP53 LOF, who harbored amplification of at least one of nine specified genes [PIK3 catalytic subunit, cyclin D1, fibroblast growth factor (FGF) 19, FGF3, FGF4, FGF receptor 1, kinase insert domain receptor, KIT proto-oncogene and platelet derived growth factor receptor α] displayed the longest progression-free survival (PFS). By contrast, patients with TP53 LOF but lacking amplification of at least one of nine genes [Amp(9G)] exhibited the worst overall survival compared with the other subgroups. Validation in the TCGA database confirmed the prognostic significance of this classification, with Amp(9G) without TP53 LOF predicting the most favorable PFS, and TP53 LOF without Amp(9G) indicating the least favorable PFS. Therefore, a composite biomarker integrating Amp(9G) and TP53 LOF was identified as a prognostic indicator for patients with LUSC treated with first-line chemotherapy. Overall, the results of the present study suggest that the absence of TP53 LOF combined with the presence of Amp(9G) could be associated with improved response to first-line chemotherapy in LUSC.
Bladder cancer is the ninth most common malignancy worldwide, with urothelial carcinoma (UC) representing the predominant histopathological subtype. UC may present as pure urothelial carcinoma (PUC), or alongside other variant histologies (VHs), with squamous differentiation in UC (SD) being the most frequently observed variant. The present study provides a population-based insight into the survival outcomes of patients with SD compared with PUC in early-stage disease. The present retrospective, observational study analyzed pathology reports from all cystectomies (n=632) performed at Uludag University Faculty of Medicine (Bursa, Turkey) between December 2010 and December 2023. A total of 23 patients with SD and 45 patients with PUC were evaluated; all of the patients had pathological stage T2N0 (pT2N0). The median follow-up period was 5.27 years (range, 0.23-16.60). Kaplan-Meier survival analysis demonstrated no statistically significant difference in disease-free survival (DFS) or overall survival (OS) between the SD and PUC groups. Univariate Cox regression analysis identified that age at diagnosis was a potential prognostic factor of both DFS and OS. The findings suggest that SD does not significantly affect DFS or OS in patients with pT2N0 UC. However, further prospective, multicenter, large-scale studies are warranted to validate and expand upon these findings.
The present study aimed to investigate the role and expression of large tumor suppressor kinase 2 (LATS2) in lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC). The expression levels of LATS2 in LUAD and LUSC, as well as their association with clinical characteristics and patient survival, were analyzed using data obtained from The Cancer Genome Atlas. A total of 100 LATS2-related genes were screened to conduct Kyoto Encyclopedia of Genes and Genomes and Gene Ontology enrichment analyses. The association between LATS2 expression and immune cell infiltration, particularly CD4+ and CD8+ tumor-infiltrating lymphocytes (TILs), was analyzed. The role of LATS2 in tumor cells was validated by observing the changes in proliferation, apoptosis, migration and invasion of LUAD and LUSC cells following LATS2 overexpression. LATS2 expression was low in both LUAD and LUSC. In LUAD, high expression of LATS2 was associated with lymph node metastasis, distant metastasis and TNM stage and served as an independent risk factor for both overall survival and progression-free survival. Conversely, in LUSC, LATS2 exhibited a weak association with clinical characteristics and survival. In LUAD and LUSC, LATS2-related genes exhibited differences in their associated functional pathways and biological processes. In LUAD, LATS2 was positively associated with CD4+ TIL proportions and CD4+/CD8+ TIL proportions, while exhibiting a negative association with CD8+ TIL proportions. In LUSC, no such associations were observed. In vitro experiments demonstrated that overexpression of LATS2 inhibited proliferation, migration and invasion, while promoting apoptosis, in both LUAD and LUSC cell lines, with notably stronger effects observed in LUAD cells. In conclusion, LATS2 exerts tumor-suppressive functions in both LUAD and LUSC. In LUAD, LATS2 is an independent risk factor for patient survival, possibly due to its close association with CD8+ TIL levels; however, this relationship is not pronounced in LUSC.
Current data on BRCA status and response to neoadjuvant pembrolizumab plus chemotherapy are limited. This study evaluated the association between BRCA status and pathological complete response (pCR) in patients with early triple-negative breast cancer (TNBC). BRCAPATH was a French multicenter retrospective study including 288 patients with early TNBC; 234 received neoadjuvant pembrolizumab plus chemotherapy and 54 received chemotherapy alone. pCR was defined as ypT0/TisN0 (TNM 8th edition). Associations between BRCA status and pCR were evaluated using Fisher's exact test and multivariable logistic regression. Survival was analyzed using the Kaplan-Meier method. In the pembrolizumab-treated cohort, 35 patients (15.0%) carried BRCA pathogenic variants (PV) and pCR was achieved in 88.6% of BRCA PV carriers versus 52.1% of non-carriers (p < 0.001). In multivariable analysis, BRCA PV remained independently associated with pCR (OR 8.47, 95% CI 2.65-27.04; p < 0.001). In exploratory subgroup analyses, BRCA1 pathogenic variants remained significantly associated with pCR, whereas findings for BRCA2 were limited by the small number of carriers. No statistically significant survival difference was observed for BRCA PV carriers. BRCA PV, particularly BRCA1, were strongly associated with pCR in pembrolizumab-treated early TNBC. These findings should be considered hypothesis-generating and warrant confirmation in larger prospective cohorts.
