Background Preterm delivery (PTD) has been a significant cause of neonatal morbidity and mortality. Maternal serum ferritin, a biomarker of both iron stores and systemic inflammation, has shown inconsistent associations with PTD risk in individual studies. Objective This systematic review and meta-analysis aimed to clarify the relationship between maternal serum ferritin levels and the risk of PTD. Methods Following the PRISMA guidelines, we searched PubMed, Scopus, Web of Science, and Google Scholar up to August 2025. Twenty-four observational studies with more than 10000 participants were included. Pooled standardized mean differences (SMDs) and odds ratios (ORs) were calculated using random-effects models. The ROBINS-1 tool was used to assess the quality of the studies and the risk of bias. Results Ferritin levels were significantly higher in pregnancies ending in PTD (random-effects SMD 0.82, 95% CI 0.28-1.36; I 2 = 97.3%), with the strongest association observed in the second trimester (SMD 1.18, 95% CI 0.74-1.63). No independent predictive role for ferritin was shown (random-effects OR 1.05, 95% CI 0.97-1.13). High heterogeneity and evidence of publication bias were noted. Hemoglobin levels did not differ between groups. Conclusion Elevated levels of maternal serum ferritin, especially during the second trimester, are linked to PTD. However, the adjusted OR estimates have not shown statistical significance. There is considerable variability among the studies and a risk of bias that warrants cautious interpretation. Additionally, the diagnostic thresholds reported differ greatly and lack sufficient validation for clinical application. It is essential to conduct standardized prospective studies before ferritin-based clinical decision-making can be endorsed.

Background: Cluster of differentiation 15 (CD15) is a carbohydrate epitope implicated in cell adhesion, migration, and tumor progression. It is variably expressed in thyroid carcinoma (TC) subtypes. However, its diagnostic and prognostic value remains uncertain due to methodological heterogeneity and inconsistent findings. Aim: To systematically review the prevalence, clinicopathologic associations, and diagnostic utility of CD15 expression across TC subtypes. Methods and Results: Following PRISMA guidelines, a systematic search was conducted in May 2025 across PubMed, Scopus, and Web of Science. Sixteen observational studies evaluating CD15 expression in human TC were included. Risk of bias was assessed using the ROBINS‐I tool. A total of 1665 TC cases were analyzed. Classic papillary thyroid carcinoma (CPTC) showed moderate overall prevalence (0%–100%), follicular variant papillary thyroid carcinoma (FVPTC) demonstrated lower expression (17.6%–80%), while tall‐cell papillary thyroid carcinoma (TCPTC) exhibited the highest positivity (71%–100%). Follicular thyroid carcinoma (FTC) showed modest expression, whereas medullary thyroid carcinoma (MTC) and anaplastic thyroid carcinoma (ATC) demonstrated overall low positivity. CD15 showed high specificity (90%–100%) for PTC, but sensitivity was inconsistent, particularly in follicular variants. Conclusion: CD15 demonstrates high specificity for PTC. However, its limited sensitivity and variable expression in follicular‐patterned lesions make its prognostic value unclear. CD15 should not be used as a standalone marker; instead, it may improve diagnostic accuracy when combined with other markers in multiparametric immunohistochemical panels.

Introduction: Cervico‐isthmic pregnancy (CIP) is a rare form of low‐lying implantation in which the gestational sac implants between the anatomical and histological internal os. It is associated with significant maternal morbidity due to abnormal placentation and a high risk of placenta accreta spectrum (PAS). Advanced cases beyond 20 weeks are exceedingly rare and pose major diagnostic and surgical challenges. Case Presentation: A 30‐year‐old woman, gravida 2, para 1, with a history of prior cesarean section and Asherman syndrome, presented at 28 weeks and 4 days of gestation with preterm premature rupture of membranes. An ultrasound revealed a viable breech fetus located in the lower uterine segment and cervico‐isthmic region. The presence of placental lacunae and bridging vessels suggested PAS. An MRI confirmed significant thinning of the lower uterine segment, nearly complete loss of myometrial tissue, and a preserved endocervical canal, consistent with CIP and PAS. Because of the high risk of hemorrhage, a cesarean section was performed using a posterior uterine incision, followed by immediate hysterectomy due to massive bleeding. Histopathological analysis confirmed the diagnosis of placenta increta in the cervico‐isthmic area. Both maternal recovery and neonatal outcomes were favorable. Discussion: This case highlights the diagnostic difficulty of advanced low‐lying implantation disorders with features favoring CIP. In late gestation, the anatomic boundaries among CIP, cervical pregnancy, and endogenic/Type I CSP may become difficult to define because the implantation site can expand beyond its original location. Careful evaluation of placental topography using ultrasound and MRI, supported by intraoperative anatomic findings and histopathologic correlation, can help characterize the implantation site and guide diagnostic interpretation. Nevertheless, even with multimodal assessment, overlap between CIP and endogenic/Type I CSP may persist, and definitive classification may remain challenging.

Differentiated thyroid carcinoma is a morphologic diagnosis, not a direct measure of preserved thyroid function. Although most papillary, follicular, and oncocytic thyroid carcinomas retain architectural or cytologic features of follicular-cell derivation, a clinically important subset loses the molecular machinery required for effective iodine transport, organification, and radioiodine therapy. This functional divergence is central to the biology of radioiodine-indifferent and radioiodine-refractory thyroid cancer. This review examines the role of oncogenic MAPK/ERK signaling as a principal regulator of thyroid lineage suppression and therapeutic failure. Aberrant activation of the RAF–MEK–ERK axis, most prominently through BRAF^V600E, RAS alterations, and receptor tyrosine kinase fusions, does more than promote proliferation. It reshapes follicular-cell identity by repressing thyroid-lineage transcriptional programs and silencing iodine-handling genes, including SLC5A5/NIS, TPO, TG, TSHR, SLC26A4, and related components of the iodine metabolic transcriptome. This repression is mediated through coordinated transcriptional, epigenetic, and post-transcriptional mechanisms involving lineage transcription factors such as PAX8, NKX2-1, and FOXE1; chromatin-modifying programs including histone deacetylation and PRC2/EZH2-associated repression; DNA methylation; and non-coding RNA networks. Importantly, ERK-driven functional dedifferentiation is not always a fixed terminal state. Preclinical models and early clinical trials demonstrate that pharmacologic inhibition of the MAPK pathway can restore iodine avidity in selected radioiodine-refractory tumors, creating the theranostic basis for redifferentiation therapy. Iodine-124 PET/CT and lesion-level dosimetry have shown that restored iodine uptake can be measured diagnostically and then exploited therapeutically with iodine-131. However, clinical translation remains limited by inter- and intratumoral heterogeneity, incomplete durability of response, adaptive pathway reactivation, persistent epigenetic repression, tumor microenvironmental influences, and the absence of standardized dosimetric thresholds. We propose that advanced follicular-cell-derived thyroid cancers should be understood along a functional differentiation continuum rather than through morphology alone. Within this framework, radioiodine refractoriness reflects not merely treatment failure, but a therapeutically interrogable state of lineage suppression. Refinement of redifferentiation therapy will require genotype-informed patient selection, functional imaging, standardized dosimetry, rational combination strategies, and prospective trials capable of distinguishing true restoration of radioiodine therapeutic efficacy from the antiproliferative effects of kinase inhibition alone.