Comprehensive table with examples of most the published pre-clinical glioma models and their specifics over the last 30+ years
| Model . | Origin . | Name . | Characteristics . | Citations . |
|---|---|---|---|---|
| Established cell lines | Human GBM | U87 | High proliferation, non-diffuse, infiltrative patterns, widely used, well-characterized | Clark et al. (2010), Allen et al. (2016) |
| Established cell line | Human GBM | U251 | High proliferation, necrotic regions, high Ki-67 positivity, maintains some tumor cell infiltrative patterns | Torsvik et al. (2014), Li et al. (2017) |
| Established cell line | Human GBM | T98G | High ACTA2 expression, motility, minimally tumorigenic in mice | Kiseleva et al. (2016), Rubenstein et al. (1999) |
| Established cell line | Human GBM | A172 | High proliferation | Fenstermaker et al. (1998), Kiseleva et al. (2016) |
| Established cell line | Human GBM | LN229 | High proliferation, useful for studying MGMT methylation and drug response | Beckner et al. (2005), Demircan et al. (2021) |
| Established cell line | Human GBM | SF8628 | H3.3K27M mutation, used in pediatric glioma studies | Damanskienė et al. (2022), Olow et al. (2016) |
| Established cell line | Human GBM | U373 | High proliferation, widely used, well-characterized | Dranoff et al. (1985), Takiguchi et al. (1985) |
| Established cell line | Human GBM | SF9402 | H3.3 wild type, used in combination therapy studies | Hashizume et al. (2014), Wang et al. (2021) |
| Established cell line | Human GBM | SF7761 | H3.3K27M mutation, used in pediatric glioma studies | Hashizume et al. (2012), Abe et al. (2020) |
| Established cell line | Human GBM | GBM12 | High proliferation, used in xenograft studies | Sarkaria et al. (2006), Paraskevakou et al. (2007) |
| Established cell line | Human oligodendroglioma | Hs683 | High proliferation, useful for studying TMZ response | Tasiou et al. (2001), Konduri et al. (2001) |
| Established cell line | Mouse GBM | GL261 | High MHC I, MHC II expression, RAS and p53 mutations. Widely used in immunotherapy studies | Wu et al. (2008), Rappa et al. (2008) |
| Established cell line | Rat gliosarcoma | 9L | High proliferation, aggressive tumor growth in vivo | Ghods et al. (2007), Kruse et al. (1994) |
| Established cell line | Rat GBM | C6 | High proliferation, aggressive tumor growth in vivo | Giakoumettis et al. (2018), Kondo et al. (2004) |
| 3D models | Human GBM | GSCs | Retains patient’s molecular subtypes | Singh et al. (2004), Lee et al. (2006) |
| 3D models | Human GBM | PDOs | Recapitulates inter- and intra-tumoral heterogeneity. Requires fresh tumor samples | Chen et al. (2022), Jacob et al. (2020) |
| 3D models | Human GBM | GLICOs | Allows for diffuse infiltration of glioma cells, mimicking human brain integration. Represents epigenomic-mediated transcriptomic states | da Silva et al. (2018), Linkous et al. (2019) |
| 3D models | Human GBM | Cerebral organoids with CRISPR-Cas9 (GBM organoids) | Genetically manipulated to develop oncogenic properties. Limited tumor heterogeneity | Ogawa et al. (2018), Bian et al. (2018) |
| 3D models | Human GBM | Tumor organoids | Represents hypoxic niches and oxygen gradients. Lack interactions with normal host brain cells | Hubert et al. (2016), Heaster et al. (2019) |
| 3D models | Human and rodent brain tissue | Brain slice cultures (explants) | Allows interaction with normal brain cells and ECM. Limited by the stress and eventual death of normal brain constituents | Ohnishi et al. (1998), Eisemann et al. (2018) |
