Carcinoid heart disease (CHD) is a complication of carcinoid syndrome that results from chronic exposure of the endocardium to circulating vasoactive substances, particularly serotonin. It leads to progressive right-sided valvular dysfunction and right heart failure. Presentation as cardiogenic shock is uncommon and may delay recognition of the underlying disease. We present the case of a 44-year-old woman with no prior medical history who developed progressive dyspnea, ascites, and lower extremity edema over four months and was admitted with cardiogenic shock. Transthoracic echocardiography revealed massive tricuspid regurgitation and moderate-to severe pulmonary regurgitation with marked right ventricular dilation with preserved conventional systolic indices. Abdominal imaging demonstrated hepatomegaly with multiple hypervascular hepatic lesions, and liver biopsy confirmed metastatic neuroendocrine tumor. Urinary 5-hydroxyindoleacetic acid was markedly elevated at 305 mg/24 hours with pro-B-type natriuretic peptide (pro-BNP) at 2,450 pg/mL, supporting the diagnosis of carcinoid syndrome with cardiac involvement. Lanreotide was initiated for biochemical and symptomatic control of the underlying carcinoid syndrome. Despite intensive hemodynamic support with inotropic and vasopressor therapy, the patient developed refractory cardiogenic shock and died from progressive right-sided heart failure. This case highlights an unusual and aggressive presentation of carcinoid disease manifesting as cardiogenic shock. Clinicians should maintain a high index of suspicion for CHD in patients with unexplained right-sided valvular dysfunction and systemic congestion, as early recognition may allow timely therapeutic intervention.

Malignant serous effusion (MSE) is a life-threatening complication of advanced cancers with limited effective treatments. Here, we present a protocol for the preparation of LIN28B siRNA-loaded nanoparticles and their combination with PARP inhibition for therapeutic evaluation in malignant ascites (MA). We describe steps for nanoparticle formulation, establishment of murine ascites models, and in vivo administration of therapeutic agents. We then detail procedures for assessing tumor progression, vascular permeability, and endothelial junction integrity to evaluate treatment efficacy and microenvironmental remodeling. For complete details on the use and execution of this protocol, please refer to Fang et al.[1].

Background and clinical significance: Gestational deciduosis is a benign, progesterone-related ectopic decidual reaction that commonly involves pelvic and peritoneal surfaces and usually regresses after delivery. Although generally asymptomatic, diffuse peritoneal deciduosis may present as multiple nodular implants and closely mimic peritoneal carcinomatosis, mesothelioma, or miliary tuberculosis, creating a challenging intraoperative differential diagnosis. Prompt histopathological assessment is essential to prevent unnecessary staging procedures or oncological treatment. Case presentation: A 30-year-old primigravida at 40 weeks' gestation underwent unplanned intrapartum cesarean section after a premature rupture of membranes, the induction of labor, and failed progression. Multiple friable, gray-yellow subcentimetric nodules were incidentally observed on the uterine serosa, adnexa, omentum, visceral intestinal peritoneum, and appendix. The macroscopic appearance raised concern for peritoneal carcinomatosis and abdominal miliary tuberculosis. No ascites or intra-abdominal masses were identified. CA-125 was elevated (207.7 U/mL), Quantiferon testing was indeterminate, and postoperative chest computed tomography showed no pulmonary disease. Histological examination showed ectopic decidual cells with abundant eosinophilic cytoplasm in a perivascular and septal distribution. The cells showed diffuse vimentin, CD10, and progesterone-receptor expression and lacked epithelial and mesothelial marker expression, supporting diffuse peritoneal deciduosis. The postoperative course was uncomplicated, and pelvic ultrasonography at 40 days postpartum showed no residual lesions. Conclusions: Diffuse peritoneal deciduosis should be considered when disseminated peritoneal nodules are encountered during pregnancy or cesarean delivery. In this setting, elevated CA-125 is nonspecific and may heighten concern for tuberculosis or malignancy without distinguishing among these entities. Correlation of the clinical context, operative findings, morphology, and targeted immunohistochemistry is essential to avoid unnecessary oncological treatment or extensive staging procedures.

Colorectal cancers (CRCs) include stroma-dominant tumors with desmoplasia and differentiated, gland-forming tumors with little stroma. We asked whether this difference reflects stromal abundance alone or also involves a distinct cancer cell state. HEST-1K sections were classified as M-type (stroma-dominant; five patient/tissue units) or D-type (differentiated and cancer cell-dominant; seven units). Prespecified EMT/pEMT, ECM/integrin, YAP/TAZ-TEAD, and DTP/persister gene sets were examined across spatial, bulk, and single-cell datasets and patient-derived malignant ascites cultures. M-type tumors contained broader CAF-rich compartments and higher activity of all four programs in EPCAM/KRT-high regions, including epithelial-dense tumor cores. Activity was greatest near CAF-rich areas. In GSE39582, EMT/pEMT, ECM/integrin, DTP/persister, and invasive epithelial programs were independently associated with recurrence. Ascites-derived cultures from stroma-dominant tumors showed higher ECM/integrin and survival programs. Independent institutional analyses supported the public data findings: focused real-time PCR showed higher MAPK/TGF-beta-related gene expression in M-type-derived than in D-type-derived ascites cells, and IHC showed stronger epithelial CD44v6 expression in M-type primary tumors and metastatic lymph node lesions. CAF co-culture increased VIM-promoter activity. These findings characterize stroma-dominant CRC as a spatially organized ecosystem in which a CAF-rich compartment is associated with stress-adapted cancer cell programs. Its poor prognosis may therefore involve not only stromal abundance but also a morphology-associated cancer cell state detectable after dissemination.

