LINK LUDWIG APRIL 2020 1 4 | A distinguished 4 |Adistinguished Douglas Hanahan joins Renowned scientist the Lausanne Branch Lausanne the scholar IN THIS ISSUE IN THIS

LIFE-CHANGING SCIENCE LIFE-CHANGING The Ludwig MIT MIT Ludwig The 18 | 18 Director on his science, science, his on Director Robert WeinbergRobert his mentors more and Q&A with Q&A

LUDWIG LINK | APRIL 2020 2

LUDWIG LINK | APRIL 2020 LETTER Senior Vice President for Communications President Vice Senior Rachel Reinhardt Sincerely, research pioneer. a with interview engaging an include and colleagues your on bestowed honors and awards discoveries, intriguing with brim which pages, following the in that of evidence ample find sure, You we’re will, humanity. of wellbeing to is the it important how of you remind will newsletter this hope we and passes, pandemic the when resume will time.work Your difficult this in healthy and safe staying are ones loved your and you We hope please do not hesitate to contact us. efforts, your in you help to of be can York New office the If requires. institution host your measures safety and mitigating whatever following and pandemic this end to help part your doing all are you that We recognize efforts. your in best the all you wish and everyone for uncertainty tremendous of atime is this that We appreciate protected. and to assure that critical research resources are preserved work time, same the at and, labs your to secure had have

economic fallout, many of you you of many fallout, economic its and pandemic COVID-19 the by caused worry the with coping from Aside beyond. and community Ludwig the in everyone for time challenging professionally and a personally at arrives Link Ludwig of issue This 3 LUDWIG LINK ludwigcancerresearch.org atter of fat of atter undone duo eadly roundup News enriching or science model or ALS on taking or distinctions and Awards TABLE OF CONTENTS Required reading ascientist Ask with Weinberg Robert Q&A boost and Prime trials Clinical needs imple ectric discovery down slowing of advantage he alternatives ncogenic DC of tribes he predictionsmpowering lock link profile low eadly yperactive nuclear hoops strategy wo-hit signals tuning and esigning TDO racking ar-T revival malignant balance attack roader uppressor suppression For immunometabolic insight For miracles miniature scholar Ludwig aWelcoming distinguished A m D F F F S El T O T E C D H T D T C A A b S Microhelper

APRIL 2020 APRIL

2 2 1 1 1 1 1 1 1 13 16 1 1 1 1 1 1 1 4 4 8 5 0 0 7 7 4 4 4 2 9 9 8 8 3 6 6 6 5 5 5 5 7 7 7 7 1 1

LUDWIG LINK | APRIL 2020 Awards distinctions and Ludwig San Diego San Ludwig Don Cleveland Ludwig Lausanne Douglas Hanahan

FOR TAKING ON ALS SCHOLAR DISTINGUISHED LUDWIG A WELCOMING of other neurodegenerative disorders anumber and ALS of forms other for promise holds approach The trials. clinical in evaluated being already is intervention ASO and ALS, to inherited linked been have gene SOD1 to the mutations different 100 Over ALS. SOD1-mediated for approach atreatment as technology (ASO) development of antisense oligonucleotide and discovery their for research (ALS) innovation in amyotrophic sclerosis lateral for Prize International Center Healey inaugural the received colleagues and Cleveland Don Diego’s San Ludwig new to generate tumors by employed switch” “angiogenic the to identify models mouse these used also he Folkman, Judah response. with Collaborating the late system’s immune the and process that in of role the progression, cancer of stages the to investigate it used and cancer of models mouse transgenic first the of one developed he 80s, late the in Laboratory Harbor Spring Cold the of out Working immunology. and biology to cancer contributions landmark many made has Doug January. in Research Cancer for Institute Ludwig the of Branch Lausanne the at Scholar Distinguished Douglas Hanahan was appointed Ludwig 4 award ceremony.award here 6th. on December Australia Perth, in ALS/MND on Symposium International 30th the during award their received colleagues his and Don injury. brain temporal dementia chronic and traumatic disease,frontal Alzheimer’s including disorders, cognitive other in features that protein a tau, of identification the neurodegenerative diseases, including of biology molecular the on discoveries significant many made has Don well. as them. to disrupt strategies pharmacologic and progression tumor of drivers and stages the to explore continues laboratory His biology. cancer modern of publications influential most the among regarded widely is It progression. and initiation tumor understanding for framework conceptual aunifying to create research cancer basic of corners all from drew Cell in published and Weinberg Robert Co-director MIT Ludwig with ofCancer review Hallmarks The anti-angiogenic drugs. Doug’s seminal new of development to the led area this in work subsequent Their vessels. blood to see Don’s presentation at the the at presentation Don’s to see in 2000, 2000, in , authored Click Click

