AFP elevation

The therapeutic courses of ImT varied. Notably, cases in which treatment was applied considering ImT were highly prone to experience growing disease during treatment.

For patients with tumor stroke as the initial symptom, prompt suspicion of hemorrhagic malignant BM is essential, requiring emergent intervention and pathological confirmation. Notably, markedly elevated alpha-fetoprotein combined with extrahepatic FDG-avid masses on PET/CT strongly suggests EHCC.

Accurate diagnosis requires integration of morphology and IHC. This study expands the clinicopathologic and molecular spectrum by documenting a case arising in cervical gastric-type adenocarcinoma and identifying RICTOR amplification in this setting.

P3, N=236, Active, not recruiting, National Cancer Institute (NCI) | Trial completion date: Mar 2026 --> Mar 2027

This case highlights that HCC can occur in NCPF/IPH despite preserved liver function, the absence of severe portal hypertension, and prior nodules; it may also remain clinically silent. To our knowledge, this represents the first reported case of HCC in NCPF/IPH from India.

This case demonstrates that AFP may be a potential biomarker for PDAC, especially in the CA19-9-negative PDAC patient.

Even when HCC was undetected on imaging despite elevated tumor markers, many recurrence cases were subsequently detected, and curative treatment was possible through appropriate surveillance.

We report six cases of locally advanced, non-metastatic gastric cancer with elevated AFP, all of which demonstrated a favorable response and were well tolerated by the patients after the use of immune checkpoint inhibitors and neoadjuvant chemotherapy. This study suggests that programmed death receptor 1(PD-1) checkpoint inhibitors plus chemotherapy can benefit patients with AFPGC and provide a reference for the treatment of patients with AFPGC, and its mechanism of action deserves further study.

First-line conversion therapy with oxaliplatin, fluoropyrimidine, sintilimab (a programmed death-1 inhibitor), and later trastuzumab yielded only transient stabilization followed by clear progression: After six cycles, AFP rose to 1 546.07 μg/L and target lymph nodes enlarged to 46 mm×31 mm on CT. Given treatment failure and persistent HER2 positivity, a second-line, biology-informed regimen was initiated: Disitamab vedotin (an HER2-targeted antibody-drug conjugate delivering monomethyl auristatin E), lenvatinib (a multi-targeted tyrosine kinase inhibitor blocking vascular endothelial growth factor receptor and other pro-angiogenic pathways), tislelizumab (a programmed death-1 inhibitor), and short-course capecitabine (discontinued after 7 days due to grade 3 thrombocytopenia)...This case underscores that in HER2-positive, chemotherapy-refractory HAS, a rationally designed, multimodal regimen integrating an HER2-directed antibody-drug conjugate, antiangiogenic agent, and immune checkpoint blockade can overcome therapeutic resistance, achieve meaningful downstaging, and enable long-term disease control. Early molecular characterization and aggressive, persona-lized intervention are essential for improving outcomes in this rare malignancy.

Individualized and multimodal therapeutic approaches are fundamental to improving clinical outcomes due to the high degree of heterogeneity in AFPGC. Therefore, a comprehensive evaluation of serum AFP levels, radiological findings, and pathological characteristics is essential for the development of personalized treatment regimens.

Treatment involved a multimodal strategy combining transarterial chemoembolization (TACE), fractionated radiotherapy, and combination immunotherapy with camrelizumab plus apatinib. This case highlights the rare entity of direct renal invasion from HCC and provides practical insights into its diagnosis and comprehensive management. It illustrates the clinical feasibility and potential benefit of a combined locoregional and systemic strategy in advanced HCC with such uncommon extrahepatic renal involvement, underscoring the importance of individualized treatment in these complex presentations.

Current evidence suggests that AFP identifies biologically aggressive subsets of GEP-NENs, reflecting disease burden in specific contexts. While AFP should not be considered an independent biomarker, it holds potential as a contextual signal of aggressive tumor biology and as an adjunctive tool within integrated clinical and pathological frameworks.