Vascular diseases (VDs) including pulmonary arterial hypertension (PAH), atherosclerosis (AS) and coronary arterial diseases (CADs) contribute to the higher morbidity and mortality worldwide. ...Apolipoprotein A-I (Apo A-I) binding protein (AIBP) and Apo-AI negatively correlate with VDs. However, the mechanism by which AIBP and apo-AI regulate VDs still remains unexplained. Here, we provide an overview of the role of AIBP and apo-AI regulation of vascular diseases molecular mechanisms such as vascular energy homeostasis imbalance, oxidative and endoplasmic reticulum stress and inflammation in VDs. In addition, the role of AIBP and apo-AI in endothelial cells (ECs), vascular smooth muscle (VSMCs) and immune cells activation in the pathogenesis of VDs are explained. The in-depth understanding of AIBP and apo-AI function in the vascular system may lead to the discovery of VDs therapy.
•Stimulants such as oxidation and endoplasmice stress, DNA damage, epigenetic modification, etc., stimulate.•Stress response, classical senescence proteins, CCHOP, calcineurin/CaMKII, etc.,•Promoting ...senescence and dead cells accumulation, endocardium remodeling.•Accelerating contractile dysfunction, impaired left ventricular ejection fraction and HF in aging population.•However, attenuating senescence and dead cell retention prevents cardiac aging and HF development.
Heart failure (HF) remains one of the major causes of morbidity and mortality worldwide. Recent studies have shown that stem cells (SCs) including bone marrow mesenchymal stem (BMSC), embryonic ...bodies (EB), embryonic stem (ESC), human induced pluripotent stem (hiPSC)-derived cardiac cells generation, and transplantation treated myocardial infarction (MI) in vivo and in human. However, the immature phenotypes compromise their clinical application requiring immediate intervention to improve stem-derived cardiac cell (S-CCs) maturation. Recently, an unbiased multi-omic analysis involving genomics, transcriptomics, epigenomics, proteomics, and metabolomics identified specific strategies for the generation of matured S-CCs that may enhance patients’ recovery processes upon transplantation. However, these strategies still remain undisclosed. Here, we summarize the recently discovered strategies for the matured S-CC generation. In addition, cardiac patch formation and transplantation that accelerated HF recuperation in clinical trials are discussed. A better understanding of this work may lead to efficient generation of matured S-CCs for regenerative medicine.
Graphical abstract
Background
Gastrointestinal extrapulmonary small cell carcinoma (GI EPSCCa) is a rare, aggressive neuroendocrine tumor. Factors affecting survival, including the prognostic significance of primary ...tumor site, remain under investigation.
Methods
Data from the surveillance, epidemiology, and end results (SEER) program were extracted to identify patients diagnosed with GI EPSCCa between 2000 and 2018. Cox proportional hazard models were used to assess prognostic factors based on primary tumor site.
Results
A total of 1687 patients were included in the survival analysis. The distribution of the primary tumor location was as follows: 31.5% colorectum (CRC), 22.1% esophageal, 20.6% pancreatic, 13.3% hepatobiliary (HB), 10.6% stomach, and 1.8% small intestine (SI). Esophagogastric and SI EPSCCa were more common among Black individuals, whereas CRC, HB, and pancreatic EPSCCa were more common among White patients (
p
= 0.012). There were no racial differences in OS for GI EPSCCa. HB EPSCCa was associated with inferior OS compared with esophageal tumors (adjusted hazard ratio aHR 1.21, 95% confidence interval CI 1.00–1.46;
p
= 0.048), and SI EPSCCa was associated with prolonged survival compared with esophageal EPSCCa (aHR 0.76, 95% CI 0.48–1.20;
p
= 0.237) but did not reach statistical significance. Surgical intervention and a treatment period after 2006 were associated with superior OS.
Conclusions
The prognosis for GI ESPCCa varies based on site. Chemotherapy, radiation, and surgical resection are associated with improved outcomes; however, the prognosis for patients with EPSCCa remains dismal. Prospective studies are needed to guide therapy for this aggressive tumor.
•Research on breast cancer stem cells has increased in the past two decades but racial comparative studies in this area remains scanty.•This is a racial comparative study of breast cancer stem cells ...and their association with clinicopathological features and clinical outcomes.•ALDH1 is the most researched breast cancer stem cell marker associated with poor clinicopathological features.•CD44+/CD24−/low has been associated with TNBC/Basal like phenotype across all races.
Breast Cancer Stem Cells has become the toast of many breast cancer investigators in the past two decades owing to their crucial roles in tumourigenesis, progression, differentiation, survival and chemoresistance. Despite the growing list of research data in this field, racial or ethnic comparison studies on these stem cells remain scanty. This study is a comparative racial analysis of putative breast cancer stem cells.
Research articles on the clinicopathological significance of breast cancer stem cells within a period of 17 years (2003–2020) were reviewed across 5 major races (African/Black American, Asian, Caucasian/White, Hispanic/Latino, and American). The associations between the stem cells markers (CD44+/CD24−/low, BMI1, ALDH1, CD133, and GD2) and clinicopathological and clinical outcomes were analysed.
