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1. An affinity for brainstem microglia in pediatric high-grade gliomas of brainstem origin

Author

Massachusetts Institute of Technology. Department of Biological Engineering, Zats, Liat Peretz, Ahmad, Labiba, Casden, Natania, Lee, Meelim J, Belzer, Vitali, Adato, Orit, Bar Cohen, Shaked, Ko, Seung-Hyun B, Filbin, Mariella G, Unger, Ron, Lauffenburger, Douglas A, Segal, Rosalind A, Behar, Oded, Massachusetts Institute of Technology. Department of Biological Engineering, Zats, Liat Peretz, Ahmad, Labiba, Casden, Natania, Lee, Meelim J, Belzer, Vitali, Adato, Orit, Bar Cohen, Shaked, Ko, Seung-Hyun B, Filbin, Mariella G, Unger, Ron, Lauffenburger, Douglas A, Segal, Rosalind A, and Behar, Oded

Abstract

Background. High-grade gliomas (HGG) in children have a devastating prognosis and occur in a remarkable spatiotemporal pattern. Diffuse midline gliomas (DMG), including diffuse intrinsic pontine gliomas (DIPG), typically occur in mid-childhood, while cortical HGGs are more frequent in older children and adults. The mechanisms behind this pattern are not clear. Methods. We used mouse organotypic slice cultures and glial cell cultures to test the impact of the microenvironment on human DIPG cells. Comparing the expression between brainstem and cortical microglia identifed differentially expressed secreted proteins. The impact of some of these proteins on DIPGs was tested. Results. DIPGs, pediatric HGGs of brainstem origin, survive and divide more in organotypic slice cultures originating in the brainstem as compared to the cortex. Moreover, brainstem microglia are better able to support tumors of brainstem origin. A comparison between the two microglial populations revealed differentially expressed genes. One such gene, interleukin-33 (IL33), is highly expressed in the pons of young mice and its DIPG receptor is upregulated in this context. Consistent with this observation, the expression levels of IL33 and its receptor, IL1RL1, are higher in DIPG biopsies compared to low-grade cortical gliomas. Furthermore, IL33 can enhance proliferation and clonability of HGGs of brainstem origin, while blocking IL33 in brainstem organotypic slice cultures reduced the proliferation of these tumor cells. Conclusions. Crosstalk between DIPGs and the brainstem microenvironment, in particular microglia, through IL33 and other secreted factors, modulates spatiotemporal patterning of this HGG and could prove to be an important future therapeutic target.

Published
2023

2. TIM-3 blockade in diffuse intrinsic pontine glioma models promotes tumor regression and antitumor immune memory

Author

Ausejo-Mauleon, Iker, Labiano, Sara, de la Nava, Daniel, Laspidea, Virginia, Zalacain, Marta, Marrodán, Lucía, García-Moure, Marc, González-Huarriz, Marisol, Hervás-Corpión, Irati, Dhandapani, Laasya, Vicent, Silvestre, Collantes, Maria, Peñuelas, Iván, Becher, Oren J, Filbin, Mariella G, Jiang, Li, Labelle, Jenna, de Biagi-Junior, Carlos A O, Nazarian, Javad; https://orcid.org/0000-0002-1951-9828, Laternser, Sandra, Phoenix, Timothy N, van der Lugt, Jasper, Kranendonk, Mariette, Hoogendijk, Raoull, Mueller, Sabine; https://orcid.org/0000-0002-3452-5150, De Andrea, Carlos, Anderson, Ana C, Guruceaga, Elizabeth, Koschmann, Carl, Yadav, Viveka Nand, et al, Ausejo-Mauleon, Iker, Labiano, Sara, de la Nava, Daniel, Laspidea, Virginia, Zalacain, Marta, Marrodán, Lucía, García-Moure, Marc, González-Huarriz, Marisol, Hervás-Corpión, Irati, Dhandapani, Laasya, Vicent, Silvestre, Collantes, Maria, Peñuelas, Iván, Becher, Oren J, Filbin, Mariella G, Jiang, Li, Labelle, Jenna, de Biagi-Junior, Carlos A O, Nazarian, Javad; https://orcid.org/0000-0002-1951-9828, Laternser, Sandra, Phoenix, Timothy N, van der Lugt, Jasper, Kranendonk, Mariette, Hoogendijk, Raoull, Mueller, Sabine; https://orcid.org/0000-0002-3452-5150, De Andrea, Carlos, Anderson, Ana C, Guruceaga, Elizabeth, Koschmann, Carl, Yadav, Viveka Nand, and et al

