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1. Normal Spine Anatomy and Imaging

Author

Liaw, Peter, Kim, Charissa, Bao, Mike, Flower, Elisa, Chang, Yu-Ming, Eisenberg, Ronald L., Series Editor, Vachha, Behroze A., editor, Moonis, Gul, editor, Wintermark, Max, editor, and Massoud, Tarik F., editor

Published
2024
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4. List of contributors

Author

Abboud, Rayan, primary, Acharya, Akanksha, additional, Al-Dulaimi, Ragheed, additional, Al-Katib, Sayf, additional, Al-Nowfal, Ahmed, additional, Ali, Omair, additional, Almsaddi, Tarek, additional, Amaral, Joao, additional, Anene, Alvin, additional, Awad, Christopher, additional, Badar, Zain, additional, Balabhadra, Samyuktha, additional, Balon, Amanda Bronte, additional, Bhanot, Shelly, additional, Bircher, Walter G., additional, Bitar, Ryan, additional, Bittle, Scott, additional, Borror, William, additional, Boumezrag, Maryam, additional, Braga, Daniel, additional, Chadha, Sakshum, additional, Chapple, Kristina M., additional, Chiramel, George Koshy, additional, Chitra, R., additional, Chockalingam, Arun, additional, Choudhury, Priyam, additional, Clarke, Geoffrey D., additional, Coffman, Kimberly, additional, Cooper, Sydney, additional, Cooper, Kyle, additional, Cornejo, Santiago M., additional, Cornman-Homonoff, Joshua, additional, Covello, Brian, additional, Dandu, Chaitu, additional, Dennison, Jennifer J., additional, Deshmukh, Ashwin, additional, Dixit, Purushottam K., additional, Drummey, Rachel, additional, Duguay, Sean, additional, Dybicz, Stephanie S., additional, El Sehemawi, N., additional, Espiritu, Marvee, additional, Ewing, Brandon, additional, Farag, Ahmed, additional, Fisher, Jason A., additional, Foss, Wylie T., additional, Fourzali, Roberto, additional, Fu, Katherine Shin-Ying, additional, Gaba, Ron C., additional, Gadodia, Gaurav, additional, Garg, Tushar, additional, Ghorashi, Sona, additional, Gibney, Brianna L., additional, Gilbert, Alexandra, additional, Gordon, Andrew C., additional, Gupta, Aakash N., additional, Henry, Matthew, additional, Hernandez, Mauricio, additional, Hood, Amber, additional, Jain, Neil K., additional, Kalantari, Jalil, additional, Kamireddy, Arun, additional, Katz, Joshua, additional, Kauffman, Nathan D., additional, Kim, Charissa, additional, Kirkpatrick, Daniel, additional, Kogan, Joshua, additional, Konstantinidis, Menelaos, additional, Kovac, Stefan, additional, Krajewski, Adam Christopher, additional, Kruse, Jonas, additional, Lalla, E.A., additional, Le, Rebecca Tuan, additional, Lewandowski, Robert J., additional, Liao, Millie, additional, Liu, Tao, additional, Liu, Abraham, additional, Lopez-Reyes, G., additional, Maguire, Thaddeus, additional, Makris, Gregory C., additional, Martinek, Alexander, additional, McCain Pebror, Travis William, additional, McGuirt, Delaney, additional, Mehta, Capt. Tej Ishaan, additional, Meyer, Travis E., additional, Moattari, Syamak, additional, Mohapatra, Ashutosh, additional, Mohit, Babak, additional, Money, David Bradley, additional, Moon, John T., additional, Morar, Satya K., additional, Mor, Yechiel, additional, Moudgil, Pranav, additional, Murthy, Sandeep, additional, Murthy, Shashidhara, additional, Muthusami, Prakash, additional, Nair, Girish B., additional, Nassar, Mark, additional, Nezami, Nariman, additional, Ngo, Han G., additional, Nourouzpour, S., additional, Olivieri, Brandon, additional, Ovanez, Christopher, additional, Ozen, Merve, additional, Parker, Matt, additional, Patel, Shrey, additional, Patel, Neal, additional, Paturu, Mounica, additional, Pham, Eric, additional, Qamhawi, Zahi, additional, Ragulojan, Ranjan, additional, Raheem, Ishmael, additional, Ramasamy, Shakthi Kumaran, additional, Ramji, Husayn F., additional, Reyes, Daniel, additional, Reynolds, Conner D., additional, Rizk, Tony H., additional, Shah, Karishma, additional, Shah, Raj, additional, Sharma, Jatin, additional, Sheth, Rahul A., additional, Shing, Li Ka, additional, Shrigiriwar, Apurva, additional, Smith, Zachary T., additional, Solomon, Alex J., additional, Sreenivasulu, Kilari, additional, Taghipour, Mehdi, additional, Talluri, Tulasi, additional, Thomson, Benedict, additional, Thukral, Siddhant, additional, Tyagi, Ravi, additional, Veneranda, M., additional, Venkatraman, Siddharth, additional, Vollano, Nicholas, additional, Wagstaff, William, additional, Walker, John, additional, Webster, Linzi Arndt, additional, Windham-Herman, Austin-Marley, additional, Woodhead, Gregory J., additional, and Zhong, Jim, additional