A total of 40 studies were included in this study with 50% Asian, 25% Caucasian, 10% African, 5% American and 2.5% Hispanic/Latino, and 7.5% other mixed races. CD44+/CD24−/low has been associated with TNBC/Basal like phenotype across all races. It is generally associated with poor clinicopathological features such as age, tumour size, lymph node metastasis and lymphovascular invasion. In Asians, CD44+/CD24−/low was associated with DFS and OS but not in Caucasians. ALDH1 was the most studied breast CSC marker (40% of all studies on breast cancer stem cell markers) also associated with poor clinicopathological features including size, age, stage, lymph node metastasis and Nottingham Prognostic Index. ALDH1 was also associated with DFS and OS in Asians but not Caucasians.
Racial variations exist in breast cancer stem cell pattern and functions but ill-defined due to multiple factors. Further research is required to better understand the role of breast CSC.
Background
Severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) and the coronavirus 19 (COVID‐19) pandemic have had a lasting impact on the care of cancer patients. The impact on patients ...with gastrointestinal (GI) malignancies remains incompletely understood. We aimed to assess the impact of COVID‐19 on mortality, length of stay (LOS), and cost of care among patients with GI malignancies, and identify differences in outcomes based on primary tumor site.
Methods
We analyzed discharge encounters collected from the National Inpatient Sample (NIS) between March 2020 and December 2020 using propensity score matching (PSM) and COVID‐19 as the treatment effect.
Results
Of the 87,684 patient discharges with GI malignancies, 1892 were positive for COVID‐19 (C+) and eligible for matching in the PSM model. Following PSM analysis, C+ with GI tumors demonstrated increased incidence of mortality compared to their COVID‐19‐negative (C‐) counterparts (21.3% vs. 11.9%, p < 0.001). C+ patients with colorectal cancer (CRC) had significantly higher mortality compared to those who were C‐ (40% vs. 24%; p = 0.035). In addition, C+ patients with GI tumors had a longer mean LOS (9.4 days vs. 6.9 days; p < 0.001) and increased cost of care ($26,048.29 vs. $21,625.2; p = 0.001) compared to C‐ patients. C+ patients also had higher odds of mortality secondary to myocardial infarction relative to C‐ patients (OR = 3.54, p = 0.001).
Conclusions
C+ patients with GI tumors face approximately double the odds of mortality, increased LOS, and increased cost of care compared to their C‐ counterparts. Outcome disparities were most pronounced among patients with CRC.
Background and Objectives
Colorectal cancer (CRC) sidedness is recognized as a prognostic factor for survival; left‐sided colorectal cancer is associated with better outcomes than right‐sided colon ...cancer (RsCC). We aimed to evaluate the influence of obesity on CRC sidedness and determine how race, age, and sex affect mortality among overweight and obese individuals.
Methods
A survey‐weighted analysis was conducted using data obtained from the National Inpatient Sample between 2016 and 2019.
Results
Of the 24 549 patients with a diagnosis of CRC and a reported body mass index (BMI), 13.6% were overweight and 49.9% were obese. The race distribution was predominantly non‐Hispanic Whites (69.7%), followed by Black (15.6%), Hispanic (8.7%), and other race (6.1%). Overweight (BMI: 25−29.9) and obese (BMI: ≥30) individuals were more likely to have RsCC (adjusted OR aOR = 1.28; 95% CI: 1.17−1.39, p < 0.001 and aOR = 1.45; 95% CI: 1.37−1.54, p < 0.001, respectively). Obese Black individuals were more likely to have RsCC as compared to their White counterparts (aOR = 1.23; 95% CI: 1.09−1.38).
Conclusions
Obesity is associated with an increased risk of RsCC. In addition, racial disparities in CRC sidedness and outcomes are most pronounced among obese patients.
Early-onset pancreatic cancer (EOPC) - defined as pancreatic cancer diagnosed before the age of 50 years - is associated with a poor prognosis as compared to later-onset pancreatic cancer (LOPC). ...Emerging evidence suggests that EOPC may exhibit a genetic signature and tumor biology that is distinct from that of LOPC. We review genetic mutations that are more prevalent in EOPC relative to LOPC and discuss the potential impact of these mutations on treatment and survival.
Using PubMed and Medline, the following terms were searched and relevant citations assessed: "early onset pancreatic cancer," "late onset pancreatic cancer," "pancreatic cancer," "pancreatic cancer genes," and "pancreatic cancer targeted therapy."
Mutations in
,
, and
are significantly more common in EOPC as compared to LOPC. In addition, limited data suggest that
mutations are more frequently observed in EOPC as compared to LOPC. KRAS mutations are relatively rare in EOPC.
Genetic mutations associated with EOPC are distinct from those of LOPC. The preponderance of the evidence suggest that poor outcomes in EOPC are related both to advanced stage of presentation and unique tumor biology. The molecular and genetic features of EOPC warrant further investigation in order to optimize management.
