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2. Exploring the tumor genomic landscape of aggressive prostate cancer by whole‐genome sequencing of tissue or liquid biopsies

Author

Weiss, Simone, primary, Lamy, Philippe, additional, Rusan, Maria, additional, Nørgaard, Maibritt, additional, Ulhøi, Benedicte Parm, additional, Knudsen, Michael, additional, Kassentoft, Christine Gaasdal, additional, Farajzadeh, Leila, additional, Jensen, Jørgen Bjerggaard, additional, Pedersen, Jakob Skou, additional, Borre, Michael, additional, and Sørensen, Karina Dalsgaard, additional

Published
2024
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3. Exome and genome sequencing of nasopharynx cancer identifies NF-κB pathway activating mutations.

Author

Li, Yvonne Y, Chung, Grace TY, Lui, Vivian WY, To, Ka-Fai, Ma, Brigette BY, Chow, Chit, Woo, John KS, Yip, Kevin Y, Seo, Jeongsun, Hui, Edwin P, Mak, Michael KF, Rusan, Maria, Chau, Nicole G, Or, Yvonne YY, Law, Marcus HN, Law, Peggy PY, Liu, Zoey WY, Ngan, Hoi-Lam, Hau, Pok-Man, Verhoeft, Krista R, Poon, Peony HY, Yoo, Seong-Keun, Shin, Jong-Yeon, Lee, Sau-Dan, Lun, Samantha WM, Jia, Lin, Chan, Anthony WH, Chan, Jason YK, Lai, Paul BS, Fung, Choi-Yi, Hung, Suet-Ting, Wang, Lin, Chang, Ann Margaret V, Chiosea, Simion I, Hedberg, Matthew L, Tsao, Sai-Wah, van Hasselt, Andrew C, Chan, Anthony TC, Grandis, Jennifer R, Hammerman, Peter S, and Lo, Kwok-Wai

Subjects
Humans, Herpesvirus 4, Human, Epstein-Barr Virus Infections, Carcinoma, Nasopharyngeal Neoplasms, TNF Receptor-Associated Factor 3, NF-kappa B, Viral Matrix Proteins, Signal Transduction, Cell Proliferation, Mutation, Genome, Human, Exome, NF-KappaB Inhibitor alpha, Whole Genome Sequencing, Deubiquitinating Enzyme CYLD, Nasopharyngeal Carcinoma, Genome, Human, Herpesvirus 4
Abstract

Nasopharyngeal carcinoma (NPC) is an aggressive head and neck cancer characterized by Epstein-Barr virus (EBV) infection and dense lymphocyte infiltration. The scarcity of NPC genomic data hinders the understanding of NPC biology, disease progression and rational therapy design. Here we performed whole-exome sequencing (WES) on 111 micro-dissected EBV-positive NPCs, with 15 cases subjected to further whole-genome sequencing (WGS), to determine its mutational landscape. We identified enrichment for genomic aberrations of multiple negative regulators of the NF-κB pathway, including CYLD, TRAF3, NFKBIA and NLRC5, in a total of 41% of cases. Functional analysis confirmed inactivating CYLD mutations as drivers for NPC cell growth. The EBV oncoprotein latent membrane protein 1 (LMP1) functions to constitutively activate NF-κB signalling, and we observed mutual exclusivity among tumours with somatic NF-κB pathway aberrations and LMP1-overexpression, suggesting that NF-κB activation is selected for by both somatic and viral events during NPC pathogenesis.

Published
2017

5. Supplement Methods from RAS–MAPK Reactivation Facilitates Acquired Resistance in FGFR1-Amplified Lung Cancer and Underlies a Rationale for Upfront FGFR–MEK Blockade

Author

Bockorny, Bruno, primary, Rusan, Maria, primary, Chen, Wankun, primary, Liao, Rachel G., primary, Li, Yvonne, primary, Piccioni, Federica, primary, Wang, Jun, primary, Tan, Li, primary, Thorner, Aaron R., primary, Li, Tianxia, primary, Zhang, Yanxi, primary, Miao, Changhong, primary, Ovesen, Therese, primary, Shapiro, Geoffrey I., primary, Kwiatkowski, David J., primary, Gray, Nathanael S., primary, Meyerson, Matthew, primary, Hammerman, Peter S., primary, and Bass, Adam J., primary