Published
2023
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6. Comparative study of central intranodal lymphangiography patterns between patients with primary lymphoedema and patients with lymphatic leak.

Author

Kim, Charissa, Ali, Hamza, Tsai, Leo L., Bulman, Julie, Singhal, Dhruv, Carroll, Brett, Ahmed, Muneeb, and Weinstein, Jeffrey

Subjects
LYMPHEDEMA diagnosis, LYMPHEDEMA, LYMPHATICS, RESEARCH funding, RETROSPECTIVE studies, DESCRIPTIVE statistics, SYMPTOMS, MEDICAL records, ACQUISITION of data, LYMPHANGIOGRAPHY, CONTRAST media
Abstract

Recent descriptive findings using infra-inguinal central lymphangiography have delineated common lymphatic patterns in primary lymphoedema patients, including irregular lymph node morphology, paucity of lymph nodes on the more symptomatic laterality, lymphovenous shunting from pre-existing anastomoses between the lymphatic and venous systems, passage of contrast past midline to the contralateral lymphatics, and delayed opacification of central lymphatics. However, the specificity of the relevance of these findings to primary lymphoedema has not been investigated or compared to those with a normally structured and functioning lymphatic system. The purpose of this study was to compare central intranodal lymphangiography (IL) findings in patients with primary lymphoedema to a cohort without lymphoedema. In this retrospective study at a single-institution tertiary referral centre, a manual search was conducted of the institutional radiology report database for IL procedures performed between January 2017 and April 2022. Seventeen primary lymphoedema patients were identified and seventeen consecutive patients without peripheral lymphoedema who underwent IL for lymphatic leak were identified as controls. The IL procedure reports for the primary lymphoedema patients were reviewed for the lymphatic patterns previously noted in the literature. To determine whether these patterns were also present in lymphatic leak patients, a blinded interventional radiologist independently reviewed the IL procedure images for these patterns. Primary lymphoedema patients demonstrated a higher rate of lymphovenous shunting (8/17, 47% versus 0/17, 0%, p=0.003) and passage of contrast past midline to the contralateral lymphatics (8/17, 47% versus 0/15, 0%, p=0.003) than leak patients. Primary lymphoedema patients also failed to opacify central lymphatics on IL, with only 5/17 (29%) displaying opacification of the central lymphatics to the renal vein compared to 10/14 (71%) of patients with lymphatic leak, p=0.03 when injected from the groin lymph nodes. Contemporary central IL approach substantiates that lymphovenous shunting, passage of contrast past midline to the contralateral lymphatics, and delayed opacification of central lymphatics, are specific to lymphoedema. These findings have the potential to aid the diagnosis and add to the understanding of lymphatic flow patterns in primary lymphoedema. [ABSTRACT FROM AUTHOR]

