BIOL-18. NEWLY DEVELOPED REPLICATION REPAIR DEFICIENT (RRD) MOUSE MODELS PROVIDE INSIGHTS INTO MEDULLOBLASTOMA/GLIOMAGENESIS AND RESPONSE TO IMMUNOTHERAPY
Abstract Replication Repair Deficiency (RRD), caused by germline monoallelic (Lynch Syndrome) or biallelic (Constitutional Mismatch Repair Deficiency, CMMRD) mutations in MMR genes, is present in 5-10% of glioblastomas in children, adolescents, and young adults. RRD glioblastomas are chemoradiation-...
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| creator | Aamir, Zoya Galati, Melissa Gattoni, Emma Crump, Owen Nunes, Nuno M Das, Anirban Fernandez, Nicholas R Wong, Angel K Q Fortin, Jerome Stengs, Lucie Bianchi, Vanessa Edwards, Melissa Negm, Logine Chung, Jiil Malkin, David Egan, Sean Hawkins, Cynthia Tabori, Uri |
| description | Abstract
Replication Repair Deficiency (RRD), caused by germline monoallelic (Lynch Syndrome) or biallelic (Constitutional Mismatch Repair Deficiency, CMMRD) mutations in MMR genes, is present in 5-10% of glioblastomas in children, adolescents, and young adults. RRD glioblastomas are chemoradiation-resistant, but respond favorably to immune checkpoint inhibition (ICI). Representative immunocompetent animal models are urgently needed for 3 recently identified subgroups based on specific somatically-acquired mutations, survival, and immunotherapy response (RRD1: MMRD with POLE mutations, RRD2: MMRD associated with TP53 mutations, and RRD3: MMRD harboring IDH1 mutations). Using germline mutations and brain-specific Cre-drivers, we genetically engineered mouse models that recapitulate each human RRD-subgroup. RRD1 (Nestin- and Olig2-Cre+/ Msh2LoxP/LoxP/PoleS459F/+ and LSL-PoleP286R/+): CMMRD-like Nestin-Cre-driven mice develop posterior-fossa glioma-like or medulloblastoma (MB)-like tumors at ~2.7 months. Olig2-Cre-driven mice display hemispheric gliomas at ~10 months, suggesting distinct cell-of-origin. RRD2 (Nestin-Cre+/Trp53LoxP/LoxP and Msh2LoxP/LoxP or Mlh1-/-): CMMRD-like tumors develop in heterogenous locations at ~4.5 months (p13 months (p |
| doi_str_mv | 10.1093/neuonc/noad073.037 |
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Replication Repair Deficiency (RRD), caused by germline monoallelic (Lynch Syndrome) or biallelic (Constitutional Mismatch Repair Deficiency, CMMRD) mutations in MMR genes, is present in 5-10% of glioblastomas in children, adolescents, and young adults. RRD glioblastomas are chemoradiation-resistant, but respond favorably to immune checkpoint inhibition (ICI). Representative immunocompetent animal models are urgently needed for 3 recently identified subgroups based on specific somatically-acquired mutations, survival, and immunotherapy response (RRD1: MMRD with POLE mutations, RRD2: MMRD associated with TP53 mutations, and RRD3: MMRD harboring IDH1 mutations). Using germline mutations and brain-specific Cre-drivers, we genetically engineered mouse models that recapitulate each human RRD-subgroup. RRD1 (Nestin- and Olig2-Cre+/ Msh2LoxP/LoxP/PoleS459F/+ and LSL-PoleP286R/+): CMMRD-like Nestin-Cre-driven mice develop posterior-fossa glioma-like or medulloblastoma (MB)-like tumors at ~2.7 months. Olig2-Cre-driven mice display hemispheric gliomas at ~10 months, suggesting distinct