Abstract Introduction: The abscopal effect refers to regression of tumors outside the irradiated field following local radiotherapy and is thought to be mediated by systemic immune activation. Reports of this phenomenon have increased in the era of immune checkpoint inhibitors (ICIs), particularly in non-small cell lung cancer. However, it remains extremely rare in small cell lung cancer (SCLC). Case Presentation: We report the case of a 77-year-old man with extensive-stage SCLC (cT2aN2bM1a, Stage IVA). He received carboplatin, etoposide, and durvalumab followed by maintenance durvalumab. On Day 533, a solitary 10-mm brain metastasis developed, accompanied by a mild enlargement of the primary lung tumor to 30 mm. In contrast, hilar and mediastinal lymph node metastases had decreased in size, and contralateral pleural dissemination remained stable. Stereotactic brain radiotherapy (27 Gy in three fractions) was administered while durvalumab maintenance therapy was continued. By Day 605, follow-up CT revealed complete regression of the non-irradiated primary lung tumor (from 30 to 0 mm), with ongoing control of nodal disease and stable pleural dissemination. Disease control has been sustained for more than 1,277 days since treatment initiation. Conclusion: We report a rare case of a possible abscopal effect observed following stereotactic radiotherapy during durvalumab maintenance therapy for extensive-stage SCLC.
Abstract Introduction: Oxaliplatin-associated sinusoidal obstruction syndrome (SOS) is well recognized in patients receiving chemotherapy for colorectal liver metastases, particularly in hepatectomy specimens, but clinically manifest disease after adjuvant therapy for nonmetastatic colorectal cancer is rarely reported. We describe suspected delayed SOS identified during routine surveillance after curative-intent treatment. Case Presentation: A 42-year-old woman with stage IIC (T4bN0M0), microsatellite-stable sigmoid adenocarcinoma underwent curative resection followed by 12 cycles of adjuvant fluorouracil, leucovorin, and oxaliplatin. Oxaliplatin was dose-reduced for neuropathy. Surveillance computed tomography 1 month after treatment showed borderline splenomegaly. Thirteen months after chemotherapy, recognition of a recanalized left umbilical vein prompted hepatology evaluation. Magnetic resonance imaging confirmed the collateral without cirrhosis or steatosis, and endoscopy demonstrated no varices. Endoscopic ultrasound-guided direct measurements yielded mean portal and hepatic vein pressures of 12 and 14 mmHg, respectively, giving a gradient of −2 mmHg. Liver biopsy demonstrated centrilobular congestion, hepatocellular collapse, and prominent portal veins without significant fibrosis or central venular obliteration. These findings supported vascular liver injury, with oxaliplatin-associated SOS considered a presumptive diagnosis. Multidisciplinary expectant surveillance was pursued. Conclusion: Oxaliplatin-associated vascular liver injury may be recognized more than a year after adjuvant therapy in patients without liver metastases. Splenomegaly, platelet changes, unexplained liver enzyme abnormalities, or portosystemic collaterals on routine surveillance should prompt further evaluation. Nonspecific biopsy findings and discordant pressure measurements require cautious diagnostic interpretation.
Abstract Introduction: Sinonasal mucosal melanoma (SNMM) is a rare and biologically aggressive melanoma subtype associated with high rates of locoregional recurrence, early distant metastasis, and poor long-term survival. While surgery and radiotherapy remain the cornerstone of treatment for localized disease, systemic options for advanced or refractory SNMM are limited, and responses to immune checkpoint inhibitors are inferior to those observed in cutaneous melanoma. Comprehensive molecular profiling has therefore become increasingly important to identify actionable genomic alterations and guide precision oncology approaches. Case presentation: We report a case of FGFR3::TACC3 fusion–positive sinonasal mucosal melanoma achieving clinical and radiologic benefit from off-label treatment with the FGFR inhibitor erdafitinib. After multiple locoregional recurrences and systemic progression following surgery, adjuvant radiotherapy, and combined nivolumab–ipilimumab, comprehensive molecular profiling identified an actionable FGFR3::TACC3 fusion. Treatment with erdafitinib resulted in rapid symptomatic improvement and initial partial response according to RECIST v1.1, with toxicities that were predictable, manageable, and consistent with the known FGFR-inhibitor safety profile. Progression-free survival was seven months. Conclusion: This case highlights the clinical relevance of molecularly guided, tumor-agnostic therapeutic strategies in rare melanoma subtypes with limited standard-of-care options and supports the integration of comprehensive genomic profiling into the management of refractory SNMM.
Abstract A 50-year-old woman was diagnosed with synchronous bilateral breast cancer; triple-negative breast cancer (TNBC) in the right breast and luminal HER2-positive breast cancer in the left breast. Neoadjuvant chemotherapy using the KEYNOTE-522 regimen combined with pembrolizumab resulted in a pathological complete response (pCR) in both tumors. Next-generation sequencing (NGS) performed on pretreatment biopsy specimens identified a pathogenic BRCA1 variant in both tumors. The right tumor showed a high homologous recombination deficiency (HRD) score. These molecular findings provide a potential biological rationale for the observed sensitivity to platinum-containing chemoimmunotherapy, though further studies are required to validate this association.
Abstract Introduction Recent studies have demonstrated the efficacy and safety of BRAF/MEK inhibitors in the treatment of BRAF-mutated thyroid carcinomas. However, these agents have generally been studied in patients with an Eastern Cooperative Oncology Group performance status (PS) of 0–2, and their use in patients with severely impaired PS, particularly PS 4, has not been previously reported. Case Presentation A 66-year-old woman presented with dyspnea and neck discomfort. Chest computed tomography (CT) revealed a calcified nodule in the right thyroid lobe and multiple pulmonary nodules. The patient was then referred to our department for further evaluation and treatment. Right thyroid lobectomy and D2a lymph node dissection were performed, and the patient was diagnosed with a poorly differentiated thyroid carcinoma, pT2N1bM1 (lung), Stage IVB. Genetic testing revealed the presence of a BRAF V600E mutation. Postoperative radioactive iodine (RAI) therapy showed no uptake in the pulmonary metastases. Two months after surgery, she developed a right-sided malignant pleural effusion and was administered lenvatinib. Four months after the initiation of lenvatinib treatment, the patient presented with fatigue and was admitted for hypercalcemia and newly observed reticular opacities on chest CT. Her condition rapidly deteriorated, and CT imaging suggested disease progression with possible anaplastic transformation. Although her PS declined to 4, combination therapy with dabrafenib and trametinib was initiated. Supportive care, including morphine and betamethasone, was subsequently administered for severe dyspnea and poor oral intake. Thereafter, her general condition transiently improved, with recovery of oral intake and mobility and improvement of PS to 2, allowing temporary discharge home. Conclusion This case describes transient clinical improvement from PS 4 to PS 2 after initiation of BRAF/MEK inhibitor therapy in conjunction with supportive care in a patient with BRAF V600E-mutated poorly differentiated thyroid carcinoma and clinically suspected anaplastic transformation. Although the relative contributions of targeted therapy and supportive care to the clinical improvement cannot be determined, dabrafenib and trametinib were administered without apparent severe treatment-related adverse events, and the patient was temporarily able to return home despite her severely debilitated condition.
