Objective: This study aimed to determine whether microvessel density (MVD) in the tumor tissues could be a potential predictive marker for vascular invasion (VI).
Methods: Surgical specimens of 73 patients with colorectal adenocarcinoma in Phramongkutklao Hospital were analyzed. Tissues of patients receiving preoperative radiation or prior anti-angiogenic therapy were excluded. Tumor MVD was determined using the average number of counted CD34-stained endothelial cells from two selected fields at 200x magnification in each slide. The presence of VI was defined by tumor involvement of endothelial cell-lined spaces. The optimal cut-off value of MVD to predict VI was examined using receiver operating characteristic analysis to assess the area under the curve and accuracy.
Result: VI was detected in 17 of 73 specimens (23.3%). Colorectal cancer (CRC) specimens were classified according to MVD as low (61 specimens, 83.6%) and high density (12 specimens, 16.4%). Average MVD was slightly higher in specimens with VI (81.3±9.3) than those without VI (76.3±7.6), but without statistical significance (p = 0.736). The MVD's cut-off value of 60 vessels/200x field provided 88% sensitivity, 40% specificity, and 57.5% accuracy, with the area under the ROC curve of 0.5788. Patients with CRC having MVD of > 60 vessels/200x field were at significantly higher risk of VI than those with CRC having MVD of <60 vessels/200x field (P=0.009, Fisher's exact test). Univariate analysis revealed that MVD, nodal involvement and AJCC tumor stage were associated with the presence of VI (p <0.05). Further multivariate analysis of these three potential variables demonstrated MVD (OR, 11.994; 95% CI, 2.197 to 65.483; p <0.01) and nodal involvement (OR, 10.767; 95% CI, 1.973 to 58.748; p <0.05) as independent prognostic factors associated with VI.
Conclusion: Based on our study, MVD immunostaining was an angiogenic marker that potentially be a predictive marker for VI.
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http://dx.doi.org/10.31557/APJCP.2023.24.12.4097 | DOI Listing |
Crit Care
January 2025
División de Terapia Intensiva, Hospital Juan A. Fernández, Buenos Aires, Argentina.
The advancements in cardiovascular imaging over the past two decades have been significant. The miniaturization of ultrasound devices has greatly contributed to their widespread adoption in operating rooms and intensive care units. The integration of AI-enabled tools has further transformed the field by simplifying echocardiographic evaluations and enhancing the reproducibility of hemodynamic measurements, even for less experienced operators.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Background: Cerebral small vessel disease (CSVD), which includes cerebral amyloid angiopathy (CAA) and arteriolosclerosis, often co-occurs with Alzheimer's disease (AD) pathology. The medial temporal lobe (MTL) is susceptible to hosting multiple AD pathologies, such as neurofibrillary tangles (NFTs), amyloid-β plaques, phospho-Tar-DNA-Binding-Protein-43 (pTDP-43), as well as CSVD. Whether a causal relationship between these pathologies exists remains largely unknown, but one potential linking mechanism is the dysfunction of perivascular clearance.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
University of Buenos Aires, Buenos Aires, Argentina.
Background: Alzheimer's disease is characterized by the accumulation of aggregated amyloid peptides in the brain parenchyma and in the walls of brain vessels. The hippocampus - a complex brain structure that plays a key role in learning and memory - has been implicated in the disease. However, there is limited data on vascular changes during the pathological degeneration of Alzheimer's disease in this vulnerable structure, which has distinctive vascular features.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
J. Philip Kistler Stroke Research Center, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Background: Alzheimer's disease (AD) related pathologies (i.e., neurofibrillary tangles [NFTs], amyloid-β plaques, and phosphorylated-TAR-DNA-binding-protein-43 [pTDP-43]) differ across sexes.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Alzheimer's Center at Lewis Katz School of Medicine, Temple University, Philadelphia, PA, USA.
Background: Recent evidence suggests that cerebrovascular dysfunction may precede and contribute to amyloid beta-(Aβ)-mediated pathology in Alzheimer's Disease (AD), particularly promoting endothelial cell damage and stress, causing the cerebral blood flow impairments, cerebral hypoperfusion, and blood brain barrier (BBB) permeability that are pathologically characteristic in AD. Studies have emerged suggesting a link between cardiovascular diseases and AD pathology, showing that cerebrovascular/cardiovascular risk factors (CVRFs), including hyperhomocysteinemia (Hhcy) and hypertension (HTN), and the cerebral consequences of these CVRFs, such as cerebral hypoperfusion, contribute to AD pathology and risk. Despite this, the underlying molecular mechanisms for these associations remain unclear.
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