Gut microbiome alterations are increasingly associated with hepatocellular carcinoma (HCC), highlighting the gut-liver axis as a key contributor to tumor progression and prognosis. Taxon-based HCC microbiome studies have shown limited reproducibility because they are affected by database dependency, taxonomic ambiguity, and overlooked ecological interactions. The Two Competing Guilds (TCG) model, based on stable gut microbiome interactions, provides a structurally grounded framework for robust, generalizable biomarkers. Using shotgun metagenomic data from a newly recruited cohort of 120 surgically resectable HCC cases and 76 benign liver tumor controls, we constructed co-abundance networks to identify stably correlated genome pairs and assembled a hepatic cancer-TCG (HCC-TCG) model composed of 142 genomes. Functionally, one Guild had more genes for butyrate production from carbohydrate fermentation while the other Guild was enriched in genes for virulence factors and antibiotic resistance, highlighting its potential proinflammatory roles. Classifiers trained on the abundance profiles of HCC-TCG genomes successfully distinguished HCC from benign liver tumors (area under the receiver operating characteristic, AUROC = 0.70) and from colorectal liver metastases (CRLM) (AUROC = 0.78). In an external validation cohort, the model further discriminated against HCC from intrahepatic cholangiocarcinoma (iCCA) (AUROC = 0.72), and from healthy controls (AUROC = 0.79-0.85), demonstrating its broad applicability for tumor stratification across clinical contexts. Moreover, HCC-TCG profiles predicted post-resection recurrence risk and response to adjuvant therapies (AUROC up to 0.83). Importantly, external validation in two independent cohorts of advanced HCC patients treated with PD-1/PD-L1 inhibitors demonstrated consistent predictive performance (AUROC = 0.64-0.73), confirming the model's generalizability in nonsurgical and immunotherapy contexts. This genome-specific, ecologically structured, and database-independent framework identifies a conserved Guild-based microbiome signature for HCC. Our findings demonstrate that a fixed genome-resolved ecological structure retains transferable discriminatory signal across clinical contexts. The HCC-TCG framework provides a genome-specific, interaction-based foundation for future development of non-invasive microbiome stratification strategies requiring prospective validation.

Colorectal cancer (CRC), a leading cause of cancer-related mortality due to distant metastases, is largely driven by activating mutations in the WNT and mitogen-activated protein kinase (MAPK) pathways. Understanding the mechanism underlying the metastatic process is essential for developing effective treatments. Using serial in vivo orthotopic passaging, we developed an immunocompetent mouse model of metastatic CRC. Highly metastatic tumor cells exhibited chromosomal amplifications in MAPK pathway genes, resulting in increased MAPK pathway activity and suppression of WNT-associated transcriptional programs, including stem cell genes. Pharmacological inhibition of mutant KRAS[G12D] led to a reduction in the MAPK-high-WNT-low transcriptional state and decreased both lung and liver metastases. Analysis of CRC patient data revealed that the metastatic gene signature associated with the MAPK-high-WNT-low state correlated with poorer survival outcomes. These findings underscore the plasticity of metastasis-initiating cells in CRC driven by the opposing roles of MAPK and WNT signaling, despite their synergy observed during colon tumorigenesis.

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.

The patient was a 70-year-old male with highly advanced gastric cancer, 2 liver metastases(S3 and S8), and pancreatic invasion. Three courses of S-1+L-OHP(SOX therapy)were administered as conversion surgery chemotherapy, and total gastrectomy and combined resection of the body and tail of the pancreas and spleen and partial resection of the liver(S3 and S8)were performed as conversion surgery. S-1 therapy was continued for 1 year as postoperative adjuvant chemotherapy. A left adrenal metastasis was detected on CT 1 year and 6 months after the operation. PET-CT revealed no other areas suspicious of recurrence; therefore, left adrenalectomy was performed through the retroperitoneal space. Radical resection was not performed because of severe adhesions and scarring from the previous surgery. Paclitaxel+ramucirumab chemotherapy was initiated, and after 10 courses, tumor disappearance was observed on enhanced CT and PET-CT. The re-enlargement was observed 1 year later. The patient underwent re-administration of paclitaxel+ramucirumab, SOX+ nivolumab therapy, and nivolumab monotherapy, but all showed PD on imaging. After 8 courses of CPT-11 monotherapy, CR was again observed on imaging. Five years and 3 months after the initial surgery and 3 years and 8 months after adrenal metastasis resection, the patient was alive and well without recurrence.

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.

A man in his 70s underwent an upper gastrointestinal series during a routine medical check-up, which revealed an abnormality in the stomach. Subsequent investigations, including computed tomography, endoscopy, and pathological examination, confirmed the diagnosis of gastric neuroendocrine carcinoma, a small cell type with multiple synchronous liver metastases(cT3[SE]N1H1PXM0, Stage Ⅳ). Following a comprehensive treatment involving 35 courses of S-1+CDDP chemotherapy, the primary lesion and multiple liver metastases resolved. For the next 8 years, the patient continued maintenance therapy with S-1 alone. The patient has survived for 15 years without recurrence.

