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glass_consortium_publications.bib

@ARTICLE{Bakas2020-ee,
  title    = "{iGLASS}: imaging integration into the Glioma Longitudinal
              Analysis Consortium",
  author   = "Bakas, Spyridon and Ormond, David Ryan and Alfaro-Munoz, Kristin
              D and Smits, Marion and Cooper, Lee Alex Donald and Verhaak, Roel
              and Poisson, Laila M",
  journal  = "Neuro. Oncol.",
  volume   =  22,
  number   =  10,
  pages    = "1545-1546",
  month    =  oct,
  year     =  2020,
  url      = "http://dx.doi.org/10.1093/neuonc/noaa160",
  language = "en",
  issn     = "1522-8517, 1523-5866",
  pmid     = "32644158",
  doi      = "10.1093/neuonc/noaa160",
  pmc      = "PMC7566469"
}

@ARTICLE{Varn2022-bt,
  title     = "Glioma progression is shaped by genetic evolution and
               microenvironment interactions",
  author    = "Varn, Frederick S and Johnson, Kevin C and Martinek, Jan and
               Huse, Jason T and Nasrallah, Maclean P and Wesseling, Pieter and
               Cooper, Lee A D and Malta, Tathiane M and Wade, Taylor E and
               Sabedot, Thais S and Brat, Daniel and Gould, Peter V and
               W{\"o}ehrer, Adelheid and Aldape, Kenneth and Ismail, Azzam and
               Sivajothi, Santhosh K and Barthel, Floris P and Kim, Hoon and
               Kocakavuk, Emre and Ahmed, Nazia and White, Kieron and Datta,
               Indrani and Moon, Hyo-Eun and Pollock, Steven and Goldfarb,
               Christine and Lee, Ga-Hyun and Garofano, Luciano and Anderson,
               Kevin J and Nehar-Belaid, Djamel and Barnholtz-Sloan, Jill S and
               Bakas, Spyridon and Byrne, Annette T and D'Angelo, Fulvio and
               Gan, Hui K and Khasraw, Mustafa and Migliozzi, Simona and Ryan
               Ormond, D and Paek, Sun Ha and Van Meir, Erwin G and Walenkamp,
               Annemiek M E and Watts, Colin and Weiss, Tobias and Weller,
               Michael and Palucka, Karolina and Stead, Lucy F and Poisson,
               Laila M and Noushmehr, Houtan and Iavarone, Antonio and Verhaak,
               Roel G W and Alfaro, Kristin D and Amin, Samirkumar B and
               Ashley, David M and Bock, Christoph and Brodbelt, Andrew and
               Bulsara, Ketan R and Castro, Ana Valeria and Connelly, Jennifer
               M and Costello, Joseph F and de Groot, John F and Finocchiaro,
               Gaetano and French, Pim J and Golebiewska, Anna and Hau, Ann C
               and Hong, Chibo and Horbinski, Craig and Kannan, Kasthuri S and
               Kouwenhoven, Mathilde C M and Lasorella, Anna and LaViolette,
               Peter S and Ligon, Keith L and Lowman, Allison K and Mehta,
               Shwetal and Miletic, Hrvoje and Molinaro, Annette M and Ng, Ho
               Keung and Niclou, Simone P and Niers, Johanna M and Phillips,
               Joanna J and Rabadan, Raul and Rao, Ganesh and Reifenberger,
               Guido and Sanai, Nader and Short, Susan C and Smitt, Peter
               Sillevis and Sloan, Andrew E and Smits, Marion and Snyder, James
               M and Suzuki, Hiromichi and Tabatabai, Ghazaleh and Tanner,
               Georgette and Tomaszewski, William H and Wells, Michael and
               Westerman, Bart A and Wheeler, Helen and Xie, Jichun and Alfred
               Yung, W K and Zadeh, Gelareh and Zhao, Junfei and Verhaak, Roel
               G W",
  abstract  = "SummaryThe factors driving therapy resistance in diffuse glioma
               remain poorly understood. To identify treatment-associated
               cellular and genetic changes, we analyzed RNA and/or DNA
               sequencing data from the temporally separated tumor pairs of 304
               adult patients with isocitrate dehydrogenase (IDH)-wild-type and
               IDH-mutant glioma. Tumors recurred in distinct manners that were
               dependent on IDH mutation status and attributable to changes in
               histological feature composition, somatic alterations, and
               microenvironment interactions. Hypermutation and acquired CDKN2A
               deletions were associated with an increase in proliferating
               neoplastic cells at recurrence in both glioma subtypes,
               reflecting active tumor growth. IDH-wild-type tumors were more
               invasive at recurrence, and their neoplastic cells exhibited
               increased expression of neuronal signaling programs that
               reflected a possible role for neuronal interactions in promoting
               glioma progression. Mesenchymal transition was associated with
               the presence of a myeloid cell state defined by specific
               ligand-receptor interactions with neoplastic cells.