Abstract

Diffuse intrinsic pontine glioma (DIPG) is an aggressive brain stem tumor and the leading cause of pediatric cancer-related death. To date, these tumors remain incurable, underscoring the need for efficacious therapies. In this study, we demonstrate that the immune checkpoint TIM-3 (HAVCR2) is highly expressed in both tumor cells and microenvironmental cells, mainly microglia and macrophages, in DIPG. We show that inhibition of TIM-3 in syngeneic models of DIPG prolongs survival and produces long-term survivors free of disease that harbor immune memory. This antitumor effect is driven by the direct effect of TIM-3 inhibition in tumor cells, the coordinated action of several immune cell populations, and the secretion of chemokines/cytokines that create a proinflammatory tumor microenvironment favoring a potent antitumor immune response. This work uncovers TIM-3 as a bona fide target in DIPG and supports its clinical translation.

Published
2023

3. The landscape of tumor cell states and spatial organization in H3-K27M mutant diffuse midline glioma across age and location

Author

Liu, Ilon, Jiang, Li, Samuelsson, Erik Reinhold, Marco Salas, Sergio, Beck, Alexander, Hack, Olivia A., Jeong, Daeun, Shaw, McKenzie L., Englinger, Bernhard, LaBelle, Jenna, Mire, Hafsa M., Madlener, Sibylle, Mayr, Lisa, Quezada, Michael A., Trissal, Maria, Panditharatna, Eshini, Ernst, Kati J., Vogelzang, Jayne, Gatesman, Taylor A., Halbert, Matthew E., Palova, Hana, Pokorna, Petra, Sterba, Jaroslav, Slaby, Ondrej, Geyeregger, Rene, Diaz, Aaron, Findlay, Izac J., Dun, Matthew D., Resnick, Adam, Suvà, Mario L., Jones, David T. W., Agnihotri, Sameer, Svedlund, Jessica, Koschmann, Carl, Haberler, Christine, Czech, Thomas, Slavc, Irene, Cotter, Jennifer A., Ligon, Keith L., Alexandrescu, Sanda, Yung, W. K. Alfred, Arrillaga-Romany, Isabel, Gojo, Johannes, Monje, Michelle, Nilsson, Mats, Filbin, Mariella G., Liu, Ilon, Jiang, Li, Samuelsson, Erik Reinhold, Marco Salas, Sergio, Beck, Alexander, Hack, Olivia A., Jeong, Daeun, Shaw, McKenzie L., Englinger, Bernhard, LaBelle, Jenna, Mire, Hafsa M., Madlener, Sibylle, Mayr, Lisa, Quezada, Michael A., Trissal, Maria, Panditharatna, Eshini, Ernst, Kati J., Vogelzang, Jayne, Gatesman, Taylor A., Halbert, Matthew E., Palova, Hana, Pokorna, Petra, Sterba, Jaroslav, Slaby, Ondrej, Geyeregger, Rene, Diaz, Aaron, Findlay, Izac J., Dun, Matthew D., Resnick, Adam, Suvà, Mario L., Jones, David T. W., Agnihotri, Sameer, Svedlund, Jessica, Koschmann, Carl, Haberler, Christine, Czech, Thomas, Slavc, Irene, Cotter, Jennifer A., Ligon, Keith L., Alexandrescu, Sanda, Yung, W. K. Alfred, Arrillaga-Romany, Isabel, Gojo, Johannes, Monje, Michelle, Nilsson, Mats, and Filbin, Mariella G.

Abstract

Histone 3 lysine27-to-methionine (H3-K27M) mutations most frequently occur in diffuse midline gliomas (DMGs) of the childhood pons but are also increasingly recognized in adults. Their potential heterogeneity at different ages and midline locations is vastly understudied. Here, through dissecting the single-cell transcriptomic, epigenomic and spatial architectures of a comprehensive cohort of patient H3-K27M DMGs, we delineate how age and anatomical location shape glioma cell-intrinsic and -extrinsic features in light of the shared driver mutation. We show that stem-like oligodendroglial precursor-like cells, present across all clinico-anatomical groups, display varying levels of maturation dependent on location. We reveal a previously underappreciated relationship between mesenchymal cancer cell states and age, linked to age-dependent differences in the immune microenvironment. Further, we resolve the spatial organization of H3-K27M DMG cell populations and identify a mitotic oligodendroglial-lineage niche. Collectively, our study provides a powerful framework for rational modeling and therapeutic interventions.

