Coccydynia is a painful condition of the coccyx that is frequently misdiagnosed and managed inconsistently. This review summarizes and grades the current evidence on diagnostic strategies and treatment options. We systematically searched the literature and included 42 studies covering conservative, interventional, and surgical management. Based on these data, we propose a current best framework for diagnostic evaluation and therapeutic management. Initial assessment should include detailed history and focused examination with palpation for localized coccygeal tenderness and symptom provocation. Standard anteroposterior and lateral radiographs are recommended mainly to exclude serious pathology, while dynamic sitting-standing radiographs can be considered when mechanical pain is suspected and symptoms persist. Cross-sectional imaging with magnetic resonance imaging or computed tomography (CT) should be reserved for trauma, red-flag features, suspected neoplasm or infection, or inconclusive basic imaging. First-line treatment should consist of education, ergonomic advice, offloading strategies, nonsteroidal anti-inflammatory drugs or other simple analgesics, and physiotherapy, with extracorporeal shock wave therapy having the strongest support. In patients with persistent pain, image-guided diagnostic and therapeutic injections and radiofrequency procedures can provide substantial relief and help select candidates for more invasive treatment. Coccygectomy should be reserved for patients with chronic, function-limiting pain who have failed conservative and interventional care and show concordant findings on assessment, imaging, and diagnostic blocks, while modified incision strategies and minimally invasive techniques may be considered in selected cases.

The aim of this study was to assess the accuracy of magnifying image-enhanced endoscopy (IEE) for predicting the invasion depth of superficial esophageal neoplasm (SEN).

We searched PubMed, Embase, the Cochrane Library. The sensitivity, specificity, positive likelihood ratio (PLR), negative likelihood ratio (NLR), diagnostic odds radio (DOR) with 95% confidence interval (CI) were calculated by bivariate mixed effect model, the summary receiver operating characteristic (SROC) curve was drawn and the area under the curve (AUC) was calculated to comprehensively evaluate the diagnostic value of magnifying IEE for the invasion depth of SEN.

Twelve literatures were included. The combined effect size of magnifying IEE in the diagnosis of carcinoma in situ (Tis) or tumor infiltrating lamina propria mucosae (LPM) were: sensitivity: 0.88(95%CI 0.83-0.92), specificity: 0.85(95%CI 0.76-0.91), PLR: 5.8(95%CI 3.6-9.3), NLR: 0.14(95%CI 0.09-0.20), DOR: 42 (95%CI 23-76), AUC: 0.93(95%CI 0.91-0.95); The combined effect size of magnifying IEE in the diagnosis of tumor infiltrating muscularis mucosae (MM) or tumor infiltrating the upper third of the submucosal layer (SM1) were: sensitivity: 0.72(95%CI 0.63-0.80), specificity: 0.86(95%CI 0.79-0.90), PLR: 5.0(95%CI 3.5-7.2), NLR: 0.32(95%CI 0.24-0.44), DOR: 15(95%CI 9-26), AUC: 0.86(95%CI 0.83-0.89); The combined effect size of magnifying IEE in the diagnosis of tumor infiltrating the middle third of the submucosal layer (SM2) or deeper were: sensitivity: 0.52(95%CI 0.40-0.64), specificity: 0.99(95%CI 0.98-0.99), PLR: 37.0(95%CI 24.5-55.9), NLR: 0.49(95%CI 0.38-0.63), DOR: 76(95%CI 45-127), AUC: 0.98(95%CI 0.96-0.99).

Magnifying IEE shows good overall diagnostic performance for assessing the invasion depth of SEN, with excellent diagnostic efficacy for superficial lesions, while the diagnostic sensitivity for deep lesions is relatively low. It can provide helpful evidence for selecting appropriate clinical treatments.

The therapeutic landscape of metastatic castration-resistant prostate cancer (mCRPC) has evolved substantially over the past decade, with androgen receptor pathway inhibitors, taxanes, poly (ADP-ribose) polymerase (PARP) inhibitors, radioisotopes, bone-protecting agents, and emerging targeted therapies improving survival for patients. At the same time, earlier treatment intensification in the hormone-sensitive setting has resulted in heterogeneous clinical presentations at the onset of castration resistance, adding complexity to treatment sequencing and clinical decision making. Here, we propose a pragmatic, patient-centered framework to help guide the management of mCRPC by integrating clinical features, molecular profiling, imaging findings, and supportive care considerations. Confirmation of castration resistance remains a critical first step and requires documented biochemical or radiographic progression in the setting of castrate testosterone levels. Treatment selection should consider prior systemic therapies, disease burden and tempo, symptom profile, comorbidities, and frailty. Molecular characterization, including evaluation for homologous recombination repair alterations and mismatch repair deficiency, is highly important for identifying candidates for PARP inhibitors or immune checkpoint blockade and other emerging biomarker-driven targeted strategies. Prostate-specific membrane antigen (PSMA)-targeted radioligand therapy has emerged as a key treatment. PSMA-positron emission tomography-based selection, incorporating assessment of uptake intensity, tumor heterogeneity, and total tumor volume, may help identify patients who are most likely to benefit from this treatment. Clinical factors such as liver metastases and limited prior response to androgen receptor-directed therapy have been associated with less favorable outcomes. Early on-treatment assessment using prostate-specific antigen response and PSMA-based imaging may support adaptive treatment strategies and earlier recognition of resistance. Given the high prevalence of bone metastases, bone-protecting agents should be considered to reduce skeletal-related events. Early palliative care (EPC) is now widely recognized as a concurrent, patient-centered intervention that improves quality of life, symptom burden, coping, and satisfaction across advanced cancers. Prostate cancer represents an especially compelling setting for EPC because of prolonged advanced disease courses, cumulative symptom burden, repeated treatment transitions, and persistent unmet supportive needs.

