Castleman's disease (CD) is a rare, chronic, lymphoproliferative disorder, increasingly recognized as a clonal neoplasm of lymph node stromal cells that can affect multiple organs and tissues. Intrapulmonary unicentric Castleman's disease (UCD) represents an exceptionally uncommon subtype, primarily involving the lung parenchyma and hilum, with only a few pathologically confirmed cases reported to date. This study aimed to characterize the clinical, radiological, and pathological features of intrapulmonary UCD and to summarize diagnostic and therapeutic experiences.

We retrospectively analyzed eight patients diagnosed with intrapulmonary UCD. Clinical manifestations, laboratory data, radiologic and bronchoscopic findings, histopathological characteristics, treatment approaches, and follow-up outcomes were systematically reviewed.

No patient exhibited specific clinical symptoms or distinctive laboratory abnormalities. Chest computed tomography (CT) served as the optimal imaging modality, consistently revealing solitary, well-circumscribed, soft-tissue masses with smooth lobulated contours. Definitive diagnosis relied on histopathological examination. All patients underwent complete surgical resection, followed by regular postoperative surveillance with chest CT. During follow-up, no local recurrence or disease progression was detected.

Intrapulmonary UCD is an exceedingly rare form of Castleman's disease that can be easily misdiagnosed as primary lung tumors, lymphoma, granulomatous disease, or tuberculosis due to its nonspecific clinical and radiological features. Complete surgical excision remains the mainstay of treatment and is associated with an excellent prognosis following complete resection.

Immune checkpoint inhibitors (ICIs) have emerged as a promising treatment for various cancers, including advanced hepatocellular carcinoma (HCC). However, a significant proportion of patients with HCC, particularly those with metabolic dysfunction-associated liver disease (MASLD), exhibit resistance to ICI therapy. Studies have revealed that the presence of specific gut bacteria, such as Akkermansia, Bifidobacterium, and Lachnoclostridium, is associated with improved outcomes with ICI-treated HCC patients. Conversely, the overgrowth of bacteria like Enterobacteriaceae is linked to resistance to therapy. This review investigates the role of gut microbiota in shaping immune checkpoint inhibitor responses in MASLD-related hepatocellular carcinoma, focusing on how dysbiosis may contribute to ICI resistance and exploring microbiome modulation strategies, such as fecal microbiota transplantation and probiotics, aiming to optimize therapeutic outcomes.

Schwannomas originating from the deep motor branch of the ulnar nerve (DMBUN) are exceptionally rare, presenting with variable and often heterogeneous clinical manifestations depending on their precise anatomical location. While these tumors have been described in the literature, reports specifically involving the DMBUN are exceedingly limited, rendering postoperative prognostication challenging. This study aims to systematically review the existing literature and present a novel case, with the objective of delineating anatomical characteristics and clarifying potential postoperative outcomes.

A systematic literature search was conducted according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines, using the MEDLINE and Scopus databases. Data regarding patient demographics, clinical presentation, anatomical localization, and surgical outcomes were extracted and analyzed.

Seven articles met the inclusion criteria. A total of nine tumors were initially identified as schwannomas of the DMBUN over a 73-year period; however, only five cases - including the newly reported one - were confirmed. The median patient age was 59.6 years; complete recovery was achieved in three cases, with time to functional improvement ranging from 4 to 6 months.

In this limited series, available data suggest that accurate preoperative imaging and careful intraoperative microsurgical dissection may lead to favorable outcomes, with complete recovery achievable in schwannomas of the DMBUN. No clear association was observed between postoperative nerve function and tumor size, patient age, or time since symptom onset.

Head and neck cancer presents a significant challenge for patients. Beyond the direct impact of the disease, chemotherapy and radiotherapy, while essential for cancer control, can further compromise patients' quality of life (QoL) and emotional well-being, while also introducing additional complications. These treatments may exacerbate existing cancer-related symptoms and contribute to malnutrition. This review aimed to identify and evaluate physical prehabilitation interventions implemented before or during radiotherapy/chemotherapy treatments to determine their impact on the QoL of patients with head and neck cancer.

This scoping review was structured according to the framework proposed by the Joanna Briggs Institute (JBI) and reported following the Preferred Reporting Items for Scoping Reviews (PRISMA-ScR) guidelines.

Eight studies were included, encompassing a total sample of 819 subjects (397 in experimental groups). The interventions identified included exercises and stretching to prevent mobility issues and trismus, home-based training programs with periodic supervision, comprehensive programs with supervised physiotherapy sessions, jaw mobility exercises, dysphagia therapy, oral exercises, and preventive rehabilitation. A positive association was found between prehabilitation interventions and improved QoL in patients. Customizing interventions based on patient characteristics and treatment modalities was shown to enhance the effectiveness of these programs.

