Objective: Bladder cancer is a genitourinary disease of increasing incidence. Despite improvements in treatment, outcomes remain equivocal with high recurrence rates. It is associated with poor psychosocial outcomes due to reduced functioning of the genitourinary system. The objective of these analyses was to query whether reported loss of function or the perception of psychological burden caused by this functional impedance was the key to understanding psychosocial outcomes.
Methods: The sample comprised 119 participants with a confirmed diagnosis of bladder cancer. They completed a self-report questionnaire comprising the Bladder Cancer Index, Mini-mental Adjustment to Cancer Scale, Psychosocial Adjustment to Illness Scale and standard sociodemographic details. Simple mediation and serial mediation were used to explore the potential for psychological burden to mediate associations between loss of function and cognitive distress, and the potential additional contribution of positive partner support on these relationships. Age and duration of cancer were considered as covariates.
Results: Simple mediation demonstrated that the association between function and cognitive distress was fully mediated by perceived psychological burden. Serial mediation, which allowed for the addition of partner support, again demonstrated full mediation, with partner support being the key predictive variable.
Conclusions: These analyses emphasise the importance of an appreciation of individuals' interpretation of the burden occasioned by bladder cancer and the role of a supportive partner. The implications for management discussions and support services in alleviating negative psychological outcomes in bladder cancer are highlighted. Copyright © 2015 John Wiley & Sons, Ltd.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1002/pon.4054 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
YWHAG promotes bladder cancer metastasis by regulating TMOD3 to activate ERK1/2 and JNK phosphorylation in the MAPK pathway.
J Transl Med
December 2024
Department of Urology, Peking University First Hospital, Beijing Key Laboratory of Urogenital Diseases (Male) Molecular Diagnosis and Treatment Center, Beijing, 100034, China.
Objective: This study aims to investigate the molecular mechanisms by which YWHAG (Tyrosine 3-Monooxygenase/Tryptophan 5-Monooxygenase Activation Protein Gamma) promotes metastasis in bladder cancer. Specifically, it seeks to elucidate the role of YWHAG in driving cancer cell invasion and its potential as a prognostic marker for bladder cancer progression.
Methods: The expression pattern of YWHAG in both primary and metastatic bladder cancer tissues was analyzed using immunohistochemistry (IHC) to determine its correlation with clinical stage and prognosis in bladder cancer patients.
Programmed cell death 1 inhibitor alone or combined with chemotherapy for patients with locally advanced or metastatic urothelial carcinoma: a single-center experience.
BMC Urol
December 2024
Department of Radiation Oncology, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, 310003, China.
Background: Immune checkpoint inhibitors (ICIs) alone or in combination with standard chemotherapy for advanced urothelial carcinoma (UC) have been tested as first-line treatment in clinical trials. This study aimed to evaluate the clinical outcomes of programmed cell death 1 (PD-1) inhibitor alone or combined with chemotherapy for patients with locally advanced or metastatic UC in a real world clinical care setting, and sought to identify prognostic factors for overall survival (OS).
Methods: A retrospective, real-world study involving 35 locally advanced or metastatic UC patients treated with PD-1 inhibitor alone or in combination with chemotherapy was conducted.
Loss of YTHDC1 mA reading function promotes invasiveness in urothelial carcinoma of the bladder.
Exp Mol Med
January 2025
Division of Epigenetics, DKFZ-ZMBH Alliance, German Cancer Research Center, 69120, Heidelberg, Germany.
Bladder cancer poses significant clinical challenges due to its high metastatic potential and poor prognosis, especially when it progresses to muscle-invasive stages. Here, we show that the mA reader YTHDC1 is downregulated in muscle-invasive bladder cancer and is negatively correlated with the expression of epithelial‒mesenchymal transition genes. The functional inhibition or depletion of YTHDC1 increased the migration and invasion of urothelial cells.
View Article and Find Full Text PDFAnesthetic approaches and 2-year recurrence rates in non-muscle invasive bladder cancer: a randomized clinical trial.
Reg Anesth Pain Med
December 2024
Department of Urology, Seoul National University Hospital, Seoul National University College of Medicine, Seoul, South Korea
Background: The effect of anesthesia methods on non-muscle invasive bladder cancer (NMIBC) recurrence post-resection remains uncertain. We aimed to compare the oncological outcomes of spinal anesthesia (SA) and general anesthesia (GA) in patients with NMIBC.
Methods: This prospective randomized controlled trial recruited 287 patients with clinical NMIBC at Seoul National University Hospital from 2018 to 2020.
The Relationship of Metabolic Activity and αvβ3 Receptor Expression in Aggressive Breast Cancer Subtypes Tumors: A Preliminary Report.
In Vivo
December 2024
Gyula Petrányi Doctoral School of Clinical Immunology and Allergology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Background/aim: Angiogenesis imaging has been a valuable complement to metabolic imaging with 2-deoxy-2-[F]fluoroglucose (FDG). In our longitudinal study, we investigated the tumour heterogeneity and the relationship between FDG and [Ga]Ga-NODAGA-c(RGDfK) (RGD) accumulation in breast cancer xenografts.
Materials And Methods: Two groups of cell lines, a fast-growing (4T1) and a slow-growing cell line (MDA-MB-HER2+), were inoculated into SCID mice.
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!