| Oncogene induced syngeneic mouse models | C57BL/6 mouse | SB28 | Poor immunogenic glioma model, commonly used in PD-L immunotherapy studies | Letchuman et al. (2022), Murty et al. (2020) |
| Chemically induced syngeneic mouse models | C57BL/6 mouse | GL261 | High proliferation, aggressive tumor growth, mutation in KRAS. Genetic drift over time, limited representation of human gliomas, immunogenic. | Szatmári et al. (2006), Daviaud et al. (2024) |
| Chemically induced | C57BL/6 mouse | CT-2A | Deficient in PTEN, necrotic, chemoresistant, undergoes unregulated angiogenesis. Used in immunotherapy studies limited genetic heterogeneity | Riva et al. (2019), Casanova-Carvajal et al. (2019) |
| Chemically induced | C57BL/6 mouse | GL26 | High proliferation, mutation in KRAS, aggressive tumor growth, widely used | Wouters et al. (2020), Kim et al. (2010) |
| Spontaneous syngeneic models | C3H mouse | P560 | High proliferation, aggressive tumor growth | Kim et al. (2010), Bradford et al. (1986) |
| GEMMs | Neural progenitors or astrocytes | Ink4a-Arf/Kras/Akt | Model for studying cooperation between KRas activation and Ink4a-Arf loss in gliomagenesis | Uhrbom et al. (2002), Figg et al. (2024) |
| GEMMs | Various glioma-initiating cells | PTEN/p53/CDKN2/RB knockout | Models high-grade astrocytomas with multiple genetic alterations | Holland (2001), Alcantara Llaguno et al. (2019) |
| GEMMs | Neural stem/progenitor cells | NF1/p53 | Useful for studying NF1 and p53 interactions in gliomagenesis. Induces tumors that appear similar to astrocytomas | Zhu et al. (2005), Liu et al. (2011) |
| GEMMs | Various glioma-initiating cells | Idh1R132H | Investigates metabolic vulnerabilities of IDH1 mutant gliomas. Demonstrates extreme vulnerability to NAD+ depletion | Bardella et al. (2016), Zhang et al. (2019) |
| GEMMs | Various glioma-initiating cells | CDKN2 Knockout/EGFR/PDGFR | Studies cooperation between CDKN2 loss and growth factor signaling in gliomagenesis | Zhu et al. (2009), Yeo et al. (2021) |
| Xenograft models | Human GBM | U87MG xenograft | High proliferation, circumscribed tumors. Widely used, good reproducibility. Lacks infiltrative pattern seen in human gliomas | Mathieu et al. (2008), Donoghue et al. (2011) |
| Cell line xenograft | Human GBM | U251 xenograft | High proliferation, necrotic regions, well-characterized, widely used, limited heterogeneity, circumscribed tumors | Williams et al. (1998), Kijima et al. (2014) |
| Cell line xenograft | Human GBM | A172 xenograft | High proliferation, used in various glioma studies, limited heterogeneity | Finkelstein et al. (1994), Zhang et al. (2008) |
| LN229 xenograft | Human GBM | LN229 xenograft | High proliferation, MGMT methylation | Hlavaty et al. (2011), Nagai et al. (2023) |
| SF8628 xenograft | Human GBM | SF8628 xenograft | H3.3K27M mutation, used in pediatric glioma studies | Olow et al. (2016), Da-Veiga et al. (2023) |
| IDH1 mutant xenograft | Human GBM | IDH1mut xenograft | Retains IDH1 mutation, mimics genetic and phenotypic features of primary tumors. Challenging to maintain | Luchman et al. (2012), Rudà et al. (2024) |
| EGFRvIII xenograft | Human GBM | GLI36-EGFRvIII xenograft | Overexpression of EGFRvIII, aggressive tumor growth | Herrmann et al. (2016), Saydam et al. (2005) |
| Xenograft | Human GBM | GSC xenograft | CD133+ cells, tumor-initiating capability. Preserves tumor heterogeneity. Long latency periods | Lee et al. (2006), Tanaka et al. (2019) |
| Xenograft | Human GBM | PDX | Retains some genetic and histological features of the primary tumor. Preserves tumor heterogeneity. Requires fresh tumor samples with variable success rates | Kerstetter-Fogle et al. (2020), Vaubel et al. (2020) |