Prehabilitation interventions represent a holistic and functional approach to improving patient outcomes and QoL. Further research is needed to refine these approaches and optimize the overall QoL of head and neck cancer survivors.

Multidrug resistance (MDR) remains a major challenge in small cell lung cancer (SCLC), limiting the efficacy of chemotherapeutics like doxorubicin. This study investigates whether silencing cellular prion protein (PrP), a known MDR-associated molecule, can enhance doxorubicin-induced cell death in Adriamycin-resistant H69AR cells. Quantitative RT-PCR and immunocytochemistry were used to assess the expression of PRNP, CD44, BAX, and BECN1 under various treatment conditions, including doxorubicin exposure and PrP knockdown via siRNA. Autophagic activity was evaluated using monodansylcadaverine (MDC) staining. PrP knockdown significantly reduced PRNP expression and modulated CD44 mRNA levels, especially during doxorubicin co-treatment. However, CD44 protein levels remained unchanged, suggesting post-transcriptional regulation. BAX expression increased with doxorubicin and siRNA individually, but not in combination, indicating a PrP-independent mechanism. BECN1 expression and Beclin-1 protein levels were significantly elevated in all treatment groups, especially in siRNA/doxorubicin combination. MDC staining confirmed increased autophagic vacuole formation in this group, indicating activation of Beclin-1-mediated autophagy. In conclusion, PrP knockdown may sensitize resistant SCLC cells to doxorubicin and promote autophagy. These findings support PrP silencing as a promising strategy to reverse chemoresistance in SCLC.

Data to guide management of isolated bland cancer-associated splanchnic vein thrombosis (CA-SpVT) are limited. We aimed to assess the role of anticoagulation (AC) and bleeding and thrombosis in patients with CA-SpVT. We conducted a dual-center retrospective cohort study of adults with incident, isolated, bland CA-SpVT from 2011 to 2020. The primary outcome was major bleeding (MB); other outcomes included usual-site venous thromboembolism (VTE) recurrence and progression/recanalization of CA-SpVT. Time-to-event outcomes were analyzed with weighted Cox models adjusting for cancer type, stage, SpVT location, and whether symptomatic. For SpVT recanalization/progression, differences were estimated using weighted average treatment effects (ATEs). After excluding tumor thrombus, we included 437 patients with notable characteristics of median age 60 years, portal vein thrombosis (81.2%), and underlying hepatocellular cancer (35.9%). Of these, 29.5% received therapeutic AC. At 6 months, there were 11.9% MB and 6.4% incident usual-site VTE events. Among 308 patients with follow-up imaging, the 1-year thrombus progression rate was 19.8% and thrombus recanalization was 28.6%. In the adjusted analysis, there were numerically higher rates of MB with AC (adjusted hazard ratio [aHR] 1.93, 95% confidence interval [CI] 0.97-3.87) and no significant difference in the incidence of VTE (aHR 1.41, 95% CI 0.56-3.51). AC was associated with significantly higher likelihood of venous recanalization (ATE +24% 95% CI 13%-35%) and significantly lower likelihood of thrombus progression (ATE -14% 95% CI -23% to -5%). In patients with isolated bland CA-SpVT, AC was associated with thrombus recanalization and limited thrombus progression; effects were offset by a potentially higher risk of MB.

Hyperleukocytosis (HL) in acute leukemia is associated with increased morbidity and mortality, mainly secondary to the effects of leukostasis. Many strategies for cytoreduction exist, however prompt initiation of chemotherapy is paramount. Leukapheresis is an additional strategy, though there is conflicting data for its use in HL in acute leukemia. Below we detail a case of HL and leukostasis in newly diagnosed pediatric T-cell acute lymphoblastic leukemia and the use of leukapheresis. We highlight that leukapheresis can rapidly and safely reduce the white blood cell count, as an adjunct to symptom management, and potentially prevent life-threatening complications while not delaying chemotherapy initiation. However, this case underscores that early recognition of HL prior to the development of severe neurological complications is critical, as once cerebral leukostasis with intracranial hemorrhage is established, neither leukapheresis nor chemotherapy may alter the fatal outcome. The patient's initial presentation with epistaxis and hematemesis two days prior-without laboratory evaluation-represents a missed opportunity that may have allowed earlier recognition and intervention.

Periapical radiolucent lesions are commonly of endodontic origin; however, some persistent cases may indicate non-endodontic pathologies, including malignancies. Diffuse large B-cell lymphoma (DLBCL) is the most prevalent subtype of lymphoma affecting the oral and maxillofacial region, yet its primary occurrence in the jaws is rare. This case report highlights the diagnostic challenges in differentiating endodontic lesions from periapical lymphomas and includes a literature review of documented cases.

