Darius Filsoof

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Journals/Publications

• Chrissian, A. A., Abbas, H., Chaddha, U., Debiane, L. G., DeBiasi, E., Filsoof, D., Hashmi, M. D., Morton, C., Naselsky, W. C., Pannu, J., Ronaghi, R., Salguero, B. D., Salmon, C., Stewart, S. J., & Channick, C. L. (2025). American Association of Bronchology and Interventional Pulmonology Essential Knowledge in Interventional Pulmonology Series: Selected Topics in Malignant Pleural Disease. Journal of bronchology & interventional pulmonology, 32(1).
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  The goal of the American Association of Bronchology and Interventional Pulmonology Essential Knowledge in Interventional Pulmonology Series is to provide clinicians with concise, up-to-date reviews of important topics in the field of interventional pulmonology. This 3-year alternating rotation of primary topics will start with a focus on selected topics in malignant pleural disease. In this article, we update the reader on malignant pleural effusion in 3 parts: part 1-diagnosis, focusing on imaging and fluid biomarkers; part 2-management, with review of multimodal approaches, cost considerations, and evolving targeted therapies; and part 3-pleural mesothelioma. These reviews complement the Essential Knowledge in Interventional Pulmonology Lecture Series presented at the 2023 AABIP Annual Conference, available for viewing on the AABIP website (https://aabip.memberclicks.net/essential-knowledge-in-interventional-pulmonology-series).
• Irfan, H., Filsuf, D., Mooney, K. L., Bedi, H., & Shaller, B. D. (2023). Endobronchial Ultrasound-guided Transbronchial Needle Aspiration of Primary Cardiac Synovial Sarcoma of the Left Ventricle. American journal of respiratory and critical care medicine, 207(9), e73-e74.
• Shaller, B. D., Filsoof, D., Pineda, J. M., & Gildea, T. R. (2022). Malignant Central Airway Obstruction: What's New?. Seminars in respiratory and critical care medicine, 43(4), 512-529.
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  Malignant central airway obstruction (MCAO) is a debilitating and life-limiting complication that occurs in an unfortunately large number of individuals with advanced intrathoracic cancer. Although the management of MCAO is multimodal and interdisciplinary, the task of providing patients with prompt palliation falls increasingly on the shoulders of interventional pulmonologists. While a variety of tools and techniques are available for the management of malignant obstructive lesions, advancements and evolution in this therapeutic venue have been somewhat sluggish and limited when compared with other branches of interventional pulmonary medicine (e.g., the early diagnosis of peripheral lung nodules). Indeed, one pragmatic, albeit somewhat uncharitable, reading of this article's title might suggest a wry smile and shug of the shoulders as to imply that relatively little has changed in recent years. That said, the spectrum of interventions for MCAO continues to expand, even if at a less impressive clip. Herein, we present on MCAO and its endoscopic and nonendoscopic management-that which is old, that which is new, and that which is still on the horizon.
• Daniel, J. A., Pellegrini, M., Lee, B. S., Guo, Z., Filsuf, D., Belkina, N. V., You, Z., Paull, T. T., Sleckman, B. P., Feigenbaum, L., & Nussenzweig, A. (2012). Loss of ATM kinase activity leads to embryonic lethality in mice. The Journal of cell biology, 198(3), 295-304.
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  Ataxia telangiectasia (A-T) mutated (ATM) is a key deoxyribonucleic acid (DNA) damage signaling kinase that regulates DNA repair, cell cycle checkpoints, and apoptosis. The majority of patients with A-T, a cancer-prone neurodegenerative disease, present with null mutations in Atm. To determine whether the functions of ATM are mediated solely by its kinase activity, we generated two mouse models containing single, catalytically inactivating point mutations in Atm. In this paper, we show that, in contrast to Atm-null mice, both D2899A and Q2740P mutations cause early embryonic lethality in mice, without displaying dominant-negative interfering activity. Using conditional deletion, we find that the D2899A mutation in adult mice behaves largely similar to Atm-null cells but shows greater deficiency in homologous recombination (HR) as measured by hypersensitivity to poly (adenosine diphosphate-ribose) polymerase inhibition and increased genomic instability. These results may explain why missense mutations with no detectable kinase activity are rarely found in patients with classical A-T. We propose that ATM kinase-inactive missense mutations, unless otherwise compensated for, interfere with HR during embryogenesis.
• Daniel, J. A., Santos, M. A., Wang, Z., Zang, C., Schwab, K. R., Jankovic, M., Filsuf, D., Chen, H. T., Gazumyan, A., Yamane, A., Cho, Y. W., Sun, H. W., Ge, K., Peng, W., Nussenzweig, M. C., Casellas, R., Dressler, G. R., Zhao, K., & Nussenzweig, A. (2010). PTIP promotes chromatin changes critical for immunoglobulin class switch recombination. Science (New York, N.Y.), 329(5994), 917-23.
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  Programmed genetic rearrangements in lymphocytes require transcription at antigen receptor genes to promote accessibility for initiating double-strand break (DSB) formation critical for DNA recombination and repair. Here, we showed that activated B cells deficient in the PTIP component of the MLL3 (mixed-lineage leukemia 3)-MLL4 complex display impaired trimethylation of histone 3 at lysine 4 (H3K4me3) and transcription initiation of downstream switch regions at the immunoglobulin heavy-chain (Igh) locus, leading to defective immunoglobulin class switching. We also showed that PTIP accumulation at DSBs contributes to class switch recombination (CSR) and genome stability independently of Igh switch transcription. These results demonstrate that PTIP promotes specific chromatin changes that control the accessibility of the Igh locus to CSR and suggest a nonredundant role for the MLL3-MLL4 complex in altering antibody effector function.