Chromosomal alterations are key in the study of acute lymphoblastic leukemia (ALL) as they facilitate the establishment of risks, prognosis and treatment. The intrachromosomal amplification of chromosome 21 (iAMP21) can generate a structurally heterogeneous derivative chromosome 21 that can typically replace a normal chromosome 21 and defines a subtype of high-risk childhood ALL (iAMP21-ALL). A region commonly involved in this amplification has been delineated and includes genes such as chromatin assembly factor 1 subunit B, dual-specificity tyrosine-(Y)-phosphorylation regulated kinase 1A, erythroblast transformation-specific-related gene, high mobility group nucleosome binding domain 1 and Runt-related transcription factor 1, but its role in the development of leukemia has not yet been fully elucidated. The Down syndrome critical region on chromosome 21 (ripply transcriptional repressor 3) overlaps with a common amplification region in iAMP21. Therefore, it has been hypothesized that iAMP21-related genes may be associated with Down syndrome susceptibility to ALL. The present review described the biological role of iAMP21-related genes and their relationship with ALL development.
The features of high heterogeneity and aggressiveness of glioblastoma (GBM) predispose it to temozolomide (TMZ) resistance, which notably impairs therapeutic efficacy. Cytokine family members have been shown to activate pro-survival pathways in GBM cells and facilitate the formation of immunosuppressive microenvironments, contributing to TMZ resistance in GBM. The present study aimed to investigate the role of cytokine IL-37 in the malignant progression and TMZ resistance of GBM. Recombinant human IL-37b (rIL-37) enhanced the survival of TMZ-treated GBM U251 cells. IL-37 silencing or overexpression notably reduced or increased the survival rate of U251 cells exposed to TMZ, respectively. In TMZ-resistant U251 (U251-TR) cells, IL-37 knockdown also improved cellular sensitivity to TMZ. Consistent with these findings, rIL-37 treatment promoted proliferation and suppressed apoptosis of U251 cells under TMZ exposure, whereas IL-37 silencing significantly suppressed growth and enhanced the apoptotic responses of U251-TR cells receiving TMZ. To explore the underlying mechanisms, RNA sequencing was performed and revealed that the U251 cells undergoing TMZ exposure and rIL-37 treatment exhibited an altered transcriptomic profile, characterized by the activation of both mitogen-activated protein kinase (MAPK) pathways and senescence-related pathways. After confirming the activation of cellular MAPK cascades and senescence, Adezmapimod, a p38 MAPK-specific inhibitor, effectively counteracted rIL-37-induced improvements in cellular survival and proliferative capacity, suppression of apoptosis and activation of senescence in U251 cells under TMZ exposure, indicating the necessity of the MAPK pathway in TMZ resistance. The present study expands the current knowledge of the roles of IL-37 during the malignant progression of GBM and demonstrates that IL-37 enhances TMZ resistance in GBM cells by activating the MAPK pathway and inhibiting apoptosis, suggesting that targeted inhibition of MAPK cascades in GBM is promising in future clinical practice.
Background: Workplace victimization is a form of repeated and systematic psychological violence that can severely affect both mental and physical health. From a psychological perspective, it impacts mood states, defense mechanisms, and personality functioning. Methods: This cross-sectional study investigated the psychological and behavioural correlates of workplace victimization in a sample of 33 workers from various professional sectors, using a multidimensional assessment including standardized measures of personality traits, mood states, and defense mechanisms. Results: The MMPI-2 profile revealed elevated scores in Hypochondriasis (Hs: 72.00), Depression (D: 70.21), Hysteria (Hy: 67.61), and Paranoia (Pa: 68.76), indicating somatic symptoms, depressive features, and suspiciousness. The POMS showed increased Tension-Anxiety (T: 65.06), Depression-Dejection (D: 68.21), Anger-Hostility (A: 68.15), and Fatigue-Inertia (F: 65.24), alongside reduced Vigor-Activity (V: 43.18). The DMI analysis highlighted a high Reversal score (REV: 65.91), suggesting a predominant use of defense mechanisms such as altruism and idealization to cope with distress. Conclusions: In this selected sample of adults referred for psychological evaluation for suspected or documented workplace victimization, participants showed a clinically relevant psychological burden, including depressive symptoms, somatic concerns, Anger-Hostility, fatigue, reduced vigor, and specific defensive patterns. Given the cross-sectional design, small sample size, and absence of a control group, these findings should be interpreted as preliminary and cannot establish causality or the specificity of this profile to workplace victimization.
[This corrects the article DOI: 10.3892/ol.2021.12593.].
[This corrects the article DOI: 10.3892/ol.2021.13015.].