Published
2024

17. List of contributors

Author

Abadi, Arad, Abdoli, Sherwin, Acton, Benjamin, Adams, Alexandra M., Aderonmu, Aderinsola A., Ahuja, Rakesh, Aiyash, Saleh, Akopian, Gabriel, Allar, Benjamin G., Amendola, Michael F., Anderson, Taylor, Andreadis, Athena, Ang, Darwin N., Anghel, Ersilia, Anthony, Favour Mfonobong, Anthony, Precious Idorenyin, Apfeld, Jordan C., Aref, Youssef, Arias, Fernando D., Arnold, Margaret, Badami, Abbasali, Bakal, Jeffrey Alexander, Bansal, Varun V., Barney, J., Barson, Jessica, Beck, Lauren L., Bender, Andrew R., Bhat, Vivek, Biswas, Saptarshi, Blitzer, David, Boeckholt, Tayt, Bolton, John S., Bose, Sourav K., Bowers, Gerald M., Brindle, Mary E., Brown, Matthew A., Brunicardi, F. Charles, Burkhart, Richard A., Byk, Jennifer L., Campbell, M., Carmona Matos, Danilea M., Castro-Ochoa, Kenny J., Cendan, Juan, Charles, Shane, Chavez-Rivera, Angel D., Chen, Hao Wei, Chen, Herbert, Chen, Kevin, Chen, Wendy, Cheng, Darren C., Cherng, Nicole B., Chopra, Christina Shree, Clifton, G. Travis, Crowner, Jason, Curtis, Houston, Daramola, Temilolaoluwa O., Darbandi, Aria, Dasani, Serena, DeJarnette, Kaci, Deneve, Jeremiah, Dewan, Karuna, Dial, Marcus, DiGiacomo, Jody C., DiMatteo, Andrew L., Dirkhipa, Tsering Y., Dittman, James M., Dodd, Ashley C., Dowlat, Israel, Drawbert, Hans E., Duchesne, Juan, Elfanagely, Omar, Elfanagely, Yousef, Eliyas, Javed Khader, Eruchalu, Chukwuma N., Etheridge, James C., Faridmoayer, Erfan, Faruqi, Arjumand, Feliz, Jessica Dominique, Fleming, Martin D., Fluke, Laura M., Flynn, Jason M., Fowler, Kathryn L., Garcia, Miguel, Garg, Tushar, Gedeon, Patrick C., Gilmor, Ruby, Goldman, Julie, Gonzalez, Christian, Guenter, Rachael E., Gulack, Brian C., Handmacher, Matthew, Haskins, Ivy N., Haupt, Carl, Hemal, Kshipra, Hey, Matthew T., Holguin, Perez, Hollenbeak, Christopher S., Holmes, Andrew, Hong, Hyo Jung, Huerta, Nicholas, Hussain, Mohamad A., Inostroza-Nieves, Yaritza, Kahn, Marc J., Karhadkar, Sunil S., Kashem, Mohammed A., Kawaji, Qingwen, Kazim, Syed Faraz, Kelley, Kathryn C., Khajanchi, Monty U., Khan, Shaarif Rauf, Kieu, Quynh, Kim, Charissa, Klein, Roger, Kool, Suzanne, Kruger, Jessica S., Kulaylat, Afif N., Kulaylat, Audrey S., Laikhter, Elizabeth, Lance, Samuel, LeBlanc, Megan, Lee, David, Lefevre, Frank V., Levy, Jacob, Lile, Deacon J., Lin, Carol A., Luo, Xinyi, Machado-Aranda, David A., Majeed, Kashif, Mamidala, Madhu, Mamode, Nizam, Mane, Abhishek, Manstein, Samuel M., Maroney, Jenna, Maxwell, Jessica, McCarthy, Patrick M., McCarthy, Philip, Mejia, Hector, Menon, Pallavi, Moeller, Albert, Morris, Dennis Spalla, Nadone, Haley, Nanda, Anil, Nauta, Allison, Navarro, Matthew, Nelson, Daniel W., Neubauer, Daniel C., Nguyen, Kaitlin A., Nguyen, Louis L., Nielson, Katherine, O. McCrea, Austin, Ocaña Narváez, Delia S., Oro, Peter, Ortega, Gezzer, Osband, Adena J., Ozair, Ahmad, Palanki, Rohan, Palau, Jaime Pardo, Panichella, Juliet, Patankar, Panini, Patel, Aneri, Patel, Nirmit, Pendlebury, Gehan A., Poa-Li, Christina, Prabhakaran, Sangeetha, Qamar, Hashir, Raghupathi, Ramesh, Rahman, Faique, Ramalingam, Mohan, Razi, Syed S., Razzack, Aminah Abdul, Razzaq, Abdul, Reich, Amanda J., Reid, Christopher, Resweber, Clay, Riddle, Mark, Rojas-Alexandre, Mehida, Rowell, Susan, Roxo, Vanessa, Roy, Debosree, Russell, Jacqueline L., Sachdev, Mala, Salas-Parra, Ruben D., Salim, Ali, Sampson, John H., Sanchez, Andrea Valquiria, Sanchez, Tiffany R., Schubart, Jane R., Schwartz, C., Schwartzman, Alexander, Scott, Erin M., Seifi, Ali, Sekhani, Aditya, Shen, Chan, Shiah, Eric, Shupp, Jeffrey W., Sievers, Meaghan, Silver, Rachel E., Singh, Kirit, Sinyard, Robert D., Smith, Kevin L., Soltani, Tandis, Sonkar, Abhinav Arun, Soyland, Dallas J., Stanley, Mackinzie A., Stein, David E., Stuart, Sean C., Tran, Linh, Vierra, Andrew, Welten, Vanessa M., Whelihan, Kate, White, Brandon M., Williams-Karnesky, Rebecca L., Witt, Emily E., X. Rhodes, Heather, Yamaguchi, Seiji, Yenduri, Ravali, Yiu, Andrew, Zambetti, Benjamin R., Zino, Christa, and Zlomke, Haley A.