Published
2023
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6. Figure S4 from RAS–MAPK Reactivation Facilitates Acquired Resistance in FGFR1-Amplified Lung Cancer and Underlies a Rationale for Upfront FGFR–MEK Blockade

Author

Bockorny, Bruno, primary, Rusan, Maria, primary, Chen, Wankun, primary, Liao, Rachel G., primary, Li, Yvonne, primary, Piccioni, Federica, primary, Wang, Jun, primary, Tan, Li, primary, Thorner, Aaron R., primary, Li, Tianxia, primary, Zhang, Yanxi, primary, Miao, Changhong, primary, Ovesen, Therese, primary, Shapiro, Geoffrey I., primary, Kwiatkowski, David J., primary, Gray, Nathanael S., primary, Meyerson, Matthew, primary, Hammerman, Peter S., primary, and Bass, Adam J., primary

Published
2023
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7. Supplementary Table 3 from RAS–MAPK Reactivation Facilitates Acquired Resistance in FGFR1-Amplified Lung Cancer and Underlies a Rationale for Upfront FGFR–MEK Blockade

Author

Bockorny, Bruno, primary, Rusan, Maria, primary, Chen, Wankun, primary, Liao, Rachel G., primary, Li, Yvonne, primary, Piccioni, Federica, primary, Wang, Jun, primary, Tan, Li, primary, Thorner, Aaron R., primary, Li, Tianxia, primary, Zhang, Yanxi, primary, Miao, Changhong, primary, Ovesen, Therese, primary, Shapiro, Geoffrey I., primary, Kwiatkowski, David J., primary, Gray, Nathanael S., primary, Meyerson, Matthew, primary, Hammerman, Peter S., primary, and Bass, Adam J., primary

Published
2023
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8. Supplementary Table 1, 2 and 4 from RAS–MAPK Reactivation Facilitates Acquired Resistance in FGFR1-Amplified Lung Cancer and Underlies a Rationale for Upfront FGFR–MEK Blockade

Author

Bockorny, Bruno, primary, Rusan, Maria, primary, Chen, Wankun, primary, Liao, Rachel G., primary, Li, Yvonne, primary, Piccioni, Federica, primary, Wang, Jun, primary, Tan, Li, primary, Thorner, Aaron R., primary, Li, Tianxia, primary, Zhang, Yanxi, primary, Miao, Changhong, primary, Ovesen, Therese, primary, Shapiro, Geoffrey I., primary, Kwiatkowski, David J., primary, Gray, Nathanael S., primary, Meyerson, Matthew, primary, Hammerman, Peter S., primary, and Bass, Adam J., primary

Published
2023
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9. Data from RAS–MAPK Reactivation Facilitates Acquired Resistance in FGFR1-Amplified Lung Cancer and Underlies a Rationale for Upfront FGFR–MEK Blockade

Author

Bockorny, Bruno, primary, Rusan, Maria, primary, Chen, Wankun, primary, Liao, Rachel G., primary, Li, Yvonne, primary, Piccioni, Federica, primary, Wang, Jun, primary, Tan, Li, primary, Thorner, Aaron R., primary, Li, Tianxia, primary, Zhang, Yanxi, primary, Miao, Changhong, primary, Ovesen, Therese, primary, Shapiro, Geoffrey I., primary, Kwiatkowski, David J., primary, Gray, Nathanael S., primary, Meyerson, Matthew, primary, Hammerman, Peter S., primary, and Bass, Adam J., primary

Published
2023
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10. Figure S6 and S7 from RAS–MAPK Reactivation Facilitates Acquired Resistance in FGFR1-Amplified Lung Cancer and Underlies a Rationale for Upfront FGFR–MEK Blockade

