Despite rigorous evidence of improved quality of life and longer survival, disparities in the utilization of palliative and hospice care persist for racial and ethnic minority patients with cancer. This study evaluated the impact of psychosocial factors on utilization of these services.
Patients with advanced lung cancer were recruited at a large academic urban hospital. Patients were surveyed about their knowledge of palliative care and hospice and their beliefs regarding medical mistrust, lung cancer care, palliative care and hospice. We used univariate and multivariable logistic regression analyses to examine the association between mistrust, knowledge and beliefs among the entire cohort and minority (Black and Hispanic) and non-minority patients on utilization of palliative care consultation and hospice care use.
Ninety-nine of the enrolled participants had a mean age of 64 years. Minority patients were more likely to receive a palliative care referral (p < 0.001) and attend a consult (p = 0.003). Similarly, they were more likely to receive a hospice referral (p = 0.04), however there was no difference in hospice care use based on minority status (p = 0.102). In our adjusted model, older patients and those reporting negative lung cancer beliefs were more likely to receive hospice care (OR: 1.06, 95% CI: 1.004–1.138; OR: 1.04, 95% CI: 1.002–1.093, respectively).
Minority patients with advanced lung cancer were more likely to receive a palliative care referral and specialty level consultation when compared to non-minority patients. Our work highlights the importance of proactive referral processes in facilitating access to palliative and hospice services, particularly among younger patients.
Gastric cancer (GC) is an important cause of death. Molecular targeted therapy and immunotherapy are progressing rapidly. It is very important to explore the pathogenesis pathways of GC and provide strong support for its treatment. However, the mechanism of occurrence and development of GC is still unclear.
Online databases and immunohistochemistry (IHC) of clinical samples were used to analyze the differential expression of YTHDF1 in the GC and nearby tissues, and its effect on survival prognosis. In vitro experimental study of GC, other mechanisms and functional analyses were specifically designed and performed too.
Online data and clinical samples analysis showed that the expression of YTHDF1 in GC was markedly elevated compared to surrounding tissues. Higher YTHDF1 levels were correlated with worse survival outcomes. Analysis of correlation with clinical parameters showed that the expression level of YTHDF1 exhibited a favorable correlation with lymphatic metastases, as well as with PD-1 and PD-L1 levels. In vitro studies of YTHDF1 overexpression have demonstrated its ability to enhance GC cell growth and migration while inhibiting apoptosis. Based on our results, RELA is a downstream target of YTHDF1, and YTHDF1 triggers the NF-κB signaling pathway by regulating RELA translation.
In comparison to adjacent tissues, GC exhibits significantly elevated YTHDF1 expression. Increased YTHDF1 expression in the GC is correlated with decreased patient survival. Lymph node metastasis and the expression of PD-1 and PD-L1 are positively correlated with YTHDF1 levels. YTHDF1 inhibits apoptosis while promoting the migration and proliferation of GC. Additionally, it stimulates the NF-κB pathway and controls the translation of RELA.
To assess how centralisation of cancer services via robotic surgery influenced positive surgical margin (PSM) occurrence and its associated risk of biochemical recurrence (BCR) in cases of pT2 prostate cancer (PC).
Retrospective analysis of all radical prostatectomy (RP) cases performed in the West of Scotland during the period from January 2013 to June 2022. Primary outcomes were PSM and BCR. The secondary outcomes compared the impact of centralisation and surgical approach on PSM and BCR; and margin length and location on BCR. Propensity score matching and Cox regression models were performed using R.
A total of, 907 patients were included; 662 robot assisted radical prostatectomy (RARP), 245 open RP. PSM rate was 17.7% (161/907), similar in RARP and open cohorts. Patients with PSM had higher rates of BCR; 26.7%, compared to 8.7% in patients with no PSM. Patients with margins of ≥ 1 mm had higher risk of developing BCR. Patients who underwent open RP had increased incidence of PSM ≥ 1 mm; 40/43 (93%) compared to 83/117 (71%) in robotic approach (p = 0.003). Limitations include the study being retrospective, introduction of centralisation and robot concurrently, and evolution of practice.