Published
2022
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4. Mitogenic and progenitor gene programmes in single pilocytic astrocytoma cells

Author

Massachusetts Institute of Technology. Institute for Medical Engineering & Science, Massachusetts Institute of Technology. Department of Chemistry, Broad Institute of MIT and Harvard, Koch Institute for Integrative Cancer Research at MIT, Reitman, Zachary J., Paolella, Brenton R., Bergthold, Guillaume, Pelton, Kristine, Becker, Sarah, Jones, Robert, Sinai, Claire E., Malkin, Hayley, Huang, Ying, Grimmet, Leslie, Herbert, Zachary T., Sun, Yu, Weatherbee, Jessica L., Alberta, John A., Daley, John F., Rozenblatt-Rosen, Orit, Condurat, Alexandra L., Qian, Kenin, Khadka, Prasidda, Segal, Rosalind A., Haas-Kogan, Daphne, Filbin, Mariella G., Suva, Mario L., Regev, Aviv, Stiles, Charles D., Kieran, Mark W., Goumnerova, Liliana, Ligon, Keith L., Shalek, Alexander K, Bandopadhayay, Pratiti, Beroukhim, Rameen, Massachusetts Institute of Technology. Institute for Medical Engineering & Science, Massachusetts Institute of Technology. Department of Chemistry, Broad Institute of MIT and Harvard, Koch Institute for Integrative Cancer Research at MIT, Reitman, Zachary J., Paolella, Brenton R., Bergthold, Guillaume, Pelton, Kristine, Becker, Sarah, Jones, Robert, Sinai, Claire E., Malkin, Hayley, Huang, Ying, Grimmet, Leslie, Herbert, Zachary T., Sun, Yu, Weatherbee, Jessica L., Alberta, John A., Daley, John F., Rozenblatt-Rosen, Orit, Condurat, Alexandra L., Qian, Kenin, Khadka, Prasidda, Segal, Rosalind A., Haas-Kogan, Daphne, Filbin, Mariella G., Suva, Mario L., Regev, Aviv, Stiles, Charles D., Kieran, Mark W., Goumnerova, Liliana, Ligon, Keith L., Shalek, Alexander K, Bandopadhayay, Pratiti, and Beroukhim, Rameen

Abstract

Pilocytic astrocytoma (PA), the most common childhood brain tumor, is a low-grade glioma with a single driver BRAF rearrangement. Here, we perform scRNAseq in six PAs using methods that enabled detection of the rearrangement. When compared to higher-grade gliomas, a strikingly higher proportion of the PA cancer cells exhibit a differentiated, astrocyte-like phenotype. A smaller proportion of cells exhibit a progenitor-like phenotype with evidence of proliferation. These express a mitogen-activated protein kinase (MAPK) programme that was absent from higher-grade gliomas. Immune cells, especially microglia, comprise 40% of all cells in the PAs and account for differences in bulk expression profiles between tumor locations and subtypes. These data indicate that MAPK signaling is restricted to relatively undifferentiated cancer cells in PA, with implications for investigational therapies directed at this pathway.

