Treatment for distant metastasis in Stage Ⅳ rectal cancer is complicated. We report a case in which a patient with concurrent lung and liver metastasis achieved R0 resection through a multidisciplinary treatment combining staged surgical resection and systemic chemotherapy. The patient was a 60-year-old woman who presented with rectal bleeding and abdominal pain during defecation. Further examination revealed a type 2 tumor in the rectal RS region and suspicious metastatic tumors in the left lung S1+2 and liver S6/7, S7, leading to a diagnosis of rectal cancer Stage Ⅳb. Due to the symptom, laparoscopic low anterior resection was performed. As a diagnostic treatment, S1+2 subregional resection was performed on the lung lesions, confirming the diagnosis of lung metastasis. Ten courses of FOLFOX plus panitumumab were administered, resulting in shrinkage of the liver tumors in segments S6/7 and S7. However, a new lesion was suspected in segment S5 and partial liver resection was performed for the 3 lesions. All resected lesions showed pathological findings consistent with complete response(CR), and R0 resection was achieved.

Most cases of primary small intestinal cancer are diagnosed at an advanced stage, and when accompanied by intussusception or obstruction, emergency surgery may be required. Preoperative evaluation of small intestinal cancer is challenging. The patient was a 52-year-old man who was referred to our hospital with abdominal pain and vomiting, and was diagnosed with small intestinal intussusception. Abdominal CT at our hospital revealed bowel wall thickening at the site where the intussusception had resolved, raising suspicion for small intestinal cancer. Based on the patient's clinical history and physical findings, delayed small intestinal perforation was suspected, and emergency surgery was performed. Laparoscopy-assisted surgery was carried out to resect the small intestinal tumor and peritoneal dissemination nodules. Pathological examination revealed moderately differentiated adenocarcinoma. The final diagnosis was pT3, pN1, pM1, and Stage Ⅳ. Laparoscopic surgery for small bowel cancer can be useful both for treatment and intraoperative diagnosis. In this case, the decision to perform non-curative resection based on the Stage Ⅳ diagnosis enabled early discharge and prompt initiation of additional treatments.

The patient is a 65-year-old male. He underwent laparoscopic distal gastrectomy for advanced gastric cancer of the lower gastric body. Pathological findings were poorly differentiated adenocarcinoma, Stage ⅢC. The cancerous lesion extended over 15 cm and was extensively positive for margins on the oral side due to marked lymphatic invasion. Two months later, CT showed local peritoneal recurrence, so treatment with nivolumab+SOX was started. The recurrence was resolved, but due to appearance of anorexia 6 months later, the treatment was discontinued. His symptoms worsened further, and hospitalized to receive intravenous infusion. A marked decrease in blood cortisol and ACTH was observed, suggesting hypopituitarism as irAE. After steroid administration, the symptoms resolved quickly. Subsequently, nivolumab+SOX were administered, and a long-term complete response was achieved.

A 68-year-old male presented with upper abdominal pain and was referred to our hospital after endoscopy revealed a primary tumor in the gastric antrum. He was diagnosed with unresectable advanced gastric cancer(cT4b[liver, pancreas]N+M1[PUL], cStage ⅣB). S-1 and oxaliplatin were selected as first-line chemotherapeutic agents. After 2 courses, a CT scan showed that the primary tumor and lymph nodes had shrunk, but there was no change in the pulmonary metastases. After 7 courses, oxaliplatin was discontinued due to peripheral neuropathy, and only S-1 was subsequently administered as a single agent. Endoscopy revealed only a scar at the primary tumor site, without malignant findings on biopsy. Seven years after treatment, he continued with only S-1. The lung metastases remained unchanged, but the primary tumor and lymph nodes continued to disappear.

Herein, we report a case of nephrotic syndrome developed during chemotherapy with an anti-EGFR antibody. The patient was a 72-year-old man. He underwent surgery for sigmoid colon cancer and liver metastasis. Two months later, lung and lymph node metastases were observed, and CAPOX+anti-VEGF antibody therapy was initiated. The patient was switched to CPT-11+panitumumab due to disease progression. After 3 courses, he was diagnosed with nephrotic syndrome due to rapid weight gain with diuretic resistance, lower leg edema, and severe proteinuria. Chemotherapy was suspended, and the diuretic dose was increased. Four weeks later, laboratory data and symptoms improved, and chemotherapy with CPT-11 alone was resumed. The nephrotic syndrome did not recur. Therefore, its previous development was attributed to panitumumab treatment.

Immune checkpoint inhibitors have shown efficacy in various malignancies. However, reports of conversion surgery after nivolumab therapy for unresectable advanced esophagogastric junction(EGJ)cancers remain rare. We present the case of a 69-year-old male diagnosed with EGJ cancer(cT4a[diaphragm], N2[No. 1×1, No. 7×1, and No. 19×1], M0, cStage Ⅲ). Neoadjuvant chemotherapy with docetaxel plus S-1 regimen was administered, resulting in stable disease(SD). During treatment, microsatellite instability-high(MSI-H)status was identified, and nivolumab monotherapy was subsequently initiated per regulatory approval. Although the radiological response remained SD, the tumor showed notable shrinkage, and the conversion surgery achieved R0 resection. The pathological findings revealed a Grade 1b treatment effect. The patient continued adjuvant nivolumab therapy postoperatively and remained disease-free. This case highlights the potential role of perioperative immunotherapy with nivolumab in MSI-H EGJ cancers and the promise of personalized treatment strategies.