Author

Bockorny, Bruno, primary, Rusan, Maria, primary, Chen, Wankun, primary, Liao, Rachel G., primary, Li, Yvonne, primary, Piccioni, Federica, primary, Wang, Jun, primary, Tan, Li, primary, Thorner, Aaron R., primary, Li, Tianxia, primary, Zhang, Yanxi, primary, Miao, Changhong, primary, Ovesen, Therese, primary, Shapiro, Geoffrey I., primary, Kwiatkowski, David J., primary, Gray, Nathanael S., primary, Meyerson, Matthew, primary, Hammerman, Peter S., primary, and Bass, Adam J., primary

Published
2023
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11. Data from Suppression of Adaptive Responses to Targeted Cancer Therapy by Transcriptional Repression

Author

Rusan, Maria, primary, Li, Kapsok, primary, Li, Yvonne, primary, Christensen, Camilla L., primary, Abraham, Brian J., primary, Kwiatkowski, Nicholas, primary, Buczkowski, Kevin A., primary, Bockorny, Bruno, primary, Chen, Ting, primary, Li, Shuai, primary, Rhee, Kevin, primary, Zhang, Haikuo, primary, Chen, Wankun, primary, Terai, Hideki, primary, Tavares, Tiffany, primary, Leggett, Alan L., primary, Li, Tianxia, primary, Wang, Yichen, primary, Zhang, Tinghu, primary, Kim, Tae-Jung, primary, Hong, Sook-Hee, primary, Poudel-Neupane, Neermala, primary, Silkes, Michael, primary, Mudianto, Tenny, primary, Tan, Li, primary, Shimamura, Takeshi, primary, Meyerson, Matthew, primary, Bass, Adam J., primary, Watanabe, Hideo, primary, Gray, Nathanael S., primary, Young, Richard A., primary, Wong, Kwok-Kin, primary, and Hammerman, Peter S., primary

Published
2023
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12. Supplementary Figures 1-10 from Suppression of Adaptive Responses to Targeted Cancer Therapy by Transcriptional Repression

Author

Rusan, Maria, primary, Li, Kapsok, primary, Li, Yvonne, primary, Christensen, Camilla L., primary, Abraham, Brian J., primary, Kwiatkowski, Nicholas, primary, Buczkowski, Kevin A., primary, Bockorny, Bruno, primary, Chen, Ting, primary, Li, Shuai, primary, Rhee, Kevin, primary, Zhang, Haikuo, primary, Chen, Wankun, primary, Terai, Hideki, primary, Tavares, Tiffany, primary, Leggett, Alan L., primary, Li, Tianxia, primary, Wang, Yichen, primary, Zhang, Tinghu, primary, Kim, Tae-Jung, primary, Hong, Sook-Hee, primary, Poudel-Neupane, Neermala, primary, Silkes, Michael, primary, Mudianto, Tenny, primary, Tan, Li, primary, Shimamura, Takeshi, primary, Meyerson, Matthew, primary, Bass, Adam J., primary, Watanabe, Hideo, primary, Gray, Nathanael S., primary, Young, Richard A., primary, Wong, Kwok-Kin, primary, and Hammerman, Peter S., primary

Published
2023
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13. Data from ER Stress Signaling Promotes the Survival of Cancer “Persister Cells” Tolerant to EGFR Tyrosine Kinase Inhibitors

Author

Terai, Hideki, primary, Kitajima, Shunsuke, primary, Potter, Danielle S., primary, Matsui, Yusuke, primary, Quiceno, Laura Gutierrez, primary, Chen, Ting, primary, Kim, Tae-jung, primary, Rusan, Maria, primary, Thai, Tran C., primary, Piccioni, Federica, primary, Donovan, Katherine A., primary, Kwiatkowski, Nicholas, primary, Hinohara, Kunihiko, primary, Wei, Guo, primary, Gray, Nathanael S., primary, Fischer, Eric S., primary, Wong, Kwok-Kin, primary, Shimamura, Teppei, primary, Letai, Anthony, primary, Hammerman, Peter S., primary, and Barbie, David A., primary

Published
2023
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14. Supplementary Methods from ER Stress Signaling Promotes the Survival of Cancer “Persister Cells” Tolerant to EGFR Tyrosine Kinase Inhibitors