Cervical carcinosarcoma (CCS), also known as malignant mixed Müllerian tumor (MMMT) of the cervix, is an exceptionally rare and aggressive biphasic neoplasm composed of both epithelial and mesenchymal malignant components. Due to its rarity, optimal management strategies are not well established, particularly in low-resource settings. Most reported cases present at an advanced stage and are associated with poor prognosis. To our knowledge, this represents the first reported metastatic case of CCS from Sub-Saharan Africa. We report a case of advanced CCS in a 33-year-old woman who presented to a tertiary referral center in Northern Tanzania with a five-month history of heavy and prolonged vaginal bleeding, lower abdominal pain, headaches, palpitations, and generalized weakness. Clinical examination revealed a large vaginal mass with restricted uterine mobility and rectal involvement. Imaging demonstrated a heterogeneously enhancing cervical mass measuring 10 × 9 × 14 cm with parametrial invasion, recto-sigmoid infiltration, bilateral ovarian enlargement, peritoneal dissemination, lymphadenopathy, and ascites, consistent with FIGO stage IVB disease. Exploratory laparotomy revealed omental caking, bilateral ovarian masses, liver surface nodules, and extensive pelvic adhesions. A total abdominal hysterectomy (TAH) with bilateral salpingo-oophorectomy (BSO) was performed. Histopathological examination demonstrated a biphasic malignant tumor composed of carcinomatous elements arranged in nests and cords and sarcomatous pleomorphic spindle cells. Immunohistochemistry showed epithelial differentiation with p16 positivity and mesenchymal differentiation highlighted by desmin. Intraoperative findings and imaging confirmed ovarian and peritoneal metastases, consistent with advanced disease. Multidisciplinary review recommended systemic chemotherapy with carboplatin and paclitaxel followed by radiotherapy. Treatment was not initiated, however, due to financial constraints. The patient was subsequently lost to follow-up.

Mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS) syndrome is a rare mitochondrial disorder characterized by impaired oxidative phosphorylation and reduced ATP production, resulting in increased organ vulnerability to metabolic stress. Fluoropyrimidine agents, such as 5-fluorouracil (5-FU), are widely used to treat colorectal cancer and can induce gastrointestinal toxicity not only through inhibition of thymidylate synthase and suppression of nucleic acid synthesis but also via RNA misincorporation, translational defects, and mitochondrial dysfunction in intestinal epithelial cells. The coexistence of metabolic vulnerability associated with m.3243A>G-related mitochondrial dysfunction and drug-induced mitochondrial injury may synergistically exacerbate intestinal toxicity, potentially leading to severe enteritis. A 40-year-old woman with m.3243A>G-associated mitochondrial disease within the MELAS spectrum underwent radical resection for perforated rectal cancer with synchronous liver metastases. Her postoperative course was uneventful, and she was discharged without complications. CapeOX therapy (capecitabine plus oxaliplatin) was initiated as adjuvant chemotherapy. Ten days after the start of the third cycle, she developed intermittent fever, abdominal distension, and diarrhea. Computed tomography revealed diffuse edema throughout the small intestine with massive ascites. Malignant peritonitis was considered unlikely based on imaging, ascites analysis, and cytology, whereas infectious enteritis was not strongly suspected based on the clinical course. Chemotherapy-induced enteritis associated with CapeOX was therefore strongly suspected, and the regimen was discontinued. The gastrointestinal symptoms improved, and tumor marker levels normalized. This case suggests that underlying mitochondrial dysfunction may enhance fluoropyrimidine-related intestinal toxicity, indicating that careful risk assessment and close monitoring are required when administering chemotherapy to patients with underlying mitochondrial disorders.