Published
2023
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19. The Insurance Approval Process for Proton Radiation Therapy: A Significant Barrier to Patient Care

Author

Ning, Matthew S., primary, Gomez, Daniel R., additional, Shah, Aashish K., additional, Kim, Charissa R., additional, Palmer, Matthew B., additional, Thaker, Nikhil G., additional, Grosshans, David R., additional, Liao, Zhongxing, additional, Chapman, Bhavana V., additional, Brooks, Eric D., additional, Tang, Chad, additional, Rosenthal, David I., additional, Garden, Adam S., additional, Frank, Steven J., additional, and Gunn, G. Brandon, additional

Published
2019
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20. Selinexor (KPT-330) demonstrates anti-tumor efficacy in preclinical models of triple-negative breast cancer

Author

Arango, Natalia Paez, primary, Yuca, Erkan, additional, Zhao, Ming, additional, Evans, Kurt W., additional, Scott, Stephen, additional, Kim, Charissa, additional, Gonzalez-Angulo, Ana Maria, additional, Janku, Filip, additional, Ueno, Naoto T., additional, Tripathy, Debu, additional, Akcakanat, Argun, additional, Naing, Aung, additional, and Meric-Bernstam, Funda, additional

Published
2017
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25. Lesions of either anterior orbitofrontal cortex or ventrolateral prefrontal cortex in marmoset monkeys heighten innate fear and attenuate active coping behaviors to predator threat

Author

Shiba, Yoshiro, Kim, Charissa, Santangelo, Andrea M., Roberts, Angela C., Santangelo, Andrea [0000-0001-7727-2651], Roberts, Angela [0000-0003-2873-157X], and Apollo - University of Cambridge Repository

Subjects
emotion regulation, prefrontal cortex, snake fear, Original Research Article, anxiety, primate, Neuroscience
Abstract

The ventral prefrontal cortex is an integral part of the neural circuitry that is dysregulated in mood and anxiety disorders. However, the contribution of its distinct sub-regions to the regulation of negative emotion are poorly understood. Recently we implicated both the ventrolateral prefrontal cortex (vlPFC) and anterior orbitofrontal cortex (antOFC) in the regulation of conditioned fear and anxiety responses to a social stimulus, i.e., human intruder, in the marmoset monkey. In the present study we extend our investigations to determine the role of these two regions in regulating innate responses and coping strategies to a predator stimulus, i.e., a model snake. Both the vlPFC and antOFC lesioned groups exhibited enhanced anxiety-related responses to the snake in comparison to controls. Both groups also showed a reduction in active coping behavior. These results indicate that the vlPFC and antOFC contribute independently to the regulation of both innate fear and, as previously reported, conditioned fear, and highlight the importance of these regions in producing stimulus-appropriate coping responses. The finding that dysregulation in two distinct prefrontal regions produces the apparently similar behavioral phenotype of heightened negative emotion provides insight into the varied etiology that may underlie this symptom across a wide variety of neuropsychiatric conditions with implications for personalized treatment strategies.