Published
2020

5. Resolving medulloblastoma cellular architecture by single-cell genomics

Author

Broad Institute of MIT and Harvard, Massachusetts Institute of Technology. Department of Biology, Koch Institute for Integrative Cancer Research at MIT, Hovestadt, Volker, Smith, Kyle S., Bihannic, Laure, Filbin, Mariella G., Shaw, McKenzie L., Baumgartner, Alicia, DeWitt, John C., Groves, Andrew, Mayr, Lisa, Weisman, Hannah R., Richman, Alyssa R., Shore, Marni E., Goumnerova, Liliana, Rosencrance, Celeste, Carter, Robert A., Phoenix, Timothy N., Hadley, Jennifer L., Tong, Yiai, Houston, Jim, Ashmun, Richard A., DeCuypere, Michael, Sharma, Tanvi, Flasch, Diane, Silkov, Antonina, Ligon, Keith L., Pomeroy, Scott L., Rivera, Miguel N., Rozenblatt-Rosen, Orit, Rusert, Jessica M., Wechsler-Reya, Robert J., Li, Xiao-Nan, Peyrl, Andreas, Gojo, Johannes, Kirchhofer, Dominik, Lötsch, Daniela, Czech, Thomas, Dorfer, Christian, Haberler, Christine, Geyeregger, Rene, Halfmann, Angela, Gawad, Charles, Easton, John, Pfister, Stefan M., Gajjar, Amar, Regev, Aviv, Orr, Brent A., Slavc, Irene, Robinson, Giles W., Bernstein, Bradley E., Suvà, Mario L., Northcott, Paul A., Broad Institute of MIT and Harvard, Massachusetts Institute of Technology. Department of Biology, Koch Institute for Integrative Cancer Research at MIT, Hovestadt, Volker, Smith, Kyle S., Bihannic, Laure, Filbin, Mariella G., Shaw, McKenzie L., Baumgartner, Alicia, DeWitt, John C., Groves, Andrew, Mayr, Lisa, Weisman, Hannah R., Richman, Alyssa R., Shore, Marni E., Goumnerova, Liliana, Rosencrance, Celeste, Carter, Robert A., Phoenix, Timothy N., Hadley, Jennifer L., Tong, Yiai, Houston, Jim, Ashmun, Richard A., DeCuypere, Michael, Sharma, Tanvi, Flasch, Diane, Silkov, Antonina, Ligon, Keith L., Pomeroy, Scott L., Rivera, Miguel N., Rozenblatt-Rosen, Orit, Rusert, Jessica M., Wechsler-Reya, Robert J., Li, Xiao-Nan, Peyrl, Andreas, Gojo, Johannes, Kirchhofer, Dominik, Lötsch, Daniela, Czech, Thomas, Dorfer, Christian, Haberler, Christine, Geyeregger, Rene, Halfmann, Angela, Gawad, Charles, Easton, John, Pfister, Stefan M., Gajjar, Amar, Regev, Aviv, Orr, Brent A., Slavc, Irene, Robinson, Giles W., Bernstein, Bradley E., Suvà, Mario L., and Northcott, Paul A.

Abstract

Medulloblastoma is a malignant childhood cerebellar tumour type that comprises distinct molecular subgroups. Whereas genomic characteristics of these subgroups are well defined, the extent to which cellular diversity underlies their divergent biology and clinical behaviour remains largely unexplored. Here we used single-cell transcriptomics to investigate intra- and intertumoral heterogeneity in 25 medulloblastomas spanning all molecular subgroups. WNT, SHH and Group 3 tumours comprised subgroup-specific undifferentiated and differentiated neuronal-like malignant populations, whereas Group 4 tumours consisted exclusively of differentiated neuronal-like neoplastic cells. SHH tumours closely resembled granule neurons of varying differentiation states that correlated with patient age. Group 3 and Group 4 tumours exhibited a developmental trajectory from primitive progenitor-like to more mature neuronal-like cells, the relative proportions of which distinguished these subgroups. Cross-species transcriptomics defined distinct glutamatergic populations as putative cells-of-origin for SHH and Group 4 subtypes. Collectively, these data provide insights into the cellular and developmental states underlying subtype-specific medulloblastoma biology.