Author

Terai, Hideki, primary, Kitajima, Shunsuke, primary, Potter, Danielle S., primary, Matsui, Yusuke, primary, Quiceno, Laura Gutierrez, primary, Chen, Ting, primary, Kim, Tae-jung, primary, Rusan, Maria, primary, Thai, Tran C., primary, Piccioni, Federica, primary, Donovan, Katherine A., primary, Kwiatkowski, Nicholas, primary, Hinohara, Kunihiko, primary, Wei, Guo, primary, Gray, Nathanael S., primary, Fischer, Eric S., primary, Wong, Kwok-Kin, primary, Shimamura, Teppei, primary, Letai, Anthony, primary, Hammerman, Peter S., primary, and Barbie, David A., primary

Published
2023
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15. Supplementary Table S1 from ER Stress Signaling Promotes the Survival of Cancer “Persister Cells” Tolerant to EGFR Tyrosine Kinase Inhibitors

Author

Terai, Hideki, primary, Kitajima, Shunsuke, primary, Potter, Danielle S., primary, Matsui, Yusuke, primary, Quiceno, Laura Gutierrez, primary, Chen, Ting, primary, Kim, Tae-jung, primary, Rusan, Maria, primary, Thai, Tran C., primary, Piccioni, Federica, primary, Donovan, Katherine A., primary, Kwiatkowski, Nicholas, primary, Hinohara, Kunihiko, primary, Wei, Guo, primary, Gray, Nathanael S., primary, Fischer, Eric S., primary, Wong, Kwok-Kin, primary, Shimamura, Teppei, primary, Letai, Anthony, primary, Hammerman, Peter S., primary, and Barbie, David A., primary

Published
2023
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16. Supplementary Figure S1-S6 from ER Stress Signaling Promotes the Survival of Cancer “Persister Cells” Tolerant to EGFR Tyrosine Kinase Inhibitors

Author

Terai, Hideki, primary, Kitajima, Shunsuke, primary, Potter, Danielle S., primary, Matsui, Yusuke, primary, Quiceno, Laura Gutierrez, primary, Chen, Ting, primary, Kim, Tae-jung, primary, Rusan, Maria, primary, Thai, Tran C., primary, Piccioni, Federica, primary, Donovan, Katherine A., primary, Kwiatkowski, Nicholas, primary, Hinohara, Kunihiko, primary, Wei, Guo, primary, Gray, Nathanael S., primary, Fischer, Eric S., primary, Wong, Kwok-Kin, primary, Shimamura, Teppei, primary, Letai, Anthony, primary, Hammerman, Peter S., primary, and Barbie, David A., primary

Published
2023
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19. Næsen kan være fokus for behandling af og profylakse mod COVID-19

Author

Rusan, Maria, Ovesen, Thomas Oliver Kamarauskas, Fuursted, Kurt, and Ovesen, Therese

Subjects
biochemical phenomena, metabolism, and nutrition
Abstract

Infection with SARS-CoV-2 frequently commences in the nasal cavity, yet knowledge about this initial virus-host interaction is sparse. In this review, we update our current understanding of SARS-CoV-2 infection via the nasal epithelium and the associated local immune response. Furthermore, we present considerations to how this interaction may influence the clinical course of COVID-19 and the systemic immune response, and lastly touch upon the potential for intranasal vaccination, intranasal antiviral therapies and immunomodulatory approaches.

Published
2022

24. Clinical evaluation of antibiotic regimens in patients with surgically verified parapharyngeal abscess: a prospective observational study

Author

Klug, Tejs Ehlers, primary, Andersen, Camilla, additional, Hahn, Pernille, additional, Danstrup, Christian Sander, additional, Petersen, Niels Krintel, additional, Mikkelsen, Sophie, additional, Døssing, Helle, additional, Christensen, Anne-Louise, additional, Rusan, Maria, additional, Kjeldsen, Anette, additional, and Greve, Thomas, additional

Published
2021
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26. Acute otitis media and antibiotics:a systematic review

Author

Holm, Niels, Rusan, Maria, and Ovesen, Therese

Subjects
Anti-Bacterial Agents/therapeutic use, Tympanic Membrane Perforation, Acute Disease, otorhinolaryngologic diseases, Humans, Infant, Neoplasm Recurrence, Local, Child, Otitis Media/drug therapy
Abstract