Published
2014

27. Lesions of either anterior orbitofrontal cortex or ventrolateral prefrontal cortex in marmoset monkeys heighten innate fear and attenuate active coping behaviors to predator threat.

Author

Yoshiro Shiba, Kim, Charissa, Santangelo, Andrea M., and Roberts, Angela C.

Subjects
PREFRONTAL cortex, ANXIETY risk factors, INTERPERSONAL relations, PSYCHOLOGICAL adaptation, NEUROBEHAVIORAL disorders, THERAPEUTICS, PHYSIOLOGY
Abstract

The ventral prefrontal cortex is an integral part of the neural circuitry that is dysregulated in mood and anxiety disorders. However, the contribution of its distinct sub-regions to the regulation of negative emotion are poorly understood. Recently we implicated both the ventrolateral prefrontal cortex (vlPFC) and anterior orbitofrontal cortex (antOFC) in the regulation of conditioned fear and anxiety responses to a social stimulus, i.e., human intruder, in the marmoset monkey. In the present study we extend our investigations to determine the role of these two regions in regulating innate responses and coping strategies to a predator stimulus, i.e., a model snake. Both the vlPFC and antOFC lesioned groups exhibited enhanced anxiety-related responses to the snake in comparison to controls. Both groups also showed a reduction in active coping behavior. These results indicate that the vlPFC and antOFC contribute independently to the regulation of both innate fear and, as previously reported, conditioned fear, and highlight the importance of these regions in producing stimulus-appropriate coping responses. The finding that dysregulation in two distinct prefrontal regions produces the apparently similar behavioral phenotype of heightened negative emotion provides insight into the varied etiology that may underlie this symptom across a wide variety of neuropsychiatric conditions with implications for personalized treatment strategies. [ABSTRACT FROM AUTHOR]

Published
2015
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28. Basolateral Amygdala Lesions Facilitate Reward Choices after Negative Feedback in Rats.

Author

Izquierdo, Alicia, Darling, Chelsi, Manos, Nic, Pozos, Hilda, Kim, Charissa, Ostrander, Serena, Cazares, Victor, Stepp, Haley, and Rudebeck, Peter H.

Subjects
AMYGDALOID body, REWARD (Psychology), PREFRONTAL cortex, NEURAL circuitry, IBOTENIC acid, LABORATORY rats
Abstract

The orbitofrontal cortex (OFC) and basolateral amygdala (BLA) constitute part of a neural circuit important for adaptive, goal-directed learning. One task measuring flexibility of response to changes in reward is discrimination reversal learning. Damage to OFC produces well documented impairments on various forms of reversal learning in rodents, monkeys, and humans. Recent reports show that BLA, though highly interconnected with OFC, may be differentially involved in reversal learning. In the present experiment, we compared the effects of bilateral, ibotenic acid lesions of OFC or BLA (or SHAM) on visual discrimination and reversal learning. Specifically, we used pairwise visual discrimination methods, as is commonly administered in non-human primate studies, and analyzed how animals use positive and negative trial-by-trial feedback, domains not previously explored in a rat study. As expected, OFC lesions displayed signif-icantly slower reversal learning than SHAM and BLA rats across sessions. Rats with BLA lesions, conversely, showed facilitated reversal learning relative to SHAM and OFC groups. Furthermore, a trial-by-trial analysis of the errors committed showed the BLA group benefited more from incorrectly performed trials (or negative feedback) on future choices than either SHAM or OFC rats. This provides evidence that BLA and OFC are involved in updating responses to changes in reward contingency and that the roles are distinct. Our results are discussed in relation to a competitive framework model for OFC and BLA in reward processing. [ABSTRACT FROM AUTHOR]

Published
2013
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29. Additional file 3: of Selinexor (KPT-330) demonstrates anti-tumor efficacy in preclinical models of triple-negative breast cancer