The increasing use of neoadjuvant systemic therapy (NAC) has led to a significant paradigm shift in the locoregional treatment of breast cancer, with increasing emphasis on response-guided de-escalation. In current practice, both clinical and pathologic responses to treatment are being leveraged to minimize the extent and morbidity of local therapy while maintaining oncologic safety. In patients presenting with clinically node-negative (cN0) disease and high-risk biologic subtypes, sentinel lymph node biopsy (SLNB) omission after NAC is an area of evolving interest. For those presenting with clinically node-positive disease (cN+) yet who attain a pathologic complete response (pCR) in the lymph nodes after NAC, emerging evidence suggests that SLNB alone with omission of regional nodal irradiation (RNI) may be considered. Ongoing trials are evaluating whether cN+ patients with residual micrometastases or macrometastases after NAC may also be treated with SLNB alone, using RNI in lieu of axillary lymph node dissection to achieve adequate locoregional control. Parallel advances in radiation therapy (RT) are reshaping treatment decisions and sequencing, including when to deliver agents concurrently with radiation and when to hold them. Exceptional responders who attain a breast pCR and undergo breast conservation may have little or no residual tumor bed to justify tumor bed boost, and several trials are assessing the safety of radiation omission in these subgroups. Finally, premastectomy RT is being explored as a strategy to facilitate immediate breast reconstruction while avoiding radiation-related complications. Together, these developments highlight a shift toward individualized, response-adapted locoregional management in early-stage breast cancer.

While immune checkpoint inhibitors have transformed treatment for many cancers, their benefit remains limited across all tumor types and is constrained by immune-related toxicity. Targeted immunotherapies, including T-cell engagers (TCEs), offer a more selective strategy by directing immune activity toward tumor-associated antigens. TCEs have achieved major success in hematologic malignancies and now show promise in selected solid tumors, with the approvals of tebentafusp and tarlatamab in uveal melanoma and small cell lung cancer, respectively, establishing proof of concept that durable benefit is possible. However, TCE efficacy is balanced by class-specific toxicities such as cytokine release syndrome and neurotoxicity, as well as on-target off-tumor effects. Antibody-drug conjugates (ADCs) can also enhance the specificity of cancer treatment by directing cytotoxic activity toward tumor cells via specific targets. ADC-checkpoint inhibitor combinations are similarly reshaping solid tumor therapy, most notably in urothelial carcinoma, where enfortumab vedotin plus pembrolizumab has demonstrated substantial survival gains. Across both strategies, efficacy may be influenced by antigen density, tumor heterogeneity, microenvironmental suppression, and treatment sequencing. Emerging drug engineering approaches and biomarker-driven patient selection aim to improve efficacy while limiting toxicity. Together, these advances support a new era of precision immuno-oncology, but broader success will require improved biomarkers, rational combinations, and an understanding of resistance mechanisms.

Mantle cell lymphoma (MCL) is a biologically and clinically heterogeneous B-cell malignancy with variable prognosis, ranging from indolent, asymptomatic forms to aggressive subtypes with early treatment failure. Contemporary management emphasizes risk-adapted strategies that integrate patient characteristics, clinical disease burden, and tumor biology. Prognostic tools such as the MCL International Prognostic Index (MIPI) and its biologically integrated variant (combined MIPI), alongside assessment of Ki-67 proliferation, TP53 status, and blastoid morphology, help guide treatment selection. In younger, fit patients, first-line therapy traditionally involves dose-intensified chemoimmunotherapy with high-dose cytarabine and autologous stem-cell transplantation (ASCT). The incorporation of Bruton tyrosine kinase inhibitors (BTKi), such as ibrutinib, into induction regimens has improved survival outcomes, with emerging evidence that may limit the use of ASCT to high-risk subsets. Maintenance therapy, particularly rituximab, remains crucial for durable disease control. In older or transplant-ineligible patients, bendamustine-rituximab remains a backbone therapy, with chemotherapy-free combinations incorporating BTKi, BCL2 inhibitors, and anti-CD20 antibodies offering effective, well-tolerated alternatives. High-risk patients, including those with TP53 mutations, may benefit from targeted triplet regimens or early cellular therapies. Relapsed/refractory MCL is increasingly managed with covalent and noncovalent BTKi, BCL2 inhibitors, and T-cell-redirecting therapies including chimeric antigen receptor T-cell therapy and bispecific antibodies. Ongoing trials are evaluating optimal sequencing and combination strategies to improve outcomes, particularly in high-risk and cBTKi-exposed patients. Overall, modern MCL management emphasizes individualized therapy based on biological risk, functional status, and treatment tolerability, with novel targeted and cellular approaches reshaping the frontline and relapsed treatment landscape.