A 44-year-old male presented with a persistent periapical lesion in the anterior maxilla, unresponsive to endodontic and periodontal treatments. Clinical examination revealed facial asymmetry, gingival edema, palatal swelling, and dental mobility. Imaging showed an ill-defined hypodense lesion extending beyond the periapical region. Fine needle aspiration and incisional biopsy confirmed DLBCL through histopathology and immunohistochemistry. The patient underwent six cycles of R-CHOP chemotherapy.

After treatment, intraoral examination revealed mucosal integrity, absence of swelling, and stabilization of dental mobility. Cone-beam computed tomography demonstrated bone regeneration, and PET/CT imaging confirmed complete remission.

This case underscores the importance of considering malignancies in the differential diagnosis of persistent periapical lesions. Accurate clinicoradiographic assessment, histopathological confirmation, and interdisciplinary collaboration are essential for timely diagnosis and improved patient outcomes.

Osteofibrous dysplasia (OFD) is a benign lesion that affects long bones in children. Adamantinoma (ADA) is a rare malignancy. A new entity known as "differentiated" adamantinoma or OFD-like ADA (OFDLA), has emerged. We examined the clinical outcomes of patients with these conditions.

A single-institution chart review of 59 patients from 1958 to 2016 was performed. Patient and treatment characteristics were compared across tumor types. Logistic regression was used to assess differences in outcomes including receipt of surgery, local recurrence, and development of metastatic disease.

A total of 43 patients were diagnosed with OFD, 17 were treated surgically, and there were 6 local recurrences. Out of the 9 OFDLA patients, 7 were treated surgically, and there were 4 local recurrences. All 5 patients with ADA were treated with wide excision, there was one local recurrence treated with re-excision, and one patient developed metastatic disease after treatment. The OFDLA patients were more than four times as likely to undergo surgery compared to OFD patients (OR = 4.5, 95% CI = 1.1-26.6, P = .04). There were no differences between OFD and OFDLA patients in surgical outcomes.

OFD and OFDLA patients can be managed conservatively, with surgical intervention reserved for those with radiographically extensive or symptomatic lesions. ADA should continue to be treated with wide local resection.

(1)OFD, OFDLA, and ADA exist in a spectrum of disease, and they are rare pathological entities.(2)Historically, OFDLA and ADA were treated like true malignancies, with wide resection and reconstruction. Our data suggest that OFD and OFDLA patients can be managed conservatively, with surgical intervention reserved for those with radiographically extensive or symptomatic lesions.(3)ADA is a low-grade malignant bone tumor with indications for wide resection.

III, Retrospective Cohort Study.

Chemotherapy resistance is the main obstacle to breast cancer recurrence, metastasis, and mortality. Drug-tolerant persister (DTP) cells are a novel type of target cell associated with tumor resistance, and autophagy is a key factor in maintaining the survival of tumor DTP cells. However, it is unclear whether the activation of autophagy in breast cancer DTP cells is related to their overexpression of the transcriptional regulatory factor CDCA7.

We analyzed CDCA7 expression using public datasets and clinical samples and established breast cancer cell lines with CDCA7 overexpression and knockdown to assess the role of CDCA7 in breast cancer. Autophagy was assessed via electron microscopy, mRFP-GFP-LC3 imaging, and immunoblotting. Mechanistic studies employed ChIP-seq, dual-luciferase assays, and site-directed mutagenesis. Functional assays measured chemosensitivity (CCK-8), migration/invasion (scratch/Transwell), and in vivo tumorigenicity (mouse xenograft).

CDCA7 was significantly upregulated in breast cancer DTP cells. Overexpression of CDCA7 in breast cancer cells significantly enhanced autophagy-related biological processes and molecular functions. Through ChIP-seq and targeted knockout experiments, we identified the binding sites of CDCA7 on the autophagy-related protein genes ULK1, ATG2A, and ATG3. Using transmission electron microscopy and mRFP/mCherry-GFP-LC3B tandem fluorescent tagging, we observed that CDCA7 knockdown significantly reduced the number of autolysosomes in breast cancer DTP cells and markedly inhibited autophagic flux. Moreover, CDCA7 knockdown not only decreased drug resistance in breast cancer cells but also reduced metastasis, invasion, and tumorigenic ability in vivo, ultimately prolonging the survival of tumor-bearing mice.

CDCA7 drives breast cancer chemoresistance by transcriptionally activating a pro-survival autophagy program in DTP cells, nominating it as a promising therapeutic target.