PSMs in pT2 PC are associated with higher rates of BCR. Introduction of centralisation via the robot had no impact on PSM occurrence or BCR, although did demonstrate a reduction in PSM length.
Esophageal squamous cell carcinoma (ESCC) is one of the most prevalent and lethal malignancies worldwide. Despite progress in immunotherapy for cancer treatment, its application and efficacy in ESCC remain limited. Therefore, there is an ongoing need to explore potential molecules and therapeutic strategies related to tumor immunity in ESCC.
In this study, we integrated high-throughput sequencing data, gene chip data, single-cell sequencing data, and various bioinformatics analysis methods along with experimental approaches to identify key genes involved in immune infiltration in ESCC and investigate their relationship with immune cell development, as well as the potential of these key genes in immunotherapy.
We discovered and validated a positive correlation between macrophage infiltration and ITGB2 expression in ESCC. ITGB2 is overexpressed in ESCC and has potential as a prognostic biomarker for the disease. We present for the first time the finding that the expression of ITGB2 in infiltrating macrophages increases as these macrophages polarize toward a tumor-promoting phenotype in ESCC. Moreover, during the progression of ESCC, ITGB2 expression in infiltrating macrophages is upregulated. The higher the expression of ITGB2, the more feasible it is to target macrophages. Additionally, we found that evaluating immune therapy responses in ESCC patients through ITGB2 expression is a viable approach. Furthermore, we identified three miRNAs associated with abnormal ITGB2 expression, providing insights into the upstream molecular interactions of ITGB2.
Macrophage infiltration in ESCC is closely associated with ITGB2, which holds significant potential for immunotherapy applications in ESCC. Based on our findings and prior studies, we propose a novel hypothesis: inducing M1 macrophages in vitro, knocking out ITGB2, and then reinfusing these ITGB2-knockout M1 macrophages into ESCC patients may represent a promising new immunotherapy strategy, providing a new avenue for ESCC immunotherapy.
This study aimed to identify prognostic factors and develop a nomogram for survival in patients with brainstem ependymoma.
Data of 652 patients diagnosed with brainstem ependymoma extracted from the Surveillance, Epidemiology, and End Results (SEER) registry from 2000 to 2020 were analyzed. Univariate and multivariable Cox regression analyses were performed to examine factors influencing overall survival (OS). Receiver operating characteristic curve (ROC) and calibration curves were used to verify the nomogram. The Kaplan–Meier method was used to analyze OS based on treatment methods stratification or different age patterns.
Six independent prognostic factors of patients with brainstem ependymoma were identified, including age, race, marital status, radiation, gross total resection (GTR), and histology. A comprehensive nomogram model was developed utilizing these predictors identified through multivariable Cox regression analysis. Furthermore, we found that patients with GTR have improved overall survival than patient with no surgery and biopsy only or with partial resection (GTR vs. no: p = 0.0004, GTR vs. partial resection: p = 0.022). Patients with radiation have improved overall survival than patient without radiation (p = 0.00013). Patients with GTR combined radiation therapy have improved overall survival than patient without or with GTR or radiation therapy only (p < 0.0001). Different treatment methods have no significant difference in the overall survival probability of the elderly group.
Individuals who are Black and anaplastic ependymomas were negative risk factors for brainstem ependymoma associated with an increased risk of mortality. Patients aged < 50 years with GTR and radiation always had better survival.
Gamma-glutamyl transferase (GGT) has been shown to have associations with several diseases including cancers. Previous studies have investigated the effect of GGT levels on the gastrointestinal (GI) cancer incidence. We aim to systematically investigate these studies to provide better insights into the interrelationship between GGT and GI cancers.
Online databases were searched to find relevant studies investigating different GGT levels' effects on the incidence of GI cancers including colorectal, esophageal, liver, pancreas, gastric, and biliary duct cancers. Random-effect meta-analysis was conducted to pool the hazard ratios (HRs) of GGT quartiles (Qs) effect on cancer incidence.
