NAPSA (Napsin A Aspartic Peptidase)

Further functionalization with an RGD peptide enhanced glioblastoma-targeted cellular uptake, and DOX-loaded RGD-D44A nanocages demonstrated potent antitumor efficacy in vivo. Collectively, these findings establish a rational mutation-based approach to fine-tune channel-adjacent interfacial dynamics, providing a generalizable framework for thermoresponsive macromolecular carrier design.

This case highlights the diagnostic challenge posed by TTF-1-positive gastric tumors, which may be mistaken for metastatic lesions from lung cancer. As TTF-1 expression is not entirely specific to tissues of lung or thyroid origin, diagnosis should be based on a comprehensive evaluation of morphological and immunohistochemical findings, together with clinical information, including treatment response and disease course.

We conclude that isolated HepPar1 expression in LUAD reflects mitochondrial adaptation to STK11 mutations rather than bona fide hepatocellular differentiation, and that HepPar1-expressing solid and granular adenocarcinomas (SAGA) represent an undifferentiated (solid, TTF1-negative) variant in this spectrum of tumors. Recognition of these tumors is warranted due to their exceptionally aggressive behavior, distinct pathogenomic features and common association with diagnostic challenges.

Next-generation sequencing analysis confirmed ALK rearrangements in 3 cases. Accurate identification of this specific subtype of lung adenocarcinoma is essential for administering appropriate treatment and reducing the risk of potential misdiagnosis.

The uniqueness of this study lies in the large number of cases, with their specimens obtained via cytopathological methods and immunostained with all five common SWI markers. This study contributes to the familiarity and awareness of pathologists and oncologists by highlighting the importance of cytomorphology and immunohistochemical profile of SWI/SNF-deficient NSCLC-NOS, facilitating earlier diagnosis, and may ultimately lead to more specific and novel therapeutic targets.

TTF-1 and Napsin A immunoreactivity was present in the background gastric mucosa almost exclusively in the AMAG-associated cases. This immunoreactivity is also present in AMAG-associated adenocarcinomas more commonly than non-AMAG-associated adenocarcinomas. This knowledge may aid pathologists in avoiding the pitfall of diagnosing metastatic lung cancer, as the expression is patchy and may also be seen in atrophic background mucosa.

SIGNIFICANCE STATEMENT: To the best of our knowledge, this study is the first to detect antidepressant and procognitive effects of lithium in DOX-induced chemobrain via GSK-3β inhibition. Accordingly, lithium offers a promising therapeutic target for the management of chemotherapy-induced depression and chemobrain.

The PCD signature confers significant potential to predict prognosis of LUAD in patients, and NAPSA is promising as a new marker for predicting the efficacy of immunotherapy.

This case highlights the cytomorphological features and immunophenotype of INI-1 deficient MM diagnosed through FNA. An accurate diagnosis requires a thorough clinicopathological correlation and a comprehensive IHC panel.

Following diagnosis, the patient received postoperative radiation therapy followed by osimertinib, and she remains recurrence-free three years after surgery. This case highlights an exceptionally rare pattern of recurrence, tumor-to-tumor metastasis of EGFR-mutated lung adenocarcinoma after right upper lobectomy into a meningioma, occurring 14 years after curative surgery. Oncologists should recognize that EGFR-mutated lung cancer can recur after an exceptionally long disease-free interval through rare metastatic patterns such as tumor-to-tumor metastasis.

Symptoms resolved postoperatively with no recurrence at 6-month follow-up. This case highlights potential false-positive biopsy/IHC results from entrapped benign epithelium and the role of surgical excision for definitive diagnosis.

P=N/A, N=463, Completed, Hoffmann-La Roche | Phase classification: P4 --> P=N/A