Introduction: Although acute otitis media (AOM) is a very frequent illness in children, it remains unclear to what extent children with AOM benefit from antibiotics (ABX). This systematic review aimed to clarify this subject by including randomised clinical trials (RCTs) from the pneumococcal vaccine era only. Methods: We performed a systematic literature search in four databases from 1 January 2000 to 1 January 2019 for RCTs comparing ABX to placebo in patients with AOM. Pain was registered as the main outcome. Adverse events (AE), development of contralateral otitis media, tympanic membrane perforation, late AOM recurrence, abnormal tympanometry and time to resolution of middle ear effusion were registered as secondary outcomes. Results: Six publications based on five RCTs with 1,862 patients were included. The number needed to treat (NNT) to reduce pain varied from seven (pain at day 7-10) to 28 (pain at day 2-3). The NNT for preventing contralateral otitis was ten. AE were seen in every 13th patient treated with ABX. Conclusions: ABX appears to have a limited effect on both primary and secondary outcomes compared with placebo. A substantial number of patients experienced AE. New RCTs are needed to further clarify the effect. Ideally, RCTs could be conducted in Danish general practices in collaboration with practicing ear, nose and throat specialists to obtain large unselected populations with high rates of vaccine coverage. Until more evidence is provided, ABX should be considered among children younger than two years of age with severe symptoms of AOM, i.e. fewer and affected well-being.

Published
2020

30. Suppression of Adaptive Responses to Targeted Cancer Therapy by Transcriptional Repression

Author

Massachusetts Institute of Technology. Department of Biology, Rusan, Maria, Li, Kapsok, Li, Yvonne, Christensen, Camilla L., Abraham, Brian J., Kwiatkowski, Nicholas, Buczkowski, Kevin A., Bockorny, Bruno, Chen, Ting, Li, Shuai, Rhee, Kevin, Zhang, Haikuo, Chen, Wankun, Terai, Hideki, Tavares, Tiffany, Leggett, Alan L., Li, Tianxia, Wang, Yichen, Zhang, Tinghu, Kim, Tae-Jung, Hong, Sook-Hee, Poudel-Neupane, Neermala, Silkes, Michael, Mudianto, Tenny, Tan, Li, Shimamura, Takeshi, Meyerson, Matthew, Bass, Adam J., Watanabe, Hideo, Gray, Nathanael S., Young, Richard A., Wong, Kwok-Kin, Hammerman, Peter S., Massachusetts Institute of Technology. Department of Biology, Rusan, Maria, Li, Kapsok, Li, Yvonne, Christensen, Camilla L., Abraham, Brian J., Kwiatkowski, Nicholas, Buczkowski, Kevin A., Bockorny, Bruno, Chen, Ting, Li, Shuai, Rhee, Kevin, Zhang, Haikuo, Chen, Wankun, Terai, Hideki, Tavares, Tiffany, Leggett, Alan L., Li, Tianxia, Wang, Yichen, Zhang, Tinghu, Kim, Tae-Jung, Hong, Sook-Hee, Poudel-Neupane, Neermala, Silkes, Michael, Mudianto, Tenny, Tan, Li, Shimamura, Takeshi, Meyerson, Matthew, Bass, Adam J., Watanabe, Hideo, Gray, Nathanael S., Young, Richard A., Wong, Kwok-Kin, and Hammerman, Peter S.