A total of 26 studies were included in the final review, 12 of which underwent meta-analysis that investigated 11 million patients. Based on the meta-analysis, Q4 patients had a 69% higher hazard of GI cancer incidence (HR 1.69, 95% CI 1.41–2.02, p-value < 0.001). The hazard ratio significance was also similar for Q3 (HR 1.22, 95% CI 1.15–1.30, p-value < 0.001) and Q2 (HR 1.10, 95% CI 1.05–1.16, p-value =0.002) of GGT. Colorectal and liver cancers showed a higher hazard ratio among Q2, Q3, and Q4 of GGT compared to Q1. In pancreas and bile duct cancers, only Q4 of GGT had significantly higher HR. Q3 and Q4 of GGT levels had statistically significant associations with gastric cancer incidence.
Higher GGT levels correlate with higher rates of GI cancer incidence, especially in colorectal and hepatic cancers. Future studies should investigate this biomarker's potential role in risk assessment for digestive cancers.
The use of digital health strategies for cancer care increased dramatically in the United States over the past 4 years. However, a dearth of knowledge remains about the use of digital health for cancer prevention for some populations with heath disparities. Therefore, the purpose of the present scoping review was to identify digital health interventions for cancer prevention designed for people with disabilities.
This scoping review was guided by the Preferred Reporting Items for Systematic Reviews and Meta-Analyses extension for scoping reviews and the Arksey and O'Malley methodological framework. The Embase, PubMed, Ovid MEDLINE, and CINAHL/EBSCO databases were searched for peer-reviewed articles published from database inception to February 5, 2024. Reports published in English of studies that employed digital health strategies for cancer prevention, were conducted among people with disabilities regardless of age, and were conducted in the United States were included.
Following screening for eligibility, seven articles were identified. The types of disabilities were cancer (n = 4), bipolar I or II disorder (n = 1), obesity (n = 1), and deafness (n = 1). Interventions focused on education (n = 4), screening (n = 3), smoking cessation (n = 3), physical activity (n = 1), and cessation support (n = 1). Digital health strategies consisted of educational content delivered online, text messaging, interactive educational games, and downloadable informational applications. The common outcome of interest across all manuscripts was intervention efficacy.
Overall, limited research is available to evaluate the use of digital health for cancer prevention among people with disabilities. This review identified gaps in knowledge that, if addressed, may help guide continued innovation in the use of digital health strategies for cancer prevention among people with disabilities.
Lymphatic metastasis in gastric cancer (GC) profoundly influences its prognosis, but the precise mechanism remains elusive. In this study, we identified the long noncoding RNA MIR181A2HG as being upregulated in GC and associated with LNs metastasis and prognosis.
The expression of MIR181A2HG in GC was identified through bioinformatics screening analysis and qRT-PCR validation. Both in vitro and in vivo functional studies revealed that MIR181A2HG facilitates lymphangiogenesis and lymphatic metastasis. Techniques such as immunofluorescence, immunohistochemistry, qRT-PCR, ELISA, CHIP, RNA-pulldown, luciferase reporter assay, and Co-IP were employed to investigate the mechanism of MIR181A2HG in LNs metastasis of GC.
MIR181A2HG overexpressed in GC signifies an unfavorable prognosis and drives M2 polarization of TAMs enhancing lymphangiogenesis. Mechanistically, MIR181A2HG/miR-5680 axis as a novel ceRNA regulatory axis to upregulate versican (VCAN). On one hand, VCAN interacts with CD44 receptors on the surface of TAMs through paracrine secretion, promoting M2 macrophage polarization and subsequently enhancing the secretion of VEGF-C, ultimately facilitating lymphangiogenesis. On the other hand, VCAN binds to CD44 receptors on the surface of GC cells through autocrine secretion, activating the Hippo pathway and upregulating SP1, thereby promoting the transcription of MIR181A2HG and establishing a feedback loop driving lymphatic metastasis.
This study highlights the pivotal role of MIR181A2HG in GC progression and LNs metastasis. MIR181A2HG-based targeted therapy would represent a novel strategy for GC.
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