The therapeutic landscape of metastatic castration-resistant prostate cancer (mCRPC) has evolved substantially over the past decade, with androgen receptor pathway inhibitors, taxanes, poly (ADP-ribose) polymerase (PARP) inhibitors, radioisotopes, bone-protecting agents, and emerging targeted therapies improving survival for patients. At the same time, earlier treatment intensification in the hormone-sensitive setting has resulted in heterogeneous clinical presentations at the onset of castration resistance, adding complexity to treatment sequencing and clinical decision making. Here, we propose a pragmatic, patient-centered framework to help guide the management of mCRPC by integrating clinical features, molecular profiling, imaging findings, and supportive care considerations. Confirmation of castration resistance remains a critical first step and requires documented biochemical or radiographic progression in the setting of castrate testosterone levels. Treatment selection should consider prior systemic therapies, disease burden and tempo, symptom profile, comorbidities, and frailty. Molecular characterization, including evaluation for homologous recombination repair alterations and mismatch repair deficiency, is highly important for identifying candidates for PARP inhibitors or immune checkpoint blockade and other emerging biomarker-driven targeted strategies. Prostate-specific membrane antigen (PSMA)-targeted radioligand therapy has emerged as a key treatment. PSMA-positron emission tomography-based selection, incorporating assessment of uptake intensity, tumor heterogeneity, and total tumor volume, may help identify patients who are most likely to benefit from this treatment. Clinical factors such as liver metastases and limited prior response to androgen receptor-directed therapy have been associated with less favorable outcomes. Early on-treatment assessment using prostate-specific antigen response and PSMA-based imaging may support adaptive treatment strategies and earlier recognition of resistance. Given the high prevalence of bone metastases, bone-protecting agents should be considered to reduce skeletal-related events. Early palliative care (EPC) is now widely recognized as a concurrent, patient-centered intervention that improves quality of life, symptom burden, coping, and satisfaction across advanced cancers. Prostate cancer represents an especially compelling setting for EPC because of prolonged advanced disease courses, cumulative symptom burden, repeated treatment transitions, and persistent unmet supportive needs.

Breast cancer commonly metastasizes to the lungs, bones, liver, and brain; however, gastrointestinal involvement is uncommon. Simultaneous metastases to both the stomach and colon are extremely rare. We report the case of a 53-year-old woman with bilateral breast cancer (right invasive ductal carcinoma and left invasive lobular carcinoma [ILC]) who developed gastric and colonic metastases, presenting with rare endoscopic findings characterized by multiple polypoid lesions, along with disseminated carcinomatosis of the bone marrow. Biopsies from the stomach and colon revealed poorly differentiated adenocarcinomas that were estrogen receptor-positive and negative for E-cadherin in the colon, consistent with ILC metastases. Endocrine therapy with letrozole led to systemic improvement. However, diarrhea and abdominal pain persisted until palbociclib was initiated, after which both symptoms markedly improved. Follow-up endoscopy demonstrated regression of the gastric and colonic lesions. This case is of educational value because it demonstrates, with high-quality images, subtle mucosal changes with a polypoid appearance that are not widely recognized as typical findings of colonic metastasis from ILC, and includes a review of previously reported cases. In patients with breast cancer, particularly ILC, persistent gastrointestinal symptoms may suggest metastasis. Careful endoscopic evaluation with biopsy is essential for diagnosis and monitoring the treatment response.

Patients with breast cancer liver metastasis (BCLM) have a low survival rate and poor prognosis; thus, early and precise diagnosis and treatment are important. Here, we developed rutin-encapsulated manganese carbonate nanoparticles (RM NPs) for sensitive magnetic resonance imaging (MRI) diagnosis and effective inhibition of BCLM. RM NPs are nanoclusters consisting of manganese carbonate nanocrystals. They have pH-responsive properties and release Mn2+ following their uptake into cells, generating MRI signals. Using a 4T1 mouse liver metastasis model, we demonstrated different uptake rates of RM NPs between normal liver tissue and metastatic tumors. The 'liver-dark/tumor-bright' (tumor-to-normal liver contrast ratio reached 219%) phenomenon can be produced using a specific T1WI imaging sequence, which enables precise imaging of submillimeter (less than 1 mm) BCLM. In vitro and in vivo experiments confirmed that because of the rutin sugar groups on the surface of RM NPs, they actively target tumor cells with overexpressed glucose transporters (Gluts). After being taken up by tumor cells, RM NPs release rutin, which induces tumor cell apoptosis by upregulating cleaved cysteine protease-3 and thereby inhibiting tumor cell growth and liver metastasis. Overall, RM NPs can serve as an effective and safe theranostic platform for precise MRI and treatment of BCLM.

Pancreatic cancer is characterized by its high malignancy, aggressive nature, and exceedingly poor prognosis. While surgical resection combined with systemic therapy offers the only potential for cure, the high recurrence rate significantly compromises long-term survival, even after radical surgery. The presence of peritoneal free tumor cells, detected via peritoneal cytology, represents a form of metastatic spread distinct from traditional distant metastases and exerts a similarly negative impact on patient outcomes. Peritoneal washing cytology is a practical and valuable diagnostic tool for identifying intraperitoneal free tumor cells, providing critical insights into disease progression and prognosis. Its status retains significant prognostic relevance even after initial clinical stratification based on resectability. Furthermore, peritoneal cytology plays a pivotal role in guiding clinical decision-making. Notably, the conversion from positive to negative cytology following preoperative therapy may select patients who could benefit from conversion surgery, potentially counteracting the adverse prognostic effects associated with peritoneal dissemination. This review comprehensively examines the etiology and risk factors associated with positive peritoneal cytology, integrates its prognostic value into current stratification systems, discusses its profound implications for clinical decision-making, explores emerging detection technologies, and shares future perspectives. By synthesizing existing evidence, this review aims to contribute to optimized individualized treatment approaches and improved clinical outcomes for patients with pancreatic cancer.