Abstract

Acquired drug resistance is a major factor limiting the effectiveness of targeted cancer therapies. Targeting tumors with kinase inhibitors induces complex adap- tive programs that promote the persistence of a fraction of the original cell population, facilitating the eventual outgrowth of inhibitor-resistant tumor clones. We show that the addition of a newly identified CDK7/12 inhibitor, THZ1, to targeted therapy enhances cell killing and impedes the emergence of drug-resistant cell populations in diverse cellular and in vivo cancer models. We propose that targeted therapy induces a state of transcriptional dependency in a subpopulation of cells poised to become drug tolerant, which THZ1 can exploit by blocking dynamic transcriptional responses, promoting remodeling of enhancers and key signaling outputs required for tumor cell survival in the setting of targeted therapy. These findings suggest that the addition of THZ1 to targeted therapies is a promising broad-based strategy to hinder the emergence of drug-resistant cancer cell populations. SIGNIFICANCE: CDK7/12 inhibition prevents active enhancer formation at genes, promoting resistance emergence in response to targeted therapy, and impedes the engagement of transcriptional programs required for tumor cell survival. CDK7/12 inhibition in combination with targeted cancer therapies may serve as a therapeutic paradigm for enhancing the effectiveness of targeted therapies.

Published
2019

33. RAS–MAPK Reactivation Facilitates Acquired Resistance in FGFR1-Amplified Lung Cancer and Underlies a Rationale for Upfront FGFR–MEK Blockade

Author

Bockorny, Bruno, primary, Rusan, Maria, additional, Chen, Wankun, additional, Liao, Rachel G., additional, Li, Yvonne, additional, Piccioni, Federica, additional, Wang, Jun, additional, Tan, Li, additional, Thorner, Aaron R., additional, Li, Tianxia, additional, Zhang, Yanxi, additional, Miao, Changhong, additional, Ovesen, Therese, additional, Shapiro, Geoffrey I., additional, Kwiatkowski, David J., additional, Gray, Nathanael S., additional, Meyerson, Matthew, additional, Hammerman, Peter S., additional, and Bass, Adam J., additional

Published
2018
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34. ER Stress Signaling Promotes the Survival of Cancer “Persister Cells” Tolerant to EGFR Tyrosine Kinase Inhibitors

Author

Terai, Hideki, primary, Kitajima, Shunsuke, additional, Potter, Danielle S., additional, Matsui, Yusuke, additional, Quiceno, Laura Gutierrez, additional, Chen, Ting, additional, Kim, Tae-jung, additional, Rusan, Maria, additional, Thai, Tran C., additional, Piccioni, Federica, additional, Donovan, Katherine A., additional, Kwiatkowski, Nicholas, additional, Hinohara, Kunihiko, additional, Wei, Guo, additional, Gray, Nathanael S., additional, Fischer, Eric S., additional, Wong, Kwok-Kin, additional, Shimamura, Teppei, additional, Letai, Anthony, additional, Hammerman, Peter S., additional, and Barbie, David A., additional

Published
2018
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35. Paediatric Virology and its interaction between basic science and clinical practice (Review)

Author

Mammas, Ioannis, primary, Greenough, Anne, additional, Theodoridou, Maria, additional, Kramvis, Anna, additional, Rusan, Maria, additional, Melidou, Angeliki, additional, Korovessi, Paraskevi, additional, Papaioannou, Georgia, additional, Papatheodoropoulou, Alexia, additional, Koutsaftiki, Chryssie, additional, Liston, Maria, additional, Sourvinos, George, additional, and Spandidos, Demetrios, additional

Published
2018
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36. Suppression of Adaptive Responses to Targeted Cancer Therapy by Transcriptional Repression

Author

Rusan, Maria, primary, Li, Kapsok, additional, Li, Yvonne, additional, Christensen, Camilla L., additional, Abraham, Brian J., additional, Kwiatkowski, Nicholas, additional, Buczkowski, Kevin A., additional, Bockorny, Bruno, additional, Chen, Ting, additional, Li, Shuai, additional, Rhee, Kevin, additional, Zhang, Haikuo, additional, Chen, Wankun, additional, Terai, Hideki, additional, Tavares, Tiffany, additional, Leggett, Alan L., additional, Li, Tianxia, additional, Wang, Yichen, additional, Zhang, Tinghu, additional, Kim, Tae-Jung, additional, Hong, Sook-Hee, additional, Poudel-Neupane, Neermala, additional, Silkes, Michael, additional, Mudianto, Tenny, additional, Tan, Li, additional, Shimamura, Takeshi, additional, Meyerson, Matthew, additional, Bass, Adam J., additional, Watanabe, Hideo, additional, Gray, Nathanael S., additional, Young, Richard A., additional, Wong, Kwok-Kin, additional, and Hammerman, Peter S., additional