Published
2020

6. Rapid Generation of Somatic Mouse Mosaics with Locus-Specific, Stably Integrated Transgenic Elements.

Author

Kim, Gi Bum, Kim, Gi Bum, Rincon Fernandez Pacheco, David, Saxon, David, Yang, Amy, Sabet, Sara, Dutra-Clarke, Marina, Levy, Rachelle, Watkins, Ashley, Park, Hannah, Abbasi Akhtar, Aslam, Linesch, Paul W, Kobritz, Naomi, Chandra, Swasty S, Grausam, Katie, Ayala-Sarmiento, Alberto, Molina, Jessica, Sedivakova, Kristyna, Hoang, Kendy, Tsyporin, Jeremiah, Gareau, Daniel S, Filbin, Mariella G, Bannykh, Serguei, Santiskulvong, Chintda, Wang, Yizhou, Tang, Jie, Suva, Mario L, Chen, Bin, Danielpour, Moise, Breunig, Joshua J, Kim, Gi Bum, Kim, Gi Bum, Rincon Fernandez Pacheco, David, Saxon, David, Yang, Amy, Sabet, Sara, Dutra-Clarke, Marina, Levy, Rachelle, Watkins, Ashley, Park, Hannah, Abbasi Akhtar, Aslam, Linesch, Paul W, Kobritz, Naomi, Chandra, Swasty S, Grausam, Katie, Ayala-Sarmiento, Alberto, Molina, Jessica, Sedivakova, Kristyna, Hoang, Kendy, Tsyporin, Jeremiah, Gareau, Daniel S, Filbin, Mariella G, Bannykh, Serguei, Santiskulvong, Chintda, Wang, Yizhou, Tang, Jie, Suva, Mario L, Chen, Bin, Danielpour, Moise, and Breunig, Joshua J

Abstract

In situ transgenesis methods such as viruses and electroporation can rapidly create somatic transgenic mice but lack control over copy number, zygosity, and locus specificity. Here we establish mosaic analysis by dual recombinase-mediated cassette exchange (MADR), which permits stable labeling of mutant cells expressing transgenic elements from precisely defined chromosomal loci. We provide a toolkit of MADR elements for combination labeling, inducible and reversible transgene manipulation, VCre recombinase expression, and transgenesis of human cells. Further, we demonstrate the versatility of MADR by creating glioma models with mixed reporter-identified zygosity or with "personalized" driver mutations from pediatric glioma. MADR is extensible to thousands of existing mouse lines, providing a flexible platform to democratize the generation of somatic mosaic mice. VIDEO ABSTRACT.

Published
2019

7. Decoupling genetics, lineages, and microenvironment in IDH-mutant gliomas by single-cell RNA-seq

Author

Broad Institute of MIT and Harvard, Massachusetts Institute of Technology. Department of Biology, Koch Institute for Integrative Cancer Research at MIT, Dionne, Danielle, Golub, Todd, Getz, Gad Asher, Bernstein, Bradley, Regev, Aviv, Venteicher, Andrew S., Tirosh, Itay, Hebert, Christine, Yizhak, Keren, Neftel, Cyril, Filbin, Mariella G., Hovestadt, Volker, Escalante, Leah E., Shaw, McKenzie L., Rodman, Christopher, Gillespie, Shawn M., Luo, Christina C., Ravichandran, Hiranmayi, Mylvaganam, Ravindra, Mount, Christopher, Onozato, Maristela L., Nahed, Brian V., Wakimoto, Hiroaki, Curry, William T., Iafrate, A. John, Rivera, Miguel N., Frosch, Matthew P., Brastianos, Priscilla K., Patel, Anoop P., Monje, Michelle, Cahill, Daniel P., Rozenblatt-Rosen, Orit, Louis, David N., Suvà, Mario L., Bernstein, Bradley E., Broad Institute of MIT and Harvard, Massachusetts Institute of Technology. Department of Biology, Koch Institute for Integrative Cancer Research at MIT, Dionne, Danielle, Golub, Todd, Getz, Gad Asher, Bernstein, Bradley, Regev, Aviv, Venteicher, Andrew S., Tirosh, Itay, Hebert, Christine, Yizhak, Keren, Neftel, Cyril, Filbin, Mariella G., Hovestadt, Volker, Escalante, Leah E., Shaw, McKenzie L., Rodman, Christopher, Gillespie, Shawn M., Luo, Christina C., Ravichandran, Hiranmayi, Mylvaganam, Ravindra, Mount, Christopher, Onozato, Maristela L., Nahed, Brian V., Wakimoto, Hiroaki, Curry, William T., Iafrate, A. John, Rivera, Miguel N., Frosch, Matthew P., Brastianos, Priscilla K., Patel, Anoop P., Monje, Michelle, Cahill, Daniel P., Rozenblatt-Rosen, Orit, Louis, David N., Suvà, Mario L., and Bernstein, Bradley E.

