Ewing's sarcoma is an aggressive small round cell tumour that usually arises from bone or soft tissues in children and young adults. Primary origin within the prostate is exceptionally rare, with only isolated cases documented. We describe a man in his 20s who presented with urinary obstruction, constipation and leg pain. Imaging revealed a bulky pelvic mass arising from the prostate and bilateral hydroureteronephrosis. Histology demonstrated a round cell neoplasm with strong CD99 and FLI1 positivity, confirming Ewing's sarcoma. Staging PET-CT identified widespread metastases involving lung, liver and bone. The patient underwent urinary and bowel diversion, followed by Vincristine, Adriamycin, Cyclophosphamide alternating with Ifosfamide and Etoposide (VAC/IE) chemotherapy. He achieved complete metabolic remission, allowing colostomy reversal and is currently under surveillance. This case illustrates the need to consider rare sarcomas in the differential diagnosis of pelvic masses in young men with normal serum PSA and highlights the potential for durable response with timely systemic therapy.

Proliferative leukoplakia (PL) is an uncommon yet aggressive variant of oral leukoplakia characterized by its high rates of malignant transformation and recurrence. Primarily affecting older, non-smoking females, PL can present as homogenous, verrucous, or erythroleukoplakia lesions. PL is associated with high DNA aneuploidy, alterations in tumor suppressor genes (TP53, CDKN2A), and exhibits immune evasion markers, such as PD-L1. Histopathologically, lesions may demonstrate architectural or cytologic dysplasia. Treatment of PL remains challenging with limited options. Recent findings support further research into molecular and immune-based therapies. There are current inconsistencies in terminology and diagnostic criteria for PL which emphasize the need for an international consensus to support standardized reporting, timely management, and conduct of clinical trials.

Oral cavity squamous cell carcinoma (OCSCC) represents the 16th most prevalent cancer worldwide accounting for greater than 389,000 cases annually. Most examples of OCSCC are preceded by a diverse group of lesions exhibiting variable risk of transformation to cancer, collectively termed oral potentially malignant disorders (OPMDs). The identification of salivary, serologic, and/or tumor tissue biomarkers holds substantial promise for improving detection, prognosis, and treatment of OPMDs and OCSCC. Although certain biomarkers have become standard of care in the management of patients, continued robust validation and stringent protocol standardization efforts are critical to ensure both diagnostic accuracy and widespread utilization.

Acute promyelocytic leukemia (APL) predominantly affects younger patients with significantly prolonged survival. Therefore, controlling the incidence of secondary hematological malignancies represents a crucial therapeutic goal. Secondary, acute T-lymphoblastic leukemia (T-ALL) following APL is rare and confers a poor prognosis, with only 2 cases reported to date. Herein, we present a case of a young female with APL who attained complete remission (CR) after receiving dual induction therapy with all-trans retinoic acid (ATRA) and arsenic trioxide (ATO), followed by standard consolidation and maintenance treatment cycles. After discontinuing chemotherapy for 26 months, the patient conceived naturally and was later diagnosed with T-ALL in the first trimester of pregnancy. She attained a second CR after receiving the VDCLP chemotherapy regimen (vincristine+daunorubicin+cyclophosphamide+L-asparaginase+prednisone). She subsequently underwent allogeneic hematopoietic stem cell transplantation (allo-HSCT) and remained in sustained CR at the 18-month follow-up time point. For patients with T-ALL secondary to APL after treatment remission, early diagnosis combined with the VDCLP regimen and allo-HSCT demonstrated certain therapeutic efficacy.

Factor VII (FVII) deficiency is a clinical condition occasionally encountered in the evaluation of coagulopathy. Although acquired FVII deficiency has been documented in association with acute myeloid leukemia (AML), the coexistence of AML and inherited FVII deficiency has not been previously reported. Here, we present a case of inherited factor VII deficiency concurrently identified in a patient with acute myeloid leukemia, in which targeted F7 gene sequencing identified compound heterozygosity for likely pathogenic variants. This case underscores that coagulopathy in patients with hematologic malignancies should not be reflexively attributed solely to acquired causes. Maintaining clinical suspicion for underlying inherited coagulation disorders is essential to prevent diagnostic oversights and to facilitate tailored management.