LUDWIG LINK | APRIL 2020 Awards distinctions and alter the behavior of immune cells like like cells immune of behavior the alter effects immunometabolomic how of contributions significant made has lab His patrols. it tissues the and system immune the between conversation a molecular mediate metabolism of byproducts and nutrients cellular how explores which immunometabolism, of field the in aleader is Ping-Chih Program. Young Investigator its in membership for (EMBO) Association Biology Molecular European the by selected was Member, Associate Ludwig appointed newly Ho, Ping-Chih Lausanne’s Ludwig IMMUNOMETABOLIC INSIGHT FOR laboratory Her cancer. including disease, treat and to diagnose materials other and nanoparticles designed have and health, human to improve manufacturing tools from the of world semiconductor miniaturization harness colleagues national academies. Sangeeta three to all elected to be person 25th the just her making Engineering, of and Science of Academies National the of amember already is She Medicine. of Academy National to the elected been has Bhatia Sangeeta MIT’s Ludwig MINIATUREFOR MIRACLES to our understanding and her her and Heidelberg, Germany. in Laboratory Biology Molecular European the at facilities to core access have responsible research practices, and and skills leadership in training receive will Ping-Chih program, the of part As excellence. scientific of record proven a have and leaders group as years four first their within are who 40 of age the under researchers are Investigators Young EMBO immunotherapy. for undone pharmacologically be might mechanisms escape those how and to cancer response Tcell the disrupt tumors, in macrophages achievement commitment and to service. professional outstanding demonstrated have who individuals recognizes and medicine and health of fields the in honors highest the of one considered is Medicine of Academy National to the develop these technologies. Election biotechnology companies to further several founded have trainees her and liver. the Sangeeta of diseases treat and to model microtissues synthetic fabricate also uses computer-chip technology to 5 Ludwig MIT Bhatia Sangeeta Ludwig Lausanne Ho Ping-Chih

LUDWIG LINK | APRIL 2020 Awards distinctions and Ludwig MSK Ludwig Alexander Rudensky Hopkins Johns Ludwig

from the molecular biology and genetics genetics and biology molecular the from Treg of cells, aspect every almost on touched has work His healing. wound in participate and autoimmunity prevent responses, immune control (Tregs), which Tcells regulatory of study the in leader recognized internationally an is Alexander contributions forAssociation of Immunologists, his American the by presented award, the received He Award. Career Meritorious Fisher AAI-Thermo the of recipient 2020 the is Rudensky Alexander MSK’s Ludwig ENRICHING IMMUNOLOGYFOR charting work subsequent His world. the around taught now is “Vogelgram,” the as known popularly ago, decades three progression he developed more than cancer of model multi-step The . treating and to diagnosing approaches sophisticated more for groundwork the laid which progression, and initiation cancer of drivers molecular and principles fundamental the illuminating work transformative his for Medal Stevenson Jessie 2020 the awarded was Vogelstein Ludwig Johns Hopkins Co-director Bert SCIENCE MODEL FOR to the field of immunology. immunology. of field to the 6 Honolulu, Hawaii. in award his receives he May,in when immunity adaptive in ofrestraint virtue The cancer. He will present a lecture titled of treatment and prevention the and diseases autoimmune for therapies of development the for promise significant hold discoveries Alexander’s tumors. of surveillance immune the thwarting in role acentral play they which biology—in to cancer relevance to their function and maintenance generation, their of medical sciences. the in research outstanding for years two every Sciences of Academy National the by awarded is Medal Kovalenko Stevenson Jessie The cancers. advanced treating for approaches therapeutic gene-based new and cancers of detection earlier the for methods diagnostic novel developing on focuses mainly lab his Today, research. cancer translational and basic of aspect every virtually on amark left has of scores in expressed genes of spectrum full the

LUDWIG LINK | APRIL 2020 A MATTER OF FAT DEADLY DUO UNDONE News roundup News kidney tumors plays a critical role in how how in role acritical plays tumors kidney surrounding tissue fat the that found and (RCC) carcinoma cell renal for surgery undergoing patients from purposes research for taken samples fat studied people undergoing treatment. The team benefit actually may obesity how on light Lancetin and MSK of Hakimi Ari by led and MSK at Center Ludwig the by supported Astudy weight. normal of those than disease the to survive likely more also are people obese cancer, kidney developing of risk the increases index body-mass high avery While cancer. kidney in aparadox of something is Obesity asymmetric organization of cells—during polarity—the cell of disruption in event key a is CagA and ASPP2 suppressor tumor the between interaction that found colleagues and Lu Xin Oxford’s , Ludwig of Sciences the paper aJanuary In not. do that strains with compared cancer stomach of risk the increase significantly CagA toxin the produce that pylori H. of Strains pylori). (H. pylori Helicobacter by infection an is cancer stomach for factor risk main The Proceedings of the National Academy in December shed shed December in published in in

