Background and Objectives: breast cancer remains the most common health burden affecting females worldwide. Despite developments in breast cancer diagnostic approaches and treatment strategies, the clinical management of metastatic breast cancer remains challenging. Thus, there is a need to identify new biomarkers and novel drug targets for breast cancer diagnosis and therapy. Recently, aberrant glypican-3 (GPC3) expression in cancers has gained considerable interest in cancer research. The studies, however, have yielded contradictory results about GPC3 expression in breast cancer. Therefore, the current study aims to analyse GPC3 expression across a large panel of different breast cancer subtypes. Materials and Methods: GPC3 expression was immunohistochemically evaluated in 230 breast cancer patients along with eight normal tissues and its associations to clinical and demographic characteristics, as well as immunohistochemical biomarkers for breast cancer. Moreover, a public database consisting of breast cancer patients’ survival data and GPC3 gene expression information was used to assess the prognostic value of GPC3 in the survival of breast cancer patients. Results: GPC3 expression was only characterised in 7.5% of different histological breast cancer subtypes. None of the normal breast tissues displayed GPC3 expression. Interestingly, all cases of Paget’s disease, as well as 42.9% of intraductal and 16.7% of mucinous carcinomas were found to have GPC3 expression, where it was able to significantly discriminate Paget’s disease and intraductal carcinoma from other breast cancer subtypes. Importantly, GPC3 expression was found more often in tumours that tested positive for the expression of hormone receptors and human epidermal growth factor receptor 2 (HER2), indicating more favourable histological subtypes of breast cancer. Consequently, longer relapse-free survival (RFS) was significantly correlated with higher GPC3 mRNA expression. Conclusions: Our study proposes that GPC3 is a promising breast cancer subtype-specific biomarker. Moreover, GPC3 may have the potential to be a molecular target for the development of new therapeutics for specific subtypes of breast cancer.

Background and Objective: Ovarian cancer is a leading cause of death in females. Since its treatment is challenging and causes severe side effects, novel therapies are urgently needed. One of the potential enzymes implicated in the progression of cancers is Cytochrome 4Z1 (CYP4Z1). Its expression in ovarian cancer remains unknown. Therefore, the current study aims to assess CYP4Z1 expression in different subtypes of ovarian cancers. Materials and Methods: Immunohistochemistry was used to characterize CYP4Z1 expression in 192 cases of ovarian cancers along with eight normal ovarian tissues. The enzyme’s association with various clinicopathological characteristics and survival was determined. Results: CYP4Z1 was strongly expressed in 79% of ovarian cancers, compared to negative expression in normal ovarian samples. Importantly, significantly high CYP4Z1 expres-sion was determined in patients with advanced-stage cancer and a high depth of invasion (p < 0.05). Surprisingly, CYP4Z1 expression was significantly associated with a low patient survival rate. Univariate analysis revealed that patient survival was strongly associated with CYP4Z1 expression, tumor stage, depth of invasion, and lymph node metastasis (p < 0.05). Multivariate analysis showed that only CYP4Z1 expression was significantly associated with patient survival (p < 0.05). Conclusions: CYP4Z1 expression is correlated with shorter patient survival and has been identified as an independent indicator of a poor prognosis for ovarian cancer patients.

Background/Objectives: Cytochrome 1B1 (CYP1B1) is overexpressed in several cancers, contributing to carcinogenesis, cancer progression, and chemoresistance. Despite its known oncogenic role, its expression in bone sarcomas remains unknown. Methods: This study assessed CYP1B1 expression in osteosarcoma and chondrosarcoma using immunohistochemistry on tissue microarrays and analyzed corresponding transcriptomic profiles from public RNA-seq datasets. Associations with clinicopathological features, survival, drug sensitivity, and protein–protein interaction networks were also investigated. Results: CYP1B1 was overexpressed in 72.3% of bone sarcomas (78% of osteosarcomas and 82.1% of chondrosarcomas) and was significantly underexpressed in normal bone (12.5%, p < 0.001). Importantly, high CYP1B1 expression was found in younger patients (≤34 years; p = 0.013), but no other associations with tumor grade, size, or metastasis were observed. The mean survival rate of CYP1B1-positive patients was insignificantly shorter than that of negative patients (58.8 vs. 62.8 months; p = 0.170). Although not confirmed in the multivariate analysis, CYP1B1-positive patients had poorer survival in the univariate analysis, which may reflect tumor aggressiveness rather than prognostic value. Transcriptomic data showed significantly lower CYP1B1 mRNA in osteosarcoma versus normal bone, suggesting post-transcriptional or translational regulation. Drug sensitivity analysis revealed both positive and negative correlations between CYP1B1 expression and response to various compounds in the GDSC dataset, highlighting potential therapeutic implications. Conclusions: Despite low mRNA levels, CYP1B1 protein is consistently and selectively overexpressed in bone sarcomas, particularly in younger patients. While not prognostic, its expression profile warrants further investigation and evaluation as a therapeutic target or diagnostic biomarker, especially in refractory or advanced cases.