Follicular lymphoma (FL) is an indolent non-Hodgkin lymphoma with rare parotid gland involvement. Histological transformation to diffuse large B-cell lymphoma (DLBCL) manifesting as gastric relapse complicated by rupture and perforation is extremely rare and clinically challenging. This case report aims to clarify its clinical characteristics, treatment strategies and prognostic significance.

A 60-year-old male was diagnosed with grade 1 FL of the bilateral parotid glands in 2014 and discontinued regular follow-up thereafter. In December 2025, he was presented with recurrent chest pain, anemia and melena. Gastroscopy and histopathology confirmed DLBCL of the gastric lesser curvature, Ann Arbor stage IIIB. The patient refused chemotherapy and was discharged. In February 2026, he was readmitted due to syncope and progressive hematochezia. Abdominal imaging suggested gastric lymphoma rupture and suspected perforation. He received palliative distal subtotal gastrectomy, and postoperative pathology verified DLBCL of the distal stomach. Subsequently, he was treated with Polatuzumab vedotin combined with Rituximab and CEP regimen, and is currently in stable condition.

This rare case emphasizes that long-term regular follow-up is essential for patients with parotid FL. Emergency surgery is a life-saving intervention for transformed DLBCL with gastric rupture and perforation. Further large-sample studies are needed to optimize the surveillance and treatment protocols for this rare condition.

Loss of sensation in the nipple-areolar complex (NAC) after mastectomy negatively affects quality of life, body image, and psychological well-being. Although direct nipple reinnervation has been described in immediate implant-based reconstruction, data on expander-based reconstruction is limited.

The aim of this study was to present our experience with nipple neurotization performed during second-stage implant exchange and evaluate its role in improving sensory outcomes in patients undergoing alloplastic breast reconstruction.

A prospective study was conducted by including patients who underwent nipple-sparing mastectomy with neurotization during expander-to-implant exchange between 2021 and 2025. Demographic and clinical data were collected. Each breast was divided into five regions and assessed using the British Medical Research Council (BMRC) scale and Semmes-Weinstein monofilament testing. Evaluations were conducted preoperatively and at 6 and 12 months postoperatively. Outcomes were compared using the Friedman test.

Thirteen patients (18 breasts), with a median age of 42 years, were included. Preoperatively, median NAC sensation was S0, which improved to S1 at 6 months and S3+ at 12 months (p < 0.01). The Semmes-Weinstein thresholds improved from >300 g preoperatively to 10 g at 6 months and 2 g at 12 months (p < 0.01).

Nipple neurotization using intercostal nerves during expander-to-implant exchange is a feasible technique associated with improved sensory outcomes in implant-based breast reconstruction. Further comparative studies are needed to determine its efficacy relative to standard reconstruction.

Determining whether pancreatic and ampullary neoplasms harbor invasive carcinoma is crucial for clinical management but can be challenging. Fibroblast activation protein (FAP) is a transmembrane serine protease that is upregulated in tumor-associated stroma. In this study, we aim to evaluate FAP expression by immunohistochemistry (IHC) in the stroma of pancreatic and ampullary neoplasms to assess its potential utility as a marker of invasion. A total of 42 patients with resection specimens of pancreatic intraductal neoplasms (n = 14), pancreatic ductal adenocarcinoma (PDAC) arising from intraductal neoplasms (n = 10), ampullary adenomatous neoplasms (n = 9), ampullary adenocarcinoma (n = 8), and chronic pancreatitis (n = 1) were included. FAP-stained sections were evaluated, and its expression was scored by two practicing pathologists independently with consensus. An immunoreactive score (IRS) was generated by multiplying stain percentage and intensity. FAP expression was significantly increased in the stroma of invasive adenocarcinomas compared to non-invasive precursor lesions (p < 0.05). FAP was positive (mildly or strongly) in 29% (4/14) of pancreatic intraductal neoplasms, 100% (10/10) of PDAC, 0% (0/9) of ampullary adenomatous neoplasms, and 100% (8/8) of ampullary adenocarcinomas. Two cases of intraductal papillary mucinous neoplasms (IPMNs) showed strong FAP expression in the stroma associated with erosion/denudation of epithelial lining and mucin extravasation. This study, although limited in size, suggests FAP as a potentially useful adjunct to morphology in diagnosing invasive adenocarcinoma in pancreas and ampulla. It is important to be aware that FAP is not a specific marker for desmoplastic stroma.