Pseudomyxoma peritonei (PMP) is a rare peritoneal malignancy. Its typical clinical manifestations include abdominal distension, increased abdominal girth, or abdominopelvic masses. It is extremely rare for an umbilical hernia to be the initial manifestation, so this can easily lead to clinical misdiagnosis. A 60-year-old woman presented with a reducible umbilical mass for 10 months. Physical examination revealed marked abdominal distension and a 6-cm firm, irreducible umbilical mass. Serum tumor markers were normal. Computed tomography (CT) showed diffuse low-density abdominopelvic masses consistent with PMP, an appendiceal cystic lesion suggestive of mucinous neoplasm, omental thickening, and periumbilical tumor extension. Ultrasound revealed 9.4-cm ascites with mucin particles and septations. She underwent cytoreductive surgery with hyperthermic intraperitoneal chemotherapy. Intraoperatively, extensive gelatinous mucin, a ruptured cystic appendix, and periumbilical tumor involvement were noted. Postoperative pathology confirmed a high-grade appendiceal mucinous tumor with PMP. The immunohistochemistry results were as follows: cytokeratin 20 positive, caudal type homeobox 2 positive, and Ki-67 labeling index of 30%. Telephone follow-up 3 months after surgery indicated that the patient was doing well. PMP presenting with umbilical hernia as the initial symptom is relatively rare and is often misdiagnosed as a simple umbilical hernia. For middle-aged and elderly female patients with umbilical hernia who have concurrent ascites, thickened peritoneum, or a hard and fixed hernia mass, abdominopelvic CT and ultrasound should be performed to rule out PMP to avoid blindly performing hernia repair and delaying diagnosis and treatment.

High-grade serous ovarian carcinoma (HGSOC) remains the most lethal gynecologic malignancy, characterized by a high recurrence rate and poor long-term survival. Although daily statin use is associated with improved survival in ovarian cancer patients, the underlying mechanism of this benefit remains unclear, in part due to the use of non-clinical high doses and reliance on immunodeficient murine models in preclinical studies. Here, we analyzed data from the TriNetX US Collaborative Network to evaluate the association between statin use and survival in ovarian cancer patients, confirming a survival benefit in a large U.S. cohort. We next investigated the protective effects in a syngeneic ascites tumor model of ovarian cancer. Mice treated with clinically relevant doses of lipophilic atorvastatin (ATO) exhibited prolonged survival. Single-cell transcriptomic analyses further revealed enhanced CD8 [+] T-cell activation programs and pro-inflammatory macrophage remodeling. Flow cytometry identified increased M1-like macrophages and activated CD8 [+] T-cell populations. Cytokine profiling and transcriptomic analyses indicated that IL-15 signaling was significantly elevated following ATO treatment. Multiplex immunofluorescence analyses demonstrated enhanced tertiary lymphoid structure (TLS)-associated immune organization in metastatic tumor tissues after ATO treatment, with increased T- and B-cell markers. Ex vivo culture of primary T cells with ascites supernatant from ATO-treated mice resulted in enhanced T-cell activation and migratory capacity compared with supernatant from DMSO-treated mice. Collectively, our results suggest that daily statin use may remodel the body environment into a more immune-activated state, leading to a long-term beneficial effect on survival in cancer patients, as observed in large epidemiological studies.

BACKGROUND Chylous ascites is a rare, potentially life-threatening complication of pelvic surgery, characterized by progressive malnutrition, immune dysfunction, and massive fluid accumulation. When the condition is refractory, its management represents a complex challenge requiring sequential escalation across multiple therapeutic modalities. CASE REPORT A 72-year-old man developed refractory chylous ascites after robot-assisted radical prostatectomy with extended pelvic lymph node dissection for high-grade prostate cancer (Gleason score 5+4=9). Despite conservative measures, consisting of low-fat diet and continuous subcutaneous octreotide infusion, the ascites persisted. Repeated large-volume paracentesis with cell-free concentrated ascites reinfusion therapy (CART) and total parenteral nutrition (TPN) were required to manage worsening malnutrition. Lymphangiography and N-butyl cyanoacrylate (NBCA) embolization provided no sustained relief. Subsequent surgical lymphatic ligation identified active leakage alongside floating solidified NBCA in the internal iliac region, confirming the prior embolization site. Although the leak was temporarily controlled by ligation, chylous drainage recurred on postoperative day 2. Repeat lymphangiography revealed a new, anatomically distinct leak in the external iliac region, suggesting dynamic redistribution of lymphatic flow through a collateral pathway. Repeat NBCA embolization of this secondary site achieved definitive resolution. Supported by TPN and CART, the patient was discharged on postoperative day 117 with improved nutritional status. He had no recurrence over a 5-year follow-up, with clinical and laboratory assessment every 3 months. CONCLUSIONS This case suggests that lymphatic leak sites may shift during treatment. Repeat lymphangiography may be considered when chylous drainage recurs after apparently successful intervention. Multidisciplinary management, including TPN and CART, was integral to sustaining this patient through a prolonged and complex treatment course.

Tjalma syndrome, also named pseudo-pseudo Meigs syndrome, is a rare complication of serositis in patients with systemic lupus erythematosus (SLE). It is associated with a high level of the ovarian tumor marker CA-125 and pleural effusion and ascites, which can suggest an ovarian tumor (benign or malignant), in patients with SLE. Available literature data include case reports of female patients with SLE ranging in age from 14 to 82. Patients under 50 years of age predominate. Our own experience led us to analyze the observations in this review against the background of our experience with a female patient with late-onset SLE. This review discusses why exploration of paraneoplastic syndrome can delay immunosuppressive therapy for this serious SLE manifestation. The main goal of this case-based review is to compare the clinical and laboratory findings of our patient with those reported in the literature and to raise awareness of this rare entity.