cell-of-origin. RRD2 (Nestin-Cre+/Trp53LoxP/LoxP and Msh2LoxP/LoxP or Mlh1-/-): CMMRD-like tumors develop in heterogenous locations at ~4.5 months (p<0.0001), classifying primarily as MB-like in hindbrain, and glioma-like in other brain regions. Strikingly, germline Mlh1 tumors occur earlier than Nestin-Cre-driven RRD2 tumors, indicating early developmental mutation accumulation in CMMRD-patients. Lynch-like RRD1/2 mice succumb exclusively to gliomas >13 months (p<0.0001). RRD3 (Olig2-Cre+/Msh2LoxP/LoxP/Trp53LoxP/LoxP/LSL-Idh1R132H/+): brain tumors occur later and are hemispheric. These observations recapitulate human data, where CMMRD-patients develop glioblastoma/MB earlier than Lynch-patients (8.6 vs. 14-years; p<0.0001), and posterior-fossa glioblastoma/MB presents earlier than hemispheric gliomas (p=0.04). Additionally, tumor onset and location vary (RRD1: 7.6-years, RRD2: 8.3-years, hemispheric/posterior-fossa; RRD3: 12-years, hemispheric; p=0.005). In both mice and humans, RRD1 exhibits ultra-hypermutation, high immune infiltration, and response to ICI, whereas RRD2 harbors lower mutational burden, are immune-cold, and ICI-monotherapy resistant. Temporal dynamics of RRD tumor development is currently being tracked by serial MRI to define biologically relevant time points. Our models accurately mimic the human condition and provide unique insights into RRD tumorigenesis, allowing optimization of subgroup-tailored therapeutic approaches.</description><identifier>ISSN: 1522-8517</identifier><identifier>EISSN: 1523-5866</identifier><identifier>DOI: 10.1093/neuonc/noad073.037</identifier><language>eng</language><publisher>US: Oxford University Press</publisher><subject>Final Category: Basic Biology/Stem Cells/Models - BIOL</subject><ispartof>Neuro-oncology (Charlottesville, Va.), 2023-06, Vol.25 (Supplement_1), p.i9-i10</ispartof><rights>The Author(s) 2023. Published by Oxford University Press on behalf of the Society for Neuro-Oncology. 2023</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10259929/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10259929/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids></links><search><creatorcontrib>Aamir, Zoya</creatorcontrib><creatorcontrib>Galati, Melissa</creatorcontrib><creatorcontrib>Gattoni, Emma</creatorcontrib><creatorcontrib>Crump, Owen</creatorcontrib><creatorcontrib>Nunes, Nuno M</creatorcontrib><creatorcontrib>Das, Anirban</creatorcontrib><creatorcontrib>Fernandez, Nicholas R</creatorcontrib><creatorcontrib>Wong, Angel K Q</creatorcontrib><creatorcontrib>Fortin, Jerome</creatorcontrib><creatorcontrib>Stengs, Lucie</creatorcontrib><creatorcontrib>Bianchi, Vanessa</creatorcontrib><creatorcontrib>Edwards, Melissa</creatorcontrib><creatorcontrib>Negm, Logine</creatorcontrib><creatorcontrib>Chung, Jiil</creatorcontrib><creatorcontrib>Malkin, David</creatorcontrib><creatorcontrib>Egan, Sean</creatorcontrib><creatorcontrib>Hawkins, Cynthia</creatorcontrib><creatorcontrib>Tabori, Uri</creatorcontrib><title>BIOL-18. NEWLY DEVELOPED REPLICATION REPAIR DEFICIENT (RRD) MOUSE MODELS PROVIDE INSIGHTS INTO MEDULLOBLASTOMA/GLIOMAGENESIS AND RESPONSE TO IMMUNOTHERAPY</title><title>Neuro-oncology (Charlottesville, Va.)</title><description>Abstract