Rationale: Keratitis-ichthyosis-deafness (KID) syndrome is a rare ectodermal disorder caused by pathogenic mutations in GJB2 gene, which encodes the gap junction protein connexin 26. While the condition is traditionally defined by a triad of keratitis, ichthyosis, and sensorineural hearing loss, emerging evidence suggests that connexin 26 dysfunction may lead to broader systemic involvement. This case highlights a rare presentation with neurological and musculoskeletal abnormalities. Patient concerns: A 3-year-old female born at 31 weeks of gestation presented with a history of global developmental delay, recurrent seizures, photophobia, and thick hyperkeratotic skin changes. At birth, she was encased in a collodion membrane and exhibited bilateral eyelid malposition. Her development was marked by delayed milestones, joint stiffness, and poor weight gain. Diagnoses: Clinical findings included vascularizing keratitis, lamellar ichthyosis, and right-sided sensorineural hearing loss confirmed by auditory brainstem response testing. Brain imaging revealed moderate enlargement of the cerebral ventricles, and skeletal surveys demonstrated developmental dysplasia of the hip and congenital muscular torticollis. A clinical diagnosis of KID syndrome was made based on the constellation of cutaneous, auditory, neurological, and musculoskeletal abnormalities. While genetic testing was unavailable, the phenotype was strongly suggestive of a pathogenic GJB2 mutation. Although KID syndrome is most commonly caused by autosomal dominant, frequently de novo, mutations-particularly the D50N variant-the apparent autosomal recessive pattern in this pedigree may reflect parental mosaicism, reduced penetrance, or variable expressivity. Interventions: The patient received coordinated multidisciplinary care. Dermatologic management involved intensive emollient therapy. Ophthalmologic care included lubricants and surgical correction of eyelid malposition. Antiepileptic medication was initiated for seizure control. Physical therapy addressed joint contractures and improved motor function. Outcomes: Following early intervention, dermatologic symptoms stabilized, seizure activity diminished, and gradual improvements in physical function were observed. However, developmental delay and structural brain abnormalities persisted, requiring long-term follow-up and therapy. Parental compliance multidisciplinary care were essential for optimizing care. Lessons: This case highlights potential atypical manifestations of KID syndrome, including seizures, ventriculomegaly, torticollis, and hip dysplasia, that may reflect a broader but under-recognized phenotypic range.

Background: Placenta previa carry high morbidity and mortality due to massive hemorrhage occur during surgery. So, there should be a standard surgical approach with less morbidity. Methods: This is a retrospective study that reviewed all deliveries in Al-karak governmental hospital between 2019–2022. Placenta previa cases were divided into two groups according to management. Group A was managed by incising the uterus at the level of fundus to avoid opening through the placenta, while Group B was managed by opening the lower uterine segment and delivering the baby through placenta after incising it. Result: This study included 26 cases of placenta previa, 12 of them (Group A) were managed by avoiding the placenta and the other 14 cases (Group B) were managed by opening through the placenta. There was no difference between the two groups in terms of age and the number of previous caesarean sections (table 1). Patients who underwent the suggested surgical approach (Group A) had less blood loss (Mdn = 775 cc) while Group B (Mdn = 1700 cc) U = 20.0 p = 0.001 was significantly higher in terms of blood loss. Similarly, the number of blood units given for Group B (Mdn = 5 units) was significantly higher than Group A (Mdn = 1 unit) U = 29.5. p = 0.005. lastly, the duration of hospital stay for Group A (Mdn = 2 days) was significantly less than Group B (Mdn = 6 days) U = 10.0. p = 0.000 Conclusion: Incising the upper uterine segment to avoid the placenta may have better outcome regarding blood loss and its consequences.

Background: Cytochrome P450 2J2 (CYP2J2) has been implicated in tumor biology, but its expression pattern and clinical significance in prostate and renal cancers remain poorly characterized. Methods: Commercially available tissue microarrays containing 208 renal and 121 prostate tissue specimens were used for immunohistochemical (IHC) characterization of CYP2J2 protein expression. We performed transcriptomic analysis and examined correlations with clinicopathological features and survival using the OncoDB 2.0 platform. Results: CYP2J2 immunoreactivity was mainly cytoplasmic, with minimal protein expression in both cancers. We identified positive staining in 7/100 (7.0%) prostate adenocarcinomas and 2/192 (1.0%) clear cell renal cell carcinoma (ccRCC) specimens, with negative expression in corresponding normal tissues. We detected no significant associations between protein expression and clinicopathological features in either cohort (all p > 0.05). In contrast, transcriptomic analysis revealed elevated CYP2J2 mRNA expression in both malignancies, with a slight increase in prostate adenocarcinoma (log₂ fold change = 1.10) and marked overexpression in ccRCC (log₂ fold change = 5.24) compared with normal tissues. We observed significant associations between CYP2J2 mRNA expression and pathological T stage in prostate adenocarcinoma (p = 0.0019) and pathological M stage in ccRCC (p = 0.0079). Moreover, higher CYP2J2 mRNA expression was associated with longer overall survival in ccRCC (HR = 0.64, 95% CI: 0.47–0.86; log-rank p = 0.0029) but not in prostate adenocarcinoma; however, these findings remain exploratory and do not establish independent prognostic value. Conclusions: Despite elevated transcript expression, CYP2J2 protein expression was infrequent in prostate adenocarcinoma and ccRCC, suggesting limited clinicopathological relevance and warranting further investigation using functional techniques.