| Model . | Origin . | Name . | Characteristics . | Citations . |
|---|---|---|---|---|
| Established cell lines | Human GBM | U87 | High proliferation, non-diffuse, infiltrative patterns, widely used, well-characterized | Clark et al. (2010), Allen et al. (2016) |
| Established cell line | Human GBM | U251 | High proliferation, necrotic regions, high Ki-67 positivity, maintains some tumor cell infiltrative patterns | Torsvik et al. (2014), Li et al. (2017) |
| Established cell line | Human GBM | T98G | High ACTA2 expression, motility, minimally tumorigenic in mice | Kiseleva et al. (2016), Rubenstein et al. (1999) |
| Established cell line | Human GBM | A172 | High proliferation | Fenstermaker et al. (1998), Kiseleva et al. (2016) |
| Established cell line | Human GBM | LN229 | High proliferation, useful for studying MGMT methylation and drug response | Beckner et al. (2005), Demircan et al. (2021) |
| Established cell line | Human GBM | SF8628 | H3.3K27M mutation, used in pediatric glioma studies | Damanskienė et al. (2022), Olow et al. (2016) |
| Established cell line | Human GBM | U373 | High proliferation, widely used, well-characterized | Dranoff et al. (1985), Takiguchi et al. (1985) |
| Established cell line | Human GBM | SF9402 | H3.3 wild type, used in combination therapy studies | Hashizume et al. (2014), Wang et al. (2021) |
| Established cell line | Human GBM | SF7761 | H3.3K27M mutation, used in pediatric glioma studies | Hashizume et al. (2012), Abe et al. (2020) |
| Established cell line | Human GBM | GBM12 | High proliferation, used in xenograft studies | Sarkaria et al. (2006), Paraskevakou et al. (2007) |
| Established cell line | Human oligodendroglioma | Hs683 | High proliferation, useful for studying TMZ response | Tasiou et al. (2001), Konduri et al. (2001) |
| Established cell line | Mouse GBM | GL261 | High MHC I, MHC II expression, RAS and p53 mutations. Widely used in immunotherapy studies | Wu et al. (2008), Rappa et al. (2008) |
| Established cell line | Rat gliosarcoma | 9L | High proliferation, aggressive tumor growth in vivo | Ghods et al. (2007), Kruse et al. (1994) |
| Established cell line | Rat GBM | C6 | High proliferation, aggressive tumor growth in vivo | Giakoumettis et al. (2018), Kondo et al. (2004) |
| 3D models | Human GBM | GSCs | Retains patient’s molecular subtypes | Singh et al. (2004), Lee et al. (2006) |
| 3D models | Human GBM | PDOs | Recapitulates inter- and intra-tumoral heterogeneity. Requires fresh tumor samples | Chen et al. (2022), Jacob et al. (2020) |
| 3D models | Human GBM | GLICOs | Allows for diffuse infiltration of glioma cells, mimicking human brain integration. Represents epigenomic-mediated transcriptomic states | da Silva et al. (2018), Linkous et al. (2019) |
| 3D models | Human GBM | Cerebral organoids with CRISPR-Cas9 (GBM organoids) | Genetically manipulated to develop oncogenic properties. Limited tumor heterogeneity | Ogawa et al. (2018), Bian et al. (2018) |
| 3D models | Human GBM | Tumor organoids | Represents hypoxic niches and oxygen gradients. Lack interactions with normal host brain cells | Hubert et al. (2016), Heaster et al. (2019) |
| 3D models | Human and rodent brain tissue | Brain slice cultures (explants) | Allows interaction with normal brain cells and ECM. Limited by the stress and eventual death of normal brain constituents | Ohnishi et al. (1998), Eisemann et al. (2018) |
| Oncogene induced syngeneic mouse models | C57BL/6 mouse | SB28 | Poor immunogenic glioma model, commonly used in PD-L immunotherapy studies | Letchuman et al. (2022), Murty et al. (2020) |