Obesity is a major global public health concern closely linked to the development and progression of various gynaecological disorders, particularly polycystic ovary syndrome (PCOS) and endometrial cancer. Incretins, a group of gut-derived hormones primarily including glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), are widely recognised for their roles in glycemic control and insulin secretion. Accumulating evidence reveals that GLP-1 and GIP also participate in modulating inflammation, autophagy, immune response and gut-brain communication through multiple signalling pathways, thereby playing important roles in female reproductive disorders. This review provides a comprehensive overview of the mechanisms and therapeutic potential of incretins in gynaecological conditions.

We performed a comprehensive literature search across PubMed, Web of Science and Embase, covering studies published from January 1995 to July 2026. Search terms combined incretin-related keywords (GLP-1, GIP, GLP-1 receptor agonists) with gynaecological disease terms (polycystic ovary syndrome, endometriosis, endometrial cancer, ovarian cancer, intrauterine adhesion). We primarily included original research studies and authoritative reviews, and excluded meeting abstracts, case reports and non-English literature.

GLP-1 receptor agonists (GLP-1 RAs) exert multi-faceted benefits in PCOS, endometriosis, intrauterine adhesions and gynaecologic cancers through cAMP/PKA, PI3K and AMPK signalling pathways. Special emphasis is placed on the multi-faceted benefits of GLP-1 RAs, while evidence supporting GIP-based therapies in gynaecology remains relatively limited and largely preclinical. The current status of clinical application, safety considerations and future directions are further discussed.

Incretin-based therapies offer novel approaches for metabolic and oncological gynaecological diseases, with significant translational value. Large-scale clinical studies and deeper mechanistic exploration are warranted to realise their full therapeutic potential.

This study aims to unveil whether WWOX modulates epithelial-mesenchymal transition (EMT), proliferation, and invasive capacity of gastric cancer (GC) cells via regulating the Wnt/β-catenin signaling pathway.

WWOX expression in GC cell lines was assessed by Western blotting (WB) and immunofluorescence. Gain- and loss-of-function approaches were employed by establishing stable WWOX-overexpressing (oe WWOX) MKN28 and HGC27 cell lines and performing siRNA-mediated WWOX (si WWOX) knockdown in the same cell lines. Cell proliferation and invasion were evaluated using CCK-8 and Transwell assays, and EMT-related protein expression was examined by WB. To determine whether WWOX functions through the Wnt/β-catenin pathway, oe WWOX cells were treated with the pathway agonist SKL2001, and WWOX-silenced cells were treated with the β-catenin inhibitor XAV939; β-catenin levels in whole-cell lysates, as well as nuclear and cytoplasmic fractions, were analyzed by WB. The in vivo effects of WWOX overexpression and knockdown were assessed using subcutaneous xenograft models in nude mice.

WWOX expression was markedly reduced in GC cells. WWOX overexpression significantly suppressed proliferation, invasion, and EMT, accompanied by decreased β-catenin levels in total cell lysates as well as in nuclear and cytoplasmic fractions. Conversely, WWOX knockdown promoted malignant phenotypes and increased β-catenin expression in both fractions. SKL2001 treatment effectively counteracted the tumor-suppressive effects of WWOX overexpression, whereas XAV939 treatment reversed the tumor-promoting effects induced by WWOX knockdown. In vivo, WWOX overexpression suppressed tumor growth and reversed EMT, while WWOX knockdown promoted tumor growth and EMT progression; these changes were associated with reciprocal alterations in WWOX and β-catenin expression in tumor tissues.

WWOX suppresses GC cell proliferation, invasion, and EMT both in vitro and in vivo by negatively regulating the Wnt/β-catenin signaling pathway. These findings provide a mechanistic basis for targeting the WWOX/Wnt/β-catenin axis as a potential therapeutic strategy for GC.