ALK negative

Consolidative allogeneic hematopoietic stem cell transplant HSCT then lead to long-term remission. This case underscores the critical role of comprehensive genomic profiling for rare histologies and supports the potential utility of JAK/STAT pathway inhibitors in select patients with ALK-negative ALCL.

While routine inflammation markers showed limited utility in predicting site-specific metastasis, LDH levels correlated significantly with liver involvement. Aggressive management strategies are warranted for ALK-positive patients presenting with liver metastases.

The tumor was located in the lower tracheal wall and showed intense activity. A follow-up FDG PET/CT after 8 cycles of chemotherapy showed complete resolution of the tumor.

In further studies, RNA sequencing confirmed the presence of NPM1::ALK gene fusion in this case; whole-exome sequencing (WES) detected somatic mutations in multiple genes of the JAK-STAT pathway (including JAK1, PTPN6, MTOR, and TYK2). It is noteworthy that such genetic alterations are more commonly observed in ALK-negative anaplastic large cell lymphoma (ALK-ALCL) but are less commonly reported in ALK+ALCL.

In alignment with our experimental findings, relapsed or refractory PTCL patients with high serum FFA exhibited superior responses to golidocitinib treatment than those with low serum FFA. Collectively, high serum FFA is related to tumor progression and indicates golidocitinib sensitivity, providing novel insights into reprogramming lipid metabolism to dually target the tumor and microenvironment in PTCL.

To date, surgical resection remains the mainstay of treatment for IMT. For ALK-negative IMT cases, molecular profiling to identify targetable genomic alterations may assist in selecting individualized targeted therapies.

P=N/A, N=160, Recruiting, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine

This case demonstrates the potential synergistic efficacy of whole-brain radiotherapy, 125I brachytherapy, and antiangiogenic therapy in advanced epidermal growth factor receptor/anaplastic lymphoma kinase wild-type lung adenocarcinoma, providing a novel salvage strategy for chemotherapy-refractory metastatic disease. Prospective clinical trials are warranted to validate the survival benefits of this multimodal approach in molecularly unselected, high-risk populations.

In the present manuscript, we provide a subsequent long-term follow-up report of the same patient, offering an extended 88-month postoperative course and additional radiologic and pathologic details not included in the earlier publication. This follow-up report highlights the long-term benign behavior of the tumor despite positive surgical margins and anaplastic lymphoma kinase (ALK)-negative immunohistochemistry, contributing meaningful information to the scarce literature on adult duodenal IMTs.

Among the molecular analytic modalities included in this study, the combination of HBZ-ISH and HTLV-1-qPCR represented the results obtained from the other more expensive modalities, indicating that this combination is effective in daily practice. When T-cell neoplasms arise in HTLV-1 carriers and exhibit atypical clinical, phenotypical, or genetic features for ATLL, it is recommended to perform HBZ-ISH and HTLV-1-qPCR to distinguish non-ATLL TCLs.

Careful assessment of nuclear morphology and cell distribution patterns can provide valuable diagnostic clues to prevent misdiagnosis. This rare cytological presentation offers critical educational insights for cytopathologists and underscores the diagnostic value of FNA cytology, particularly when integrated with immunophenotypic analysis and retrospective morphological review in evaluating morphologically challenging lymphoid malignancies.

In this case, however, the patient achieved a remarkable PFS of over 4 years following a multimodal regimen combining SRT, PD-1 inhibition, and GM-CSF. This tri-modality strategy emerges as a promising therapeutic paradigm for NSCLC-associated LM.