| Chemically induced syngeneic mouse models | C57BL/6 mouse | GL261 | High proliferation, aggressive tumor growth, mutation in KRAS. Genetic drift over time, limited representation of human gliomas, immunogenic. | Szatmári et al. (2006), Daviaud et al. (2024) |
| Chemically induced | C57BL/6 mouse | CT-2A | Deficient in PTEN, necrotic, chemoresistant, undergoes unregulated angiogenesis. Used in immunotherapy studies limited genetic heterogeneity | Riva et al. (2019), Casanova-Carvajal et al. (2019) |
| Chemically induced | C57BL/6 mouse | GL26 | High proliferation, mutation in KRAS, aggressive tumor growth, widely used | Wouters et al. (2020), Kim et al. (2010) |
| Spontaneous syngeneic models | C3H mouse | P560 | High proliferation, aggressive tumor growth | Kim et al. (2010), Bradford et al. (1986) |
| GEMMs | Neural progenitors or astrocytes | Ink4a-Arf/Kras/Akt | Model for studying cooperation between KRas activation and Ink4a-Arf loss in gliomagenesis | Uhrbom et al. (2002), Figg et al. (2024) |
| GEMMs | Various glioma-initiating cells | PTEN/p53/CDKN2/RB knockout | Models high-grade astrocytomas with multiple genetic alterations | Holland (2001), Alcantara Llaguno et al. (2019) |
| GEMMs | Neural stem/progenitor cells | NF1/p53 | Useful for studying NF1 and p53 interactions in gliomagenesis. Induces tumors that appear similar to astrocytomas | Zhu et al. (2005), Liu et al. (2011) |
| GEMMs | Various glioma-initiating cells | Idh1R132H | Investigates metabolic vulnerabilities of IDH1 mutant gliomas. Demonstrates extreme vulnerability to NAD+ depletion | Bardella et al. (2016), Zhang et al. (2019) |
| GEMMs | Various glioma-initiating cells | CDKN2 Knockout/EGFR/PDGFR | Studies cooperation between CDKN2 loss and growth factor signaling in gliomagenesis | Zhu et al. (2009), Yeo et al. (2021) |
| Xenograft models | Human GBM | U87MG xenograft | High proliferation, circumscribed tumors. Widely used, good reproducibility. Lacks infiltrative pattern seen in human gliomas | Mathieu et al. (2008), Donoghue et al. (2011) |
| Cell line xenograft | Human GBM | U251 xenograft | High proliferation, necrotic regions, well-characterized, widely used, limited heterogeneity, circumscribed tumors | Williams et al. (1998), Kijima et al. (2014) |
| Cell line xenograft | Human GBM | A172 xenograft | High proliferation, used in various glioma studies, limited heterogeneity | Finkelstein et al. (1994), Zhang et al. (2008) |
| LN229 xenograft | Human GBM | LN229 xenograft | High proliferation, MGMT methylation | Hlavaty et al. (2011), Nagai et al. (2023) |
| SF8628 xenograft | Human GBM | SF8628 xenograft | H3.3K27M mutation, used in pediatric glioma studies | Olow et al. (2016), Da-Veiga et al. (2023) |
| IDH1 mutant xenograft | Human GBM | IDH1mut xenograft | Retains IDH1 mutation, mimics genetic and phenotypic features of primary tumors. Challenging to maintain | Luchman et al. (2012), Rudà et al. (2024) |
| EGFRvIII xenograft | Human GBM | GLI36-EGFRvIII xenograft | Overexpression of EGFRvIII, aggressive tumor growth | Herrmann et al. (2016), Saydam et al. (2005) |
| Xenograft | Human GBM | GSC xenograft | CD133+ cells, tumor-initiating capability. Preserves tumor heterogeneity. Long latency periods | Lee et al. (2006), Tanaka et al. (2019) |
| Xenograft | Human GBM | PDX | Retains some genetic and histological features of the primary tumor. Preserves tumor heterogeneity. Requires fresh tumor samples with variable success rates | Kerstetter-Fogle et al. (2020), Vaubel et al. (2020) |