Replication Repair Deficiency (RRD), caused by germline monoallelic (Lynch Syndrome) or biallelic (Constitutional Mismatch Repair Deficiency, CMMRD) mutations in MMR genes, is present in 5-10% of glioblastomas in children, adolescents, and young adults. RRD glioblastomas are chemoradiation-resistant, but respond favorably to immune checkpoint inhibition (ICI). Representative immunocompetent animal models are urgently needed for 3 recently identified subgroups based on specific somatically-acquired mutations, survival, and immunotherapy response (RRD1: MMRD with POLE mutations, RRD2: MMRD associated with TP53 mutations, and RRD3: MMRD harboring IDH1 mutations). Using germline mutations and brain-specific Cre-drivers, we genetically engineered mouse models that recapitulate each human RRD-subgroup. RRD1 (Nestin- and Olig2-Cre+/ Msh2LoxP/LoxP/PoleS459F/+ and LSL-PoleP286R/+): CMMRD-like Nestin-Cre-driven mice develop posterior-fossa glioma-like or medulloblastoma (MB)-like tumors at ~2.7 months. Olig2-Cre-driven mice display hemispheric gliomas at ~10 months, suggesting distinct cell-of-origin. RRD2 (Nestin-Cre+/Trp53LoxP/LoxP and Msh2LoxP/LoxP or Mlh1-/-): CMMRD-like tumors develop in heterogenous locations at ~4.5 months (p<0.0001), classifying primarily as MB-like in hindbrain, and glioma-like in other brain regions. Strikingly, germline Mlh1 tumors occur earlier than Nestin-Cre-driven RRD2 tumors, indicating early developmental mutation accumulation in CMMRD-patients. Lynch-like RRD1/2 mice succumb exclusively to gliomas >13 months (p<0.0001). RRD3 (Olig2-Cre+/Msh2LoxP/LoxP/Trp53LoxP/LoxP/LSL-Idh1R132H/+): brain tumors occur later and are hemispheric. These observations recapitulate human data, where CMMRD-patients develop glioblastoma/MB earlier than Lynch-patients (8.6 vs. 14-years; p<0.0001), and posterior-fossa glioblastoma/MB presents earlier than hemispheric gliomas (p=0.04). Additionally, tumor onset and location vary (RRD1: 7.6-years, RRD2: 8.3-years, hemispheric/posterior-fossa; RRD3: 12-years, hemispheric; p=0.005). In both mice and humans, RRD1 exhibits ultra-hypermutation, high immune infiltration, and response to ICI, whereas RRD2 harbors lower mutational burden, are immune-cold, and ICI-monotherapy resistant. Temporal dynamics of RRD tumor development is currently being tracked by serial MRI to define biologically relevant time points. Our models accurately mimic the human condition and provide unique insights into RRD tumorigenesis, allowing optimization of subgroup-tailored therapeutic approaches.</description><subject>Final Category: Basic Biology/Stem Cells/Models - BIOL</subject><issn>1522-8517</issn><issn>1523-5866</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>TOX</sourceid><recordid>eNqNUctu2zAQFIIGqJv2B3risT3I1pKWRJ4K2WJsApQoSLIDnwhaj9ZFIhlSXSC_kq8NHRsFcutld4DZmV3sOM5X8KbgMTLrmlPfVbOuN7UXkqlHwhtnAj4mrk-D4MMbxi71IfzofBrH356HwQ9g4rwshJIu0ClK-YPcoZhvuVQZj1HOMymWUSlUesaRyC15L5aCpyX6lufxd5SoTcFtjbksUJarrYg5EmkhVuuysKBUKOHxRkq1kFFRqiSaraSwbcVTXogCRel5T5Gp1PrYaZEkm1SVa55H2e6zc9uax7H5cu13zuael8u1K9XKHibdCiiEbkVY4NN5PccU9gwMhnnYENYSCGhImakbHJCWBSb0W4qrJqigrX0DLTHUfqUid86Pi-_xtH9q6qrp_gzmUR-Hw5MZnnVvDvo90x1-6Z_9Xw0e9hnDzDrgi0M19OM4NO0_MXj6nI--5KOv-WibjxW5F1F_Ov7P_CvuAYte</recordid><startdate>20230612</startdate><enddate>20230612</enddate><creator>Aamir, Zoya</creator><creator>Galati, Melissa</creator><creator>Gattoni, Emma</creator><creator>Crump, Owen</creator><creator>Nunes, Nuno