               Collectively, these recurrence-associated phenotypes represent
               potential targets to alter disease progression.",
  journal   = "Cell",
  publisher = "Elsevier",
  volume    =  0,
  number    =  0,
  month     =  may,
  year      =  2022,
  url       = "http://www.cell.com/article/S0092867422005360/abstract",
  language  = "en",
  issn      = "0092-8674, 1097-4172",
  doi       = "10.1016/j.cell.2022.04.038"
}

@ARTICLE{Barthel2019-kv,
  title    = "Longitudinal molecular trajectories of diffuse glioma in adults",
  author   = "Barthel, Floris P and Johnson, Kevin C and Varn, Frederick S and
              Moskalik, Anzhela D and Tanner, Georgette and Kocakavuk, Emre and
              Anderson, Kevin J and Abiola, Olajide and Aldape, Kenneth and
              Alfaro, Kristin D and Alpar, Donat and Amin, Samirkumar B and
              Ashley, David M and Bandopadhayay, Pratiti and Barnholtz-Sloan,
              Jill S and Beroukhim, Rameen and Bock, Christoph and Brastianos,
              Priscilla K and Brat, Daniel J and Brodbelt, Andrew R and Bruns,
              Alexander F and Bulsara, Ketan R and Chakrabarty, Aruna and
              Chakravarti, Arnab and Chuang, Jeffrey H and Claus, Elizabeth B
              and Cochran, Elizabeth J and Connelly, Jennifer and Costello,
              Joseph F and Finocchiaro, Gaetano and Fletcher, Michael N and
              French, Pim J and Gan, Hui K and Gilbert, Mark R and Gould, Peter
              V and Grimmer, Matthew R and Iavarone, Antonio and Ismail, Azzam
              and Jenkinson, Michael D and Khasraw, Mustafa and Kim, Hoon and
              Kouwenhoven, Mathilde C M and LaViolette, Peter S and Li, Meihong
              and Lichter, Peter and Ligon, Keith L and Lowman, Allison K and
              Malta, Tathiane M and Mazor, Tali and McDonald, Kerrie L and
              Molinaro, Annette M and Nam, Do-Hyun and Nayyar, Naema and Ng, Ho
              Keung and Ngan, Chew Yee and Niclou, Simone P and Niers, Johanna
              M and Noushmehr, Houtan and Noorbakhsh, Javad and Ormond, D Ryan
              and Park, Chul-Kee and Poisson, Laila M and Rabadan, Raul and
              Radlwimmer, Bernhard and Rao, Ganesh and Reifenberger, Guido and
              Sa, Jason K and Schuster, Michael and Shaw, Brian L and Short,
              Susan C and Smitt, Peter A Sillevis and Sloan, Andrew E and
              Smits, Marion and Suzuki, Hiromichi and Tabatabai, Ghazaleh and
              Van Meir, Erwin G and Watts, Colin and Weller, Michael and
              Wesseling, Pieter and Westerman, Bart A and Widhalm, Georg and
              Woehrer, Adelheid and Yung, W K Alfred and Zadeh, Gelareh and
              Huse, Jason T and De Groot, John F and Stead, Lucy F and Verhaak,
              Roel G W and Barthel, Floris P and Johnson, Kevin C and Varn,
              Frederick S and Moskalik, Anzhela D and Tanner, Georgette and
              Kocakavuk, Emre and Anderson, Kevin J and Aldape, Kenneth and
              Alfaro, Kristin D and Amin, Samirkumar B and Ashley, David M and
              Bandopadhayay, Pratiti and Barnholtz-Sloan, Jill S and Beroukhim,
              Rameen and Bock, Christoph and Brastianos, Priscilla K and Brat,
              Daniel J and Brodbelt, Andrew R and Bulsara, Ketan R and
              Chakrabarty, Aruna and Chuang, Jeffrey H and Claus, Elizabeth B
              and Cochran, Elizabeth J and Connelly, Jennifer and Costello,
              Joseph F and Finocchiaro, Gaetano and Fletcher, Michael N and
              French, Pim J and Gan, Hui K and Gilbert, Mark R and Gould, Peter
              V and Iavarone, Antonio and Ismail, Azzam and Jenkinson, Michael
              D and Khasraw, Mustafa and Kim, Hoon and Kouwenhoven, Mathilde C
              M and LaViolette, Peter S and Lichter, Peter and Ligon, Keith L
              and Lowman, Allison K and Malta, Tathiane M and McDonald, Kerrie
              L and Molinaro, Annette M and Nam, Do-Hyun and Ng, Ho Keung and
              Niclou, Simone P and Niers, Johanna M and Noushmehr, Houtan and
              Ormond, D Ryan and Park, Chul-Kee and Poisson, Laila M and
              Rabadan, Raul and Radlwimmer, Bernhard and Rao, Ganesh and
              Reifenberger, Guido and Sa, Jason K and Short, Susan C and Smitt,
              Peter A Sillevis and Sloan, Andrew E and Smits, Marion and
              Suzuki, Hiromichi and Tabatabai, Ghazaleh and Van Meir, Erwin G
              and Watts, Colin and Weller, Michael and Wesseling, Pieter and
              Westerman, Bart A and Woehrer, Adelheid and Yung, W K Alfred and
              Zadeh, Gelareh and Huse, Jason T and De Groot, John F and Stead,
              Lucy F and Verhaak, Roel G W and {The GLASS Consortium}",
  abstract = "The evolutionary processes that drive universal therapeutic
              resistance in adult patients with diffuse glioma remain