Author

Arango, Natalia, Yuca, Erkan, Zhao, Ming, Evans, Kurt, Scott, Stephen, Kim, Charissa, Gonzalez-Angulo, Ana, Janku, Filip, Ueno, Naoto, Debu Tripathy, Argun Akcakanat, Aung Naing, and Meric-Bernstam, Funda

Subjects
3. Good health
Abstract

Effects of selinexor on the cell cycle. SUM-159PT and MDA-MB-468 cells were treated with 1 nM paclitaxel alone (2 nM for MDA-MB-468), 400 nM selinexor alone, and the combination of both. After 72Â hours, cells were stained with propidium iodide and analyzed via flow cytometry. (DOCX 514 kb)

30. Additional file 1: of Selinexor (KPT-330) demonstrates anti-tumor efficacy in preclinical models of triple-negative breast cancer

Author

Arango, Natalia, Yuca, Erkan, Zhao, Ming, Evans, Kurt, Scott, Stephen, Kim, Charissa, Gonzalez-Angulo, Ana, Janku, Filip, Ueno, Naoto, Debu Tripathy, Argun Akcakanat, Aung Naing, and Meric-Bernstam, Funda

Subjects
neoplasms, 3. Good health
Abstract

PIK3CA, PTEN, TP53 and Ras/Raf status of cell lines in panel. A panel of breast cancer cell lines was tested with selinexor, and cell growth was measured after 72Â hours of treatment using the SRB assay. IC50 was then calculated using isobologram curves. The mutation statuses for PIK3CA, PTEN, TP53, and Ras/Raf status are reported. (DOCX 23 kb)

32. Additional file 2: of Selinexor (KPT-330) demonstrates anti-tumor efficacy in preclinical models of triple-negative breast cancer

Author

Arango, Natalia, Yuca, Erkan, Zhao, Ming, Evans, Kurt, Scott, Stephen, Kim, Charissa, Gonzalez-Angulo, Ana, Janku, Filip, Ueno, Naoto, Debu Tripathy, Argun Akcakanat, Aung Naing, and Meric-Bernstam, Funda

Subjects
3. Good health
Abstract

Effects of selinexor in breast cancer models. A Eight breast cancer cell lines were treated with vehicle or 5 ΟM selinexor. Cells were lysed and blotted with the indicated antibodies. B The bands were quantified and normalized to their respective β-actin controls. Data are shown as relative protein levels vs vehicle control of cell lines treated with selinexor. (DOCX 397 kb)

33. Additional file 1: of Selinexor (KPT-330) demonstrates anti-tumor efficacy in preclinical models of triple-negative breast cancer

Author

Arango, Natalia, Yuca, Erkan, Zhao, Ming, Evans, Kurt, Scott, Stephen, Kim, Charissa, Gonzalez-Angulo, Ana, Janku, Filip, Ueno, Naoto, Debu Tripathy, Argun Akcakanat, Aung Naing, and Meric-Bernstam, Funda

Subjects
neoplasms, 3. Good health
Abstract

PIK3CA, PTEN, TP53 and Ras/Raf status of cell lines in panel. A panel of breast cancer cell lines was tested with selinexor, and cell growth was measured after 72Â hours of treatment using the SRB assay. IC50 was then calculated using isobologram curves. The mutation statuses for PIK3CA, PTEN, TP53, and Ras/Raf status are reported. (DOCX 23 kb)

34. Additional file 4: of Selinexor (KPT-330) demonstrates anti-tumor efficacy in preclinical models of triple-negative breast cancer

Author

Arango, Natalia, Yuca, Erkan, Zhao, Ming, Evans, Kurt, Scott, Stephen, Kim, Charissa, Gonzalez-Angulo, Ana, Janku, Filip, Ueno, Naoto, Debu Tripathy, Argun Akcakanat, Aung Naing, and Meric-Bernstam, Funda

Subjects
3. Good health
Abstract

Actionable DNA alterations in PDXs. BCX 6, BCX 10, BCX 11, and BCX 22 were analyzed by targeted exome sequencing of 202 cancer-relevant targets and whole-exome sequencing. BCX 51 was analyzed using targeted exome sequencing of 265 genes that included XPO1. HDEL: copy number 4. (DOCX 15 kb)