M</creator><creator>Das, Anirban</creator><creator>Fernandez, Nicholas R</creator><creator>Wong, Angel K Q</creator><creator>Fortin, Jerome</creator><creator>Stengs, Lucie</creator><creator>Bianchi, Vanessa</creator><creator>Edwards, Melissa</creator><creator>Negm, Logine</creator><creator>Chung, Jiil</creator><creator>Malkin, David</creator><creator>Egan, Sean</creator><creator>Hawkins, Cynthia</creator><creator>Tabori, Uri</creator><general>Oxford University Press</general><scope>TOX</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>5PM</scope></search><sort><creationdate>20230612</creationdate><title>BIOL-18. NEWLY DEVELOPED REPLICATION REPAIR DEFICIENT (RRD) MOUSE MODELS PROVIDE INSIGHTS INTO MEDULLOBLASTOMA/GLIOMAGENESIS AND RESPONSE TO IMMUNOTHERAPY</title><author>Aamir, Zoya ; Galati, Melissa ; Gattoni, Emma ; Crump, Owen ; Nunes, Nuno M ; Das, Anirban ; Fernandez, Nicholas R ; Wong, Angel K Q ; Fortin, Jerome ; Stengs, Lucie ; Bianchi, Vanessa ; Edwards, Melissa ; Negm, Logine ; Chung, Jiil ; Malkin, David ; Egan, Sean ; Hawkins, Cynthia ; Tabori, Uri</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c1817-c396584d4281b91a2147e39f3168789ade263f96a75f82ce6c1fd5a1f3a8152c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Final Category: Basic Biology/Stem Cells/Models - BIOL</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Aamir, Zoya</creatorcontrib><creatorcontrib>Galati, Melissa</creatorcontrib><creatorcontrib>Gattoni, Emma</creatorcontrib><creatorcontrib>Crump, Owen</creatorcontrib><creatorcontrib>Nunes, Nuno M</creatorcontrib><creatorcontrib>Das, Anirban</creatorcontrib><creatorcontrib>Fernandez, Nicholas R</creatorcontrib><creatorcontrib>Wong, Angel K Q</creatorcontrib><creatorcontrib>Fortin, Jerome</creatorcontrib><creatorcontrib>Stengs, Lucie</creatorcontrib><creatorcontrib>Bianchi, Vanessa</creatorcontrib><creatorcontrib>Edwards, Melissa</creatorcontrib><creatorcontrib>Negm, Logine</creatorcontrib><creatorcontrib>Chung, Jiil</creatorcontrib><creatorcontrib>Malkin, David</creatorcontrib><creatorcontrib>Egan, Sean</creatorcontrib><creatorcontrib>Hawkins, Cynthia</creatorcontrib><creatorcontrib>Tabori, Uri</creatorcontrib><collection>Oxford Journals Open Access Collection</collection><collection>CrossRef</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Neuro-oncology (Charlottesville, Va.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Aamir, Zoya</au><au>Galati, Melissa</au><au>Gattoni, Emma</au><au>Crump, Owen</au><au>Nunes, Nuno M</au><au>Das, Anirban</au><au>Fernandez, Nicholas R</au><au>Wong, Angel K Q</au><au>Fortin, Jerome</au><au>Stengs, Lucie</au><au>Bianchi, Vanessa</au><au>Edwards, Melissa</au><au>Negm, Logine</au><au>Chung, Jiil</au><au>Malkin, David</au><au>Egan, Sean</au><au>Hawkins, Cynthia</au><au>Tabori, Uri</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>BIOL-18. NEWLY DEVELOPED REPLICATION REPAIR DEFICIENT (RRD) MOUSE MODELS PROVIDE INSIGHTS INTO MEDULLOBLASTOMA/GLIOMAGENESIS AND RESPONSE TO IMMUNOTHERAPY</atitle><jtitle>Neuro-oncology (Charlottesville, Va.)</jtitle><date>2023-06-12</date><risdate>2023</risdate><volume>25</volume><issue>Supplement_1</issue><spage>i9</spage><epage>i10</epage><pages>i9-i10</pages><issn>1522-8517</issn><eissn>1523-5866</eissn><abstract>Abstract
