Background: This study aims to describe the factors associated with dysplastic changes in sinonasal inverted papilloma (SIP) including somatic EGFR mutation, FoxM1 expression, HPV status, and their association with dysplastic changes.
Methods: A cross-sectional, analytical study was conducted comprising 34 samples of histologically-confirmed diagnosis of SIP. The samples were further grouped into 2 groups: 20 samples without associated dysplastic changes, and 14 samples with associated dysplastic changes. The numbers of FoxM1 positively-expressed cells, EGFR mutation, and HPV status were compared among two groups using appropriate comparative statistics.
Results: There was statistically-significant difference of FoxM1 expression between SIP and SIP with dysplasia (10% vs 100%; p<0.001). EGFR mutation was identified in 6 samples (30.0%) of the SIP and 5 samples (35.7%) of SIP with dysplasia. No difference of EGFR mutant proportion among two groups. HPV DNA was detected in 5 samples (25.0%) of SIP versus 9 samples (64.3%) of SIP with dysplasia. There was significant difference of HPV status among two groups (p=0.022). The high-risk subtypes were found in most HPV positive samples (57.1%), while low-risk subtypes and out panel subtypes were found 14.3% and 21.4%, respectively.
Conclusions: FoxM1 was overexpressed in SIP with malignant transformation. FoxM1 along with HPV status is associated with dysplastic changes in the SIP. FoxM1 immunostaining is potential to be a biomarker of malignant transformation in SIP.
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http://dx.doi.org/10.31557/APJCP.2022.23.12.4293 | DOI Listing |
J Oral Biol Craniofac Res
January 2025
Centre of Molecular Medicine and Diagnostics (COMManD), Department of Biochemistry, Saveetha Dental College and Hospitals, Saveetha Institute of Medical and Technical Sciences, Saveetha University, Chennai, 600077, India.
Objective: This study explores the role of MALAT1 as a valuable target for creating minimally-invasive diagnostic methods and personalized treatments in the management of OSCC. It focuses on evaluating the role of exosomal MALAT1 in the progression of dysplasia to OSCC by influencing the PI3K/AKT pathway.
Method: This cross-sectional study evaluated MALAT1 expression and PI3K/AKT pathway components in exosomes derived from plasma samples of patients with various stages of oral dysplasia, OSCC and compared with normal.
Am J Sports Med
January 2025
Department of Orthopaedics, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, USA.
Background: Trochlear dysplasia is a consistent risk factor for recurrent patellofemoral instability (PFI), but there is limited understanding of how the trochlea develops during growth. The aim of this study was to evaluate serial magnetic resonance imaging (MRI) studies performed in skeletally immature patients with and without PFI to characterize changes in trochlear anatomy over time.
Hypothesis: PFI leads to progressive worsening of trochlear dysplasia over time.
J Am Soc Nephrol
January 2025
Renal Division, Department of Internal Medicine, Xin Hua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200092, China.
Background: Many congenital anomalies of the kidney and urinary tract involve deficits in the number of nephrons, which are associated with a higher risk of hypertension and chronic kidney disease later in life. Prior work has implicated histone modifications in regulating kidney lineage-specific gene transcription and nephron endowment. Our earlier study suggested that ASH2L, a core subunit of the H3K4 methyltransferase complex, plays a role in ureteric bud morphogenesis during mammalian kidney development.
View Article and Find Full Text PDFBiomedicines
December 2024
Department of Oral and Maxillofacial Clinical Sciences, Faculty of Dentistry, Universiti Malaya, Kuala Lumpur 50603, Malaysia.
Oral potentially malignant disorders (OPMD) are a group of lesions carrying the risk of developing into cancer. The gold standard to predict which lesions are more likely to undergo malignant transformation is the presence of dysplasia histologically. However, not all dysplastic lesions progress, and non-dysplastic lesions may also undergo malignant transformation.
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