Seetu Palo

Choriocarcinoma, a rare yet highly aggressive gestational trophoblastic neoplasia, is uniquely responsive to chemotherapy. The serum marker β-human chorionic gonadotropin (β- hCG) has long been central to its diagnosis and monitoring, but not without limitations. Persistent false positives, poor specificity for residual disease or resistance, and slow detection of relapse are a few to mention. Advances in precision oncology have introduced novel biomarkers, such as ctDNA, circulating tumor cells (CTCs), exosomes, miRNAs, and exosomal miRNAs, that promise improved specificity, early relapse detection, and personalized monitoring. This review encapsulates the current landscape of emerging biomarkers in choriocarcinoma, categorizes them by methodological class and clinical utility, discusses integration challenges, and outlines future research directions toward multi-marker precision diagnostics.

Alopecia, a prevalent and distressing condition with diverse aetiologies, encompasses both scarring and non-scarring types and necessitates accurate diagnostic approaches for effective management. Apart from optimal biopsy site selection based on clinical suspicion, such as active borders for scarring alopecias and lesion borders for non-scarring alopecias, choice of appropriate method for grossing of alopecic scalp biopsies also forms a key step. Historically, debates on ‘One (biopsy) Vs Two (biopsies)’ and ‘Vertical/Longitudinal Vs Horizontal/Transverse’ sections persist, each approach carrying its advantages and disadvantages. Traditional methods, such as those proposed by Headington and Whiting, describe the landmarks for slicing a biopsy for transverse section. Newer innovative strategies, including the HoVert technique and the Tyler technique, aim to obtain both vertical and horizontal sections from a single biopsy. This article meticulously presents all the methodologies employed in the grossing of alopecic scalp biopsies in a simplified manner, presents a comprehensive overview of their strengths and limitations, and offers evidence-based recommendation for choosing optimal grossing techniques based on clinical scenarios.

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Purpose: Human papillomavirus is the dominant etiological factor underlying atypical cervical squamous epithelial cell abnormalities and cervical carcinoma. Currently, only a limited number of drugs targeting specific biomarkers in cervical cancer are available. This study aimed to assess the expression of estrogen receptor (ER), human epidermal growth factor receptor 2 (HER2), and the Ki-67 proliferative index (Ki-67) in p16-positive cervical squamous premalignant and malignant lesions, which may help clarify the potential role of targeted therapies in cervical cancer.Methods: In p16-positive, histologically proven premalignant and malignant cervical lesions, ER, HER2, and Ki-67 expression were evaluated according to predefined criteria.Results: p16 showed strong nuclear and cytoplasmic positivity in 54 of 56 cases. Patchy nuclear positivity was mainly observed in low-grade squamous intraepithelial lesion (LSIL) cases (2/56). Ki-67 demonstrated a variable proliferative index ranging from 5% to 95% across all cases, with higher indices predominantly observed in squamous cell carcinomas (SCC). ER positivity in LSIL, high-grade squamous intraepithelial lesion, and SCC was 100% (2/2), 66.7% (10/15), and 46.15% (18/39), respectively. HER2 expression was predominantly negative, observed in 78.6% (44/56) of cases, equivocal in 17.8% (10/56), and positive in 3.6% (2/56). Both HER2-positive cases were SCC. ER and HER2 interpretations were analyzed and were not significantly correlated with clinical or pathological parameters.Conclusion: ER positivity decreased with progression of cervical squamous lesions, and HER2 expression was rare in cervical squamous neoplasia. No statistically significant correlation was identified between ER or HER2 expression and clinicopathological parameters. The findings of the current study may help fill gaps in the existing literature and provide essential foundational knowledge for optimizing emerging therapeutic strategies, including ER- and HER2-related therapies.

ObjectiveDysregulation of leukocyte cell number as a cause of heavy menstrual bleeding (HMB) has not been investigated much. The present study compares the changes in the number of uterine natural killer (uNK) cells, T cells, and macrophages in endometrial samples from women with normal menstrual cycles versus those with HMB.MethodsWe analyzed endometrial tissue from 98 patients (73 with HMB; 25 with normal cycles) using immunohistochemistry to semi-quantitatively estimate the degree of cluster of differentiation (CD)56+, CD8+, CD4+, and CD68+ cell infiltration.ResultsNo statistically significant differences were observed in the CD4+, CD8+, CD56+, or CD68+ cell counts between women with HMB and controls during either the proliferative or secretory phases of the menstrual cycle. CD56+ natural killer cells were relatively reduced in the HMB group during the proliferative phase, with higher counts in the control group (P=0.071). CD68+ macrophages/high-power field (hpf) showed a strong positive correlation with CD4+ T cells (r, 0.481; P<0.001), CD8+ T cells (r, 0.641; P<0.001), and CD56+ uNK cells (r, 0.404; P<0.001). CD8+ cells/hpf demonstrated a significant positive correlation with uterine volume, CD4+ cells/hpf, CD68+ cells/hpf, and CD56+ cells/hpf.ConclusionAlthough no single immune cell type was independently associated with HMB compared with controls, the observed significant correlations among CD4+, CD8+, CD56+, and CD68+ highlight the interconnected nature of endometrial immune activity.

Choriocarcinoma, a highly malignant variant of gestational trophoblastic neoplasia, is characterized by rapid proliferation, hematogenous dissemination, and excessive secretion of human chorionic gona

The human placenta is the nexus of maternal–fetal exchange, with its function reflected in histological features such as syncytial knots. These nuclear aggregations within the syncytiotrophoblast, historically termed Tenney–Parker changes when excessive, serve as critical markers of both placental maturation and maladaptation. This narrative review synthesizes the current understanding of their structural, ultrastructural, and molecular features, emphasizing the biological significance of the syncytial knot index as a quantitative marker of placental function. The syncytial knot index rises progressively with gestation but increases prematurely in conditions such as preeclampsia, fetal growth restriction, maternal vascular malperfusion, and chronic hypoxia, reflecting accelerated syncytiotrophoblast aging and oxidative injury. This review also highlights the mechanistic pathways – apoptosis, senescence, hypoxia-driven signaling, and disturbed trophoblast turnover – that determine knot formation. Emerging evidence on syncytiotrophoblast-derived microparticles illustrates their potential role in mediating maternal endothelial dysfunction and systemic manifestations of placental disease. Despite its diagnostic value, the syncytial knot index remains underutilized due to methodological variability; however, digital pathology, stereology, and 3D imaging now offer promising avenues for standardized assessment.