Background: Anaplastic lymphoma kinase (ALK) tyrosine kinase inhibitors (TKIs) improve outcomes for non-small-cell lung cancer (NSCLC) patients with ALK fusions. Nevertheless, ALK TKI resistance will inevitably occur. Histological transformation is one of the causes of TKI resistance in NSCLC. Reports of ALK-rearranged adenocarcinoma with histological transformation are limited.
Case Presentation: A case of an invasive lung adenocarcinoma patient with ALK rearrangement who experienced histological transformation into sarcomatoid carcinoma after ALK TKI resistance is reported, and ALK fusion, MET amplification and TP53 mutation were detected after transformation.
Conclusions: This case first reported a patient with invasive lung adenocarcinoma harboring ALK rearrangement who underwent histological transformation into sarcomatoid carcinoma after ALK TKI resistance, and MET amplification might represent the cause. After transformation, the patient benefited from targeted therapy combined with chemotherapy, which represents a promising option for patients with sarcomatoid carcinoma transformation.
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http://dx.doi.org/10.1007/s00432-022-04022-0 | DOI Listing |
Transl Oncol
January 2025
Department of Hepatobiliary Pancreatic Surgery, Changhai Hospital, Naval Medical University (Second Military Medical University), 168 Changhai Road, Shanghai 200433, China. Electronic address:
Purpose The present study aimed to clarify the distribution pattern of carcinoma associated fibroblasts (CAFs) across pancreatic ductal adenocarcinoma (PDAC) and its prognostic prediction value. Methods Data of two cohorts were retrospectively collected from consecutive patients who underwent primary pancreatic resection from January 2015 to December 2017. We used tumor specimens to screen out the most suitable markers for the spatial distribution analysis for CAFs subpopulations.
View Article and Find Full Text PDFHepatology
January 2025
Division of Gastroenterology and Hepatology, University of California, San Francisco, San Francisco, CA.
Background Aims: Patients with hepatocellular carcinoma (HCC) meeting UNOS-downstaging (DS) criteria have excellent post-liver transplantation (LT) outcomes. Studies on HCC beyond UNOS-DS criteria ("All-comers" (AC)) have been limited by small sample size and short follow-up time, prompting this analysis.
Approach Results: 326 patients meeting UNOS-DS and 190 meeting AC criteria from 9 LT centers across 5 UNOS regions were enrolled from 2015 to 2023 and prospectively followed.
Hepatology
January 2025
Division of Digestive and Liver Diseases, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Preventive interventions are expected to substantially improve the prognosis of patients with primary liver cancer, predominantly hepatocellular carcinoma (HCC) and cholangiocarcinoma. HCC prevention is challenging in the face of the evolving etiological landscape, particularly the sharp increase in obesity-associated metabolic disorders, including metabolic dysfunction-associated steatotic liver disease (MASLD). Next-generation anti-HCV and HBV drugs have substantially reduced, but not eliminated, the risk of HCC and have given way to new challenges in identifying at-risk patients.
View Article and Find Full Text PDFHepatology
January 2025
Department of Hepatobiliary and Pancreatic Surgery, the First Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, China.
Background Aims: The role of adjuvant transarterial chemoembolization (TACE) for hepatocellular carcinoma (HCC) following curative resection remains controversial. We aimed to determine the effectiveness of postoperative adjuvant TACE in HCC patients.
Approach Results: In this randomized phase 3 trial, histologically confirmed HCC patients (AJCC TNM stage I and II) were randomly assigned (1:1) to adjuvant TACE or observation groups.
Proc Natl Acad Sci U S A
January 2025
Shenzhen Hospital, Southern Medical University, Shenzhen 518000, China.
ADAR is highly expressed and correlated with poor prognosis in hepatocellular carcinoma (HCC), yet the role of its constitutive isoform ADARp110 in tumorigenesis remains elusive. We investigated the role of ADARp110 in HCC and underlying mechanisms using clinical samples, a hepatocyte-specific knock-in mouse model, and engineered cell lines. ADARp110 is overexpressed and associated with poor survival in both human and mouse HCC.
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