Published
2018
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37. From epidemiology to therapeutics: An analysis of Human Papillomavirus prevalence in tonsillar infections and a study on transcriptional repression as an adjunct to targeted therapies in cancer

Author

Rusan, Maria

Abstract

Med over 8 millioner kræft-relaterede dødsfald årligt har kræft indtaget pladsen som en af verdens førende sygdomme. Der er derfor hårdt brug for fremskridt indenfor diagnosticering og behandling af kræft. En række nye stoffer der er målrettet kræftforårsagende mutationer er udviklet de senere år. ”Selvom patienterne normalt oplever gode resultater i begyndelsen af behandlingen, bliver deres kræftceller ofte forholdsvist hurtigt resistente overfor de nye behandlinger, hvilket medfører tilbagefald”, siger Maria Rusan, og fortsætter: ”Resistensen opstår fordi kræftcellerne er særdeles gode til at tilpasse sig og finde nye måder at overleve på, på trods af behandlingen.” I sit ph.d.-projekt har Maria Rusan opdaget at et nyt stof, THZ1, er i stand til at hæmme kræftcellernes evne til at tilpasse sig de målrettede terapier. ”Grunden til at vi er så begejstrede er, at den effekt vi opnår ser ud til at være gældende over en meget bred vifte af kræfttyper”, tilføjer hun. Hendes opdagelse danner grundlag for igangværende prækliniske undersøgelser ved Dana Farber Cancer Institute.

Published
2016

39. Abstract 15: Suppression of adaptive responses to targeted therapies by transcriptional inhibition

Author

Rusan, Maria, primary, Li, Kapsok, additional, Li, Yvonne, additional, Christensen, Camilla L., additional, Abraham, Brian J., additional, Kwiatkowski, Nicholas, additional, Buczkowski, Kevin, additional, Bockorny, Bruno, additional, Chen, Ting, additional, Li, Shuai, additional, Zhang, Haikuo, additional, Terai, Hideko, additional, Tavares, Tiffany, additional, Zhang, Tinghu, additional, Kim, Tae Jung, additional, Silkes, Michael, additional, Mudianto, Tenny, additional, Tan, Li, additional, Shimamura, Takeshi, additional, Meyerson, Matthew, additional, Watanabe, Hideo, additional, Gray, Nathanael S., additional, Young, Richard A., additional, Wong, Kwok-Kin, additional, and Hammerman, Peter S., additional

Published
2017
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41. Peritonsillar Abscess

Author

Klug, Tejs Ehlers, primary, Rusan, Maria, additional, Fuursted, Kurt, additional, and Ovesen, Therese, additional

Published
2016
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42. The interplay between HPV and host immunity in head and neck squamous cell carcinoma

Author

Andersen, Anne, Sølling, Anne Sophie Koldkjær, Ovesen, Therese, and Rusan, Maria

Subjects
virus diseases, female genital diseases and pregnancy complications
Abstract

Persistent infection with Human Papillomavirus (HPV) type 16 is a major risk factor for the development of head and neck squamous cell carcinoma (HNSCC), in particular oropharyngeal squamous cell carcinoma (OPSCC). The oropharyngeal epithelium differs from the mucosal epithelium at other commonly HPV16-infected sites (i.e., cervix/ anogenital region) in that it is juxtaposed with the underlying lymphatic tissue, serving a key immunologic function in the surveillance of inhaled and ingested pathogens. Therefore, the natural history of infection and immune response to HPV at this site may differ from that at other anatomic locations. This review summarizes the literature concerning the adaptive immune response against HPV in the context of HNSCC, with a focus on the T-cell response. Recent studies have shown that a broad repertoire of tumour-infiltrating HPV-specific T-cells are found in nearly all patients with HPV-positive tumours. A systemic response is found in only a proportion of these. Furthermore, the local response is more frequent in OPSCC patients than in cervical cancer patients and HPV-negative OPSCC patients. Despite this, tumour persistence may be facilitated by abnormalities in antigen processing, a skewed T-helper cell response, and an increased local prevalence of T-regulatory cells. Nonetheless, the immunologic profile of HPV-positive vs. HPV-negative HNSCC is associated with a significantly better outcome, and the HPV-specific immune response is suggested to play a role in the significantly better response to therapy of HPV-positive patients. Immunoprofiling may prove a valuable prognostic tool, and immunotherapy trials targeting HPV are underway, providing hope for decreasing treatment-related toxicity. © 2013 Wiley Periodicals, Inc.