Gastric and gastroesophageal junction cancers remain a major global cause of cancer-related mortality. Despite incremental advances in surgery and systemic therapy, durable survival gains have been limited, underscoring persistent unmet medical needs. However, the treatment paradigm has undergone a rapid transformation, driven by the integration of immunotherapy in curative-intent systemic treatment and the expansion of biomarker-guided systemic therapies. In the perioperative setting, immune checkpoint inhibitors combined with optimized cytotoxic chemotherapy have demonstrated encouraging efficacy, with recent phase III trials contributing to the establishment of combination of immunotherapy and chemotherapy as an emerging therapeutic platform. In advanced disease, precision oncology frameworks continue to expand beyond traditional biomarkers. Established targets such as human epidermal growth factor receptor 2 are now complemented by newly validated markers including claudin18.2, whereas additional actionable alterations-such as MET and TROP2-are actively under clinical investigation. These developments are redefining treatment algorithms and introducing new sequencing considerations, particularly in the context of tumor heterogeneity and biomarker coexpression. Concurrent advances in molecular diagnostics and next-generation sequencing are also facilitating the comprehensive identification of therapeutically relevant alterations. This review outlines the evolving therapeutic landscape of gastric and gastroesophageal junction cancers, spanning perioperative immunotherapy, newly validated molecular targets, and next-generation drug development platforms. By integrating biomarker-driven strategies with innovative modalities, such as antibody-drug conjugates, bispecific antibodies, chimeric antigen receptor-T-cell therapy, and vaccines, we highlight how precision therapeutics are reshaping treatment paradigms across resectable and advanced disease.

Uterine sarcomas are rare but aggressive tumors with high rates of recurrence and limited effective treatment options; a deeper understanding of their molecular and histologic diversity is critical to improving outcomes.

To provide a comprehensive overview of clinical management and current systemic treatment strategies for uterine sarcomas. Specific histologic subtypes and molecular features are also reviewed.

A thorough review of the literature was conducted using PubMed and clinical trial databases, with a focus on recent studies evaluating histology-specific management, molecular diagnostics, and novel systemic therapies across uterine sarcoma subtypes.

Uterine sarcomas comprise 3% to 5% of uterine malignancies and include multiple distinct subtypes such as leiomyosarcoma, low and high-grade endometrial stromal sarcoma, undifferentiated uterine sarcoma, and adenosarcoma. Each displays unique clinical behavior and molecular alterations that guide treatment. While surgery remains the foundation of management for early-stage disease, the role of adjuvant therapy is unclear and best guided by individual risk. In advanced disease, combination regimens such as doxorubicin and trabectedin have shown improved outcomes in the treatment of leiomyosarcomas. Targeted therapies, hormonal agents, and immunotherapy have variable activity across subtypes. Molecular diagnostics, including next-generation sequencing, are increasingly essential in diagnosis, prognostication, and treatment planning.

The landscape of uterine sarcoma treatment is rapidly evolving due to advances in molecular biology and emerging systemic therapies. Personalized management based on histology and molecular profiling, along with the development of subtype-specific clinical trials, will be essential in improving survival. Centralized, multidisciplinary care remains a cornerstone for patients with these rare tumors.

Preeclampsia before 20 weeks of gestation is an unusual clinical entity that suggests an underlying etiology, such as gestational trophoblastic disease (GTD). Among its forms, complete hydatidiform mole may evolve into gestational trophoblastic neoplasia with metastatic potential. The objective was to present the case of an adolescent patient with early-onset preeclampsia as the initial manifestation of a complete hydatidiform mole with pulmonary metastasis.

A 15-year-old patient without prenatal care was admitted due to vaginal bleeding, persistent nausea, and clinical signs of preeclampsia. A complete hydatidiform mole associated with grade IV hypovolemic shock was diagnosed. Patient underwent urgent uterine evacuation, intensive care for uterine atony, and received EMA-CO chemotherapy after pulmonary metastases were identified. 3 months after completing treatment, a viable intrauterine pregnancy was confirmed, with no evidence of tumor recurrence.

The onset of preeclampsia before 20 weeks should raise suspicion of GTD. Timely, multidisciplinary management can achieve full disease resolution, preserve fertility, and avoid long-term sequelae, even in advanced clinical scenarios.