Immune checkpoint inhibitors(ICIs)have remarkably improved survival with durable response for patients with multiple cancer type. But, the accurate predictors of response and toxicity to immunotherapy are still unclear. In recent years, the human microbiota, specially the gut microbiota, has been attracting attention in various fields, and it is one of the topics in the field of oncology. The gut microbiome, which refers to the microorganisms and their genes, affects the host immunity both locally and systemically. Modulation of the gut microbiota alters the immune systems and affects the efficacy of ICI. Many clinical trials targeting the gut microbiota, such as fecal microbiota transplantation(FMT)and biotics intervention, are currently being conducted. In this review, we consider the evidence on the role of the microbiome in cancer patients and research began the impact of FMT on the efficacy of ICIs in cancer. ln the future, research on carcinogenesis mechanisms and advance cancer treatment focusing on the human microbiota will become in creakingly active.

Recent advances in immune checkpoint inhibitors(ICIs)and molecular targeted therapies have substantially improved outcomes in lung cancer; however, marked inter-individual variability in efficacy and toxicity remains. Accumulating evidence suggests that the gut microbiota, acting through the"gut-lung axis,"is a key modifier of treatment response and tolerance in this setting. High microbial diversity and the abundance of beneficial taxa such as Akkermansia, Bifidobacterium, and Faecalibacterium have been associated with favorable ICI responses, whereas dysbiosis induced by antibiotics, proton pump inhibitors, cytotoxic chemotherapy, or lifestyle factors is linked to reduced efficacy and increased toxicity. Microbial metabolites, including short-chain fatty acids and tryptophan derivatives, shape antitumor immunity by modulating T-cell activation, regulatory T-cell differentiation, and the tumor immune microenvironment. In addition, emerging data indicate that the gut microbiota may influence the pharmacodynamics and adverse event profiles of EGFR tyrosine kinase inhibitors(EGFR- TKIs)and other targeted agents, particularly with respect to gastrointestinal toxicity. Smoking, a central etiological factor in lung carcinogenesis, also alters gut microbial composition, decreasing beneficial anti-inflammatory species and promoting pro-inflammatory taxa, thereby potentially aggravating systemic inflammation and impairing ICI responsiveness. Notably, partial restoration of a healthier microbiome appears possible with smoking cessation and rational supportive care. Interventions aimed at favorably modifying the gut ecosystem-such as high-fiber or plant-forward diets, probiotics, and fecal microbiotatransplantation-have begun to show promise in enhancing ICI efficacy without substantially increasing immune-related adverse events. Prospective trials in lung cancer are now underway to evaluate the clinical utility of microbiome-based biomarkers and interventions. Collectively, these findings position the gut microbiota as both a predictive biomarker and a modifiable therapeutic target, with the potential to refine patient stratification, optimize treatment selection, and advance truly personalized medicine in lung cancer.

Vascular lesions, including aneurysms, are rare but well-documented complications of von Recklinghausen's disease. Although aneurysms associated with this condition are often asymptomatic, rupture can lead to life-threatening events such as hemothorax. We report a 63-year-old male with von Recklinghausen's disease who presented with sudden onset of chest pain. Imaging revealed left-side hemothorax, and contrast-enhanced computed tomography( CT) suggested rupture of the left 10th intercostal artery. Given his hemodynamic stability, percutaneous coil embolization was performed. Angiography revealed two adjacent aneurysms at the origin of the left 10th intercostal artery, both of which were successfully embolized. Postoperative course was uneventful, and the patient was discharged on postoperative day 6. This case highlights the importance of considering vascular complications in von Recklinghausen's disease and supports the efficacy and safety of coil embolization in managing ruptured intercostal artery aneurysms.

The contribution of B cells to antitumor immunity remains controversial, with studies reporting varied effects across cancer types. Even less is known about the role of the endogenous humoral response, including when tumor-elicited antibodies are protective, when they are deleterious, and how they might be modulated to influence antitumor immunity. Critically, it remains unclear whether specific antigenic features govern the efficacy of humoral immune responses against cancer. We aim to define the conditions under which endogenous antibodies mediate antitumor immunity and to leverage these principles to improve neoantigen-directed immunotherapies, including cancer vaccines.

We performed a pan-cancer analysis of The Cancer Genome Atlas (TCGA) to assess associations between intratumoral IgG and clinical outcomes. Using syngeneic mouse tumor models expressing membrane or cytoplasmic neoantigens, we examined how antigen localization influences endogenous antibody responses. We evaluated strategies to enhance humoral immunity via cytokine and chemokine modulation and assessed antibody responses in the context of cancer vaccination.

Our pan-cancer TCGA analysis revealed marked heterogeneity in the prognostic impact of intratumoral IgG. In vivo, expression of membrane-localized, but not cytoplasmic, neoantigens drove potent class-switched IgG responses, activated myeloid cells, and restricted tumor growth independently of CD8 T cells. Notably, membrane-restricted antigen expression was sufficient to convert tumor types such as colorectal cancer, where IgG correlates with poor prognosis, into settings in which antibodies mediate tumor suppression. These effects required CD4 T-cell help, antigen-specific IgG, and Fc receptor engagement. Enhancing B-cell recruitment (C-X-C motif chemokine ligand 13) or B-cell help (interleukin (IL)-21) further amplified antibody-mediated tumor control, with co-expression providing the strongest benefit. Finally, we establish that antigen localization dictates vaccine efficacy: the point-mutated trophoblast cell-surface antigen 2 (Trop2) T256R, which exhibits impaired membrane localization and reduced antibody binding relative to wild-type Trop2, failed to elicit comparable vaccine-induced tumor control.

These findings identify antigen subcellular localization as a key regulator of endogenous antibody-mediated antitumor immunity and cancer vaccine efficacy, providing a mechanistic framework for leveraging humoral immunity in immunotherapeutic strategies. CXCL13 and IL-21 emerge as candidate approaches to selectively enhance antibody-mediated tumor control in settings where membrane-bound antigens are present.