Abstract

Tumor subclasses differ according to the genotypes and phenotypes of malignant cells as well as the composition of the tumor microenvironment (TME).We dissected these influences in isocitrate dehydrogenase (IDH)-mutant gliomas by combining 14,226 single-cell RNA sequencing (RNA-seq) profiles from 16 patient samples with bulk RNA-seq profiles from 165 patient samples. Differences in bulk profiles between IDH-mutant astrocytoma and oligodendroglioma can be primarily explained by distinct TME and signature genetic events, whereas both tumor types share similar developmental hierarchies and lineages of glial differentiation. As tumor grade increases, we find enhanced proliferation of malignant cells, larger pools of undifferentiated glioma cells, and an increase in macrophage over microglia expression programs in TME. Our work provides a unifying model for IDH-mutant gliomas and a general framework for dissecting the differences among human tumor subclasses., National Cancer Institute (U.S.) (Grant P30-CA14051)

Published
2018

8. Single-cell RNA-seq supports a developmental hierarchy in human oligodendroglioma

Author

Massachusetts Institute of Technology. Department of Biology, Koch Institute for Integrative Cancer Research at MIT, Golub, Todd, Regev, Aviv, Tirosh, Itay, Venteicher, Andrew S., Hebert, Christine, Escalante, Leah E., Patel, Anoop P., Yizhak, Keren, Fisher, Jonathan M., Rodman, Christopher, Mount, Christopher, Filbin, Mariella G., Neftel, Cyril, Desai, Niyati, Nyman, Jackson, Izar, Benjamin, Luo, Christina C., Francis, Joshua M., Patel, Aanand A., Onozato, Maristela L., Riggi, Nicolo, Livak, Kenneth J., Gennert, Dave, Satija, Rahul, Nahed, Brian V., Curry, William T., Martuza, Robert L., Mylvaganam, Ravindra, Iafrate, A. John, Frosch, Matthew P., Rivera, Miguel N., Getz, Gad, Rozenblatt-Rosen, Orit, Cahill, Daniel P., Monje, Michelle, Bernstein, Bradley E., Louis, David N., Suvà, Mario L., Massachusetts Institute of Technology. Department of Biology, Koch Institute for Integrative Cancer Research at MIT, Golub, Todd, Regev, Aviv, Tirosh, Itay, Venteicher, Andrew S., Hebert, Christine, Escalante, Leah E., Patel, Anoop P., Yizhak, Keren, Fisher, Jonathan M., Rodman, Christopher, Mount, Christopher, Filbin, Mariella G., Neftel, Cyril, Desai, Niyati, Nyman, Jackson, Izar, Benjamin, Luo, Christina C., Francis, Joshua M., Patel, Aanand A., Onozato, Maristela L., Riggi, Nicolo, Livak, Kenneth J., Gennert, Dave, Satija, Rahul, Nahed, Brian V., Curry, William T., Martuza, Robert L., Mylvaganam, Ravindra, Iafrate, A. John, Frosch, Matthew P., Rivera, Miguel N., Getz, Gad, Rozenblatt-Rosen, Orit, Cahill, Daniel P., Monje, Michelle, Bernstein, Bradley E., Louis, David N., and Suvà, Mario L.

Abstract

Although human tumours are shaped by the genetic evolution of cancer cells, evidence also suggests that they display hierarchies related to developmental pathways and epigenetic programs in which cancer stem cells (CSCs) can drive tumour growth and give rise to differentiated progeny. Yet, unbiased evidence for CSCs in solid human malignancies remains elusive. Here we profile 4,347 single cells from six IDH1 or IDH2 mutant human oligodendrogliomas by RNA sequencing (RNA-seq) and reconstruct their developmental programs from genome-wide expression signatures. We infer that most cancer cells are differentiated along two specialized glial programs, whereas a rare subpopulation of cells is undifferentiated and associated with a neural stem cell expression program. Cells with expression signatures for proliferation are highly enriched in this rare subpopulation, consistent with a model in which CSCs are primarily responsible for fuelling the growth of oligodendroglioma in humans. Analysis of copy number variation (CNV) shows that distinct CNV sub-clones within tumours display similar cellular hierarchies, suggesting that the architecture of oligodendroglioma is primarily dictated by developmental programs. Subclonal point mutation analysis supports a similar model, although a full phylogenetic tree would be required to definitively determine the effect of genetic evolution on the inferred hierarchies. Our single-cell analyses provide insight into the cellular architecture of oligodendrogliomas at single-cell resolution and support the cancer stem cell model, with substantial implications for disease management.

Published
2018

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