Replication Repair Deficiency (RRD), caused by germline monoallelic (Lynch Syndrome) or biallelic (Constitutional Mismatch Repair Deficiency, CMMRD) mutations in MMR genes, is present in 5-10% of glioblastomas in children, adolescents, and young adults. RRD glioblastomas are chemoradiation-resistant, but respond favorably to immune checkpoint inhibition (ICI). Representative immunocompetent animal models are urgently needed for 3 recently identified subgroups based on specific somatically-acquired mutations, survival, and immunotherapy response (RRD1: MMRD with POLE mutations, RRD2: MMRD associated with TP53 mutations, and RRD3: MMRD harboring IDH1 mutations). Using germline mutations and brain-specific Cre-drivers, we genetically engineered mouse models that recapitulate each human RRD-subgroup. RRD1 (Nestin- and Olig2-Cre+/ Msh2LoxP/LoxP/PoleS459F/+ and LSL-PoleP286R/+): CMMRD-like Nestin-Cre-driven mice develop posterior-fossa glioma-like or medulloblastoma (MB)-like tumors at ~2.7 months. Olig2-Cre-driven mice display hemispheric gliomas at ~10 months, suggesting distinct cell-of-origin. RRD2 (Nestin-Cre+/Trp53LoxP/LoxP and Msh2LoxP/LoxP or Mlh1-/-): CMMRD-like tumors develop in heterogenous locations at ~4.5 months (p<0.0001), classifying primarily as MB-like in hindbrain, and glioma-like in other brain regions. Strikingly, germline Mlh1 tumors occur earlier than Nestin-Cre-driven RRD2 tumors, indicating early developmental mutation accumulation in CMMRD-patients. Lynch-like RRD1/2 mice succumb exclusively to gliomas >13 months (p<0.0001). RRD3 (Olig2-Cre+/Msh2LoxP/LoxP/Trp53LoxP/LoxP/LSL-Idh1R132H/+): brain tumors occur later and are hemispheric. These observations recapitulate human data, where CMMRD-patients develop glioblastoma/MB earlier than Lynch-patients (8.6 vs. 14-years; p<0.0001), and posterior-fossa glioblastoma/MB presents earlier than hemispheric gliomas (p=0.04). Additionally, tumor onset and location vary (RRD1: 7.6-years, RRD2: 8.3-years, hemispheric/posterior-fossa; RRD3: 12-years, hemispheric; p=0.005). In both mice and humans, RRD1 exhibits ultra-hypermutation, high immune infiltration, and response to ICI, whereas RRD2 harbors lower mutational burden, are immune-cold, and ICI-monotherapy resistant. Temporal dynamics of RRD tumor development is currently being tracked by serial MRI to define biologically relevant time points. Our models accurately mimic the human condition and provide unique insights into RRD tumorigenesis, allowing optimization of subgroup-tailored therapeutic approaches.</abstract><cop>US</cop><pub>Oxford University Press</pub><doi>10.1093/neuonc/noad073.037</doi><oa>free_for_read</oa></addata></record> |
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| subjects | Final Category: Basic Biology/Stem Cells/Models - BIOL |
| title | BIOL-18. NEWLY DEVELOPED REPLICATION REPAIR DEFICIENT (RRD) MOUSE MODELS PROVIDE INSIGHTS INTO MEDULLOBLASTOMA/GLIOMAGENESIS AND RESPONSE TO IMMUNOTHERAPY |
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