35. Additional file 2: of Selinexor (KPT-330) demonstrates anti-tumor efficacy in preclinical models of triple-negative breast cancer

Author

Arango, Natalia, Yuca, Erkan, Zhao, Ming, Evans, Kurt, Scott, Stephen, Kim, Charissa, Gonzalez-Angulo, Ana, Janku, Filip, Ueno, Naoto, Debu Tripathy, Argun Akcakanat, Aung Naing, and Meric-Bernstam, Funda

Subjects
3. Good health
Abstract

Effects of selinexor in breast cancer models. A Eight breast cancer cell lines were treated with vehicle or 5 ΟM selinexor. Cells were lysed and blotted with the indicated antibodies. B The bands were quantified and normalized to their respective β-actin controls. Data are shown as relative protein levels vs vehicle control of cell lines treated with selinexor. (DOCX 397 kb)

36. Additional file 4: of Selinexor (KPT-330) demonstrates anti-tumor efficacy in preclinical models of triple-negative breast cancer

Author

Arango, Natalia, Yuca, Erkan, Zhao, Ming, Evans, Kurt, Scott, Stephen, Kim, Charissa, Gonzalez-Angulo, Ana, Janku, Filip, Ueno, Naoto, Debu Tripathy, Argun Akcakanat, Aung Naing, and Meric-Bernstam, Funda

Subjects
3. Good health
Abstract

Actionable DNA alterations in PDXs. BCX 6, BCX 10, BCX 11, and BCX 22 were analyzed by targeted exome sequencing of 202 cancer-relevant targets and whole-exome sequencing. BCX 51 was analyzed using targeted exome sequencing of 265 genes that included XPO1. HDEL: copy number 4. (DOCX 15 kb)

38. Additional file 3: of Selinexor (KPT-330) demonstrates anti-tumor efficacy in preclinical models of triple-negative breast cancer

Author

Arango, Natalia, Yuca, Erkan, Zhao, Ming, Evans, Kurt, Scott, Stephen, Kim, Charissa, Gonzalez-Angulo, Ana, Janku, Filip, Ueno, Naoto, Debu Tripathy, Argun Akcakanat, Aung Naing, and Meric-Bernstam, Funda

Subjects
3. Good health
Abstract

Effects of selinexor on the cell cycle. SUM-159PT and MDA-MB-468 cells were treated with 1 nM paclitaxel alone (2 nM for MDA-MB-468), 400 nM selinexor alone, and the combination of both. After 72Â hours, cells were stained with propidium iodide and analyzed via flow cytometry. (DOCX 514 kb)

39. Single-nuclear transcriptomics of lymphedema-associated adipose reveals a pro-lymphangiogenic stromal cell population.

Author

Westcott GP, Emont MP, Gulko A, Zhou Z, Kim C, Varma G, Tsai LL, O'Donnell E, Loureiro ZY, Liang W, Jacobs C, Tsai LT, Padera TP, Singhal D, and Rosen ED

Abstract

Chronic lymphedema is a progressive, disfiguring disease that results from dysfunction of the lymphatic vasculature, causing distal accumulation of interstitial fluid, localized development of tissue edema, and expansion of subcutaneous adipose tissue (SAT). As the molecular mechanisms governing SAT remodeling in this disease are unclear, we performed single-nucleus RNA sequencing on paired control and affected SAT biopsies from patients with unilateral lymphedema. Lymphedema samples were characterized by expansion of SAA + adipocytes, pro-adipogenic stem cells, and proliferation of lymphatic capillaries. A GRIA1 + lymphedema-enriched stromal cell population expressing VEGFC , ADAMTS3 , and CCBE1 was identified, suggesting an enhanced axis of communication between adipose stem and progenitor cells (ASPCs) and lymphatic endothelial cells. Furthermore, lymphedema ASPC-conditioned media promoted lymphatic endothelial tube elongation in vitro . These findings indicate a critical role for ASPCs in regulating adipocyte differentiation and lymphatic vascular remodeling in lymphedema, and provide a valuable resource for better understanding this disease.

Published
2025
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