Published
2013
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45. Clinical evaluation of intravenous ampicillin as empirical antimicrobial treatment of acute epiglottitis.

Author

Kjaerulff, Ann Marlene Gram, Rusan, Maria, and Klug, Tejs Ehlers

Subjects
*ANTIBIOTICS, *HOSPITALS, *EPIGLOTTIS diseases, *HOSPITAL care, *INTRAVENOUS therapy, *TREATMENT effectiveness, *ACUTE diseases, *AMPICILLIN, *THERAPEUTICS
Abstract

Introduction:The significant pathogens in acute epiglottitis (AE) are poorly defined in the postHaemophilus influenzatype b-vaccine era. Furthermore, there is a lack of clinical evaluations of antibiotic regimens in patients with AE. We aimed to evaluate the effectiveness of empiric intravenous ampicillin in the treatment of patients with AE. Materials & methods:All patients admitted with AE to the Ear-Nose-Throat Department, Aarhus University Hospital, Denmark, from 2001 to 2015 were included. Results:In total, 103 (51 males) patients were included in the study. The median duration of hospitalization was four days. There was no statistical significant difference between patients initially treated with intravenous ampicillin (n = 83) or other antibiotics (n = 20) (p = .26). The antibiotic regimen was altered during admission in 11% of patients, without significant difference between antibiotic groups (ampicillin 10% vs non-ampicillin 15%,p = .44). Complications potentially related to insufficient antibiotic treatment were observed in four (5%) patients initially treated with ampicillin, but in none of the patients initially treated with antibiotics other than ampicillin (p = 1.00). Throat swab cultures and blood cultures frequently yielded negative results. Conclusions:Intravenous ampicillin is efficient as empiric antibiotic therapy for AE patients, leading to a quick recovery and low complication rates. [ABSTRACT FROM PUBLISHER]

Published
2018
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50. Peritonsillar Abscess: Complication of Acute Tonsillitis or Weber's Glands Infection?

Author

Klug, Tejs Ehlers, Rusan, Maria, Fuursted, Kurt, and Ovesen, Therese

Abstract

Objective: To review the literature concerning the 2 primary hypotheses put forth to explain the pathogenesis of peritonsillar abscess: "the acute tonsillitis hypothesis" (peritonsillar abscess is a complication of acute tonsillitis) and "the Weber gland hypothesis" (peritonsillar abscess is an infection of Weber's glands).Data Sources: PubMed, EMBASE.Review Methods: Data supporting or negating one hypothesis or the other were elicited from the literature.Conclusions: Several findings support the acute tonsillitis hypothesis. First, the 2 main pathogens in peritonsillar abscess have been recovered from pus aspirates and bilateral tonsillar tissues with high concordance rates, suggesting that both tonsils are infected in patients with peritonsillar abscess. Second, studies report signs of acute tonsillitis in the days prior to and at the time of peritonsillar abscess. Third, antibiotic treatment reduces the risk of abscess development in patients with acute tonsillitis. However, some findings suggest involvement of the Weber's glands in peritonsillar abscess pathogenesis. First, high amylase levels have been found in peritonsillar pus. Second, the majority of peritonsillar abscesses are located at the superior tonsillar pole in proximity of the Weber's glands. We propose a unified hypothesis whereby bacteria initially infect the tonsillar mucosa and spread via the salivary duct system to the peritonsillar space, where an abscess is formed.Implications For Practice: Our findings support the rationale for antibiotic treatment of patients with severe acute tonsillitis to reduce the risk of abscess development. Improved understanding of peritonsillar abscess pathogenesis is important for the development of efficient prevention strategies. [ABSTRACT FROM AUTHOR]

Published
2016
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