              unclear1,2. Here we analysed temporally separated DNA-sequencing
              data and matched clinical annotation from 222 adult patients with
              glioma. By analysing mutations and copy numbers across the three
              major subtypes of diffuse glioma, we found that driver genes
              detected at the initial stage of disease were retained at
              recurrence, whereas there was little evidence of
              recurrence-specific gene alterations. Treatment with alkylating
              agents resulted in a hypermutator phenotype at different rates
              across the glioma subtypes, and hypermutation was not associated
              with differences in overall survival. Acquired aneuploidy was
              frequently detected in recurrent gliomas and was characterized by
              IDH mutation but without co-deletion of chromosome arms 1p/19q,
              and further converged with acquired alterations in the cell cycle
              and poor outcomes. The clonal architecture of each tumour
              remained similar over time, but the presence of subclonal
              selection was associated with decreased survival. Finally, there
              were no differences in the levels of immunoediting between
              initial and recurrent gliomas. Collectively, our results suggest
              that the strongest selective pressures occur during early glioma
              development and that current therapies shape this evolution in a
              largely stochastic manner.",
  journal  = "Nature",
  month    =  nov,
  year     =  2019,
  url      = "https://doi.org/10.1038/s41586-019-1775-1",
  issn     = "0028-0836, 1476-4687",
  doi      = "10.1038/s41586-019-1775-1"
}

@ARTICLE{Aldape2018-qf,
  title    = "Glioma Through the Looking {GLASS}: Molecular Evolution of
              Diffuse Gliomas and the Glioma Longitudinal {AnalySiS} Consortium",
  author   = "Aldape, Kenneth and Amin, Samirkumar B and Ashley, David M and
              Barnholtz-Sloan, Jill S and Bates, Amanda J and Beroukhim, Rameen
              and Bock, Christoph and Brat, Daniel J and Claus, Elizabeth B and
              Costello, Joseph F and de Groot, John F and Finocchiaro, Gaetano
              and French, Pim J and Gan, Hui K and Griffith, Brent and
              Herold-Mende, Christel C and Horbinski, Craig and Iavarone,
              Antonio and Kalkanis, Steven N and Karabatsou, Konstantina and
              Kim, Hoon and Kouwenhoven, Mathilde C M and McDonald, Kerrie L
              and Miletic, Hrvoje and Nam, Do-Hyun and Ng, Ho Keung and Niclou,
              Simone P and Noushmehr, Houtan and Ormond, Ryan and Poisson,
              Laila M and Reifenberger, Guido and Roncaroli, Federico and Sa,
              Jason K and Sillevis Smitt, Peter A E and Smits, Marion and
              Souza, Camila F and Tabatabai, Ghazaleh and Van Meir, Erwin G and
              Verhaak, Roel G W and Watts, Colin and Wesseling, Pieter and
              Woehrer, Adelheid and Yung, W K Alfred and Jungk, Christine and
              Hau, Ann-Christin and van Dyck, Eric and Westerman, Bart A and
              Yin, Julia and Abiola, Olajide and Zeps, Nikolaj and Grimmond,
              Sean and Buckland, Michael and Khasraw, Mustafa and Sulman, Erik
              P and Muscat, Andrea M and Stead, Lucy and {GLASS Consortium}",
  abstract = "Adult diffuse gliomas are a diverse group of brain neoplasms that
              inflict a high emotional toll on patients and their families. The
              Cancer Genome Atlas (TCGA) and similar projects have provided a
              comprehensive understanding of the somatic alterations and
              molecular subtypes of glioma at diagnosis. However, gliomas
              undergo significant cellular and molecular evolution during
              disease progression. We review the current knowledge on the
              genomic and epigenetic abnormalities in primary tumors and after
              disease recurrence, highlight the gaps in the literature, and
              elaborate on the need for a new multi-institutional effort to
              bridge these knowledge gaps and how the Glioma Longitudinal
              AnalySiS Consortium (GLASS) aims to systemically catalog the
              longitudinal changes in gliomas. The GLASS initiative will
              provide essential insights into the evolution of glioma toward a
              lethal phenotype, with the potential to reveal targetable
              vulnerabilities, and ultimately, improved outcomes for a patient
              population in need.",
  journal  = "Neuro. Oncol.",
  month    =  feb,
  year     =  2018,
  url      = "https://academic.oup.com/neuro-oncology/advance-article-abstract/doi/10.1093/neuonc/noy020/4843984",
  language = "en",
  issn     = "1522-8517, 1523-5866",
  pmid     = "29432615",
  doi      = "10.1093/neuonc/noy020"
}