as susceptible to immunotherapy. susceptible as tumors kidney flag might that biomarkers for looking and detected they response immune the exploring further now are colleagues his and Ari cells. immune relatively unpopulated with anti-cancer is, cold—that were they as response, immune an stimulating to be appear not did themselves tumors kidney the Yet, it. surprisingly, to attack tumor the of site to the cells immune draws this that and weight, normal of people in than inflamed more is people obese in fat the that found They works. atreatment well class of antimicrobial agents. anew represent might infection bacterial upon in host-cellchanges polarity prevent can that agents that suggest results The stomach. the from case this in cells, stem from derived cultures tissue three-dimensional self-organized tiny, are which organoids, in colonization bacterial reduces and polarity cell of loss blocks peptide aspecific or molecules interaction small using CagA–ASPP2 the with Interfering infection. pylori H. 7 Ludwig MSK Ludwig Ludwig Oxford Xin Lu Ari Hakimi

LUDWIG LINK | APRIL 2020 News roundup News Ludwig Harvard Peter Sorger Ludwig Harvard Rakesh Jain

PI3K pathway inhibitors. They found that that found They inhibitors. pathway PI3K of collection to adiverse cells TNBC of responses analyzed systematically Sorger Peter by led investigators Harvard Ludwig In a December paper aDecember In have been only moderately successful. therapies such But TNBCs. in overactive and mutated often are components whose inhibiting pathway, the PI3K signaling on focused have cancer deadly this for efforts development drug Many survival. overall low and relapse of rates high with (TNBC) are associated Current treatments for triple negative ATTACK BROADER A responses—to the regions around GBM immune anticancer of (MDSCs)—inhibitors cells suppressor myeloid-derived draw targets chemokine receptors, which checkpoint inhibitors. The approach to immune susceptible GBM to make strategy anew examined that December in ofSciences Academy National the a co-led Jain Rakesh Harvard’s Ludwig far. so not least at them, of one not (GBM) is multiforme cancer brain the But cancer. of types many treating in effective variously Immune checkpoint inhibitors are SUPPRESSION SUPPRESSOR study reported in the Proceedings the of in reported in Cell in Systems 8 , mTOR and PIKK inhibitors. mTOR PIKK and existing of combinations or Torin2 analogs of development the by therapeutically translated to be potential the have findings The inhibitors. pathway PI3K of class cytotoxic uniquely and distinct that Torin2 represents a mechanistically its demonstrate The researchers DNA. replicates cell cancer proliferating the when exposed vulnerabilities target to (PIKKs) kinases PI3K-like of variety a and pathways, signaling PI3K of hub mTOR, both acentral inhibits it because effective Torin2, unusually is drug, one immunotherapies for GBM. for immunotherapies to enhance cells myeloid expressing CCR2- of targeting support results The effects. similar had receptor the blocks CCR2, treatment with a molecule that expressing mice in that demonstrated checkpoint blockade. They also by induced responses to immune susceptible were themselves tumors the that and MDSCs lacked tumors GBM the around regions the that showed They 2(CCR2). receptor chemokine the lack and GBM to develop bred mice at looked initially team his and Rakesh tumors.

LUDWIG LINK | APRIL 2020 News roundup News to play a role in killer fitness—to fitness—to Tcell killer in arole to play known RNA noncoding regulatory small miR-155—a using of potential the on findings their reported Lausanne Ludwig of Romero Pedro by led investigators of ateam and Monnot Gwennaelle student TherapyMolecular Oncolytics paper aDecember In tumors. within environment the immunosuppressive by thwarted be can cells to cancer reactive highly are that Tcells even But culture. in expansion selective their after donors the into back infusion their and patients from Tcells of extraction the involve cancer for therapies cell Adoptive MICROHELPER and Peter susceptibility. cancer affect that sequences DNA in variations and HIF pathway the in involved elements DNA-binding between overlap the examined HIF. they response, particular, In hypoxic the of regulator akey of activation constitutive the by driven acancer (RCC), carcinoma cell clear renal in hypothesis this examined colleagues and Ratcliffe Peter Oxford’s Ludwig growth. tumor drive and to survive cell the allow others consequences are in harmony with that of only those altered pathways whose cells, cancer in accumulate alterations such as that suggests This question. in cell the for good them of all not effects, of avariety have can cells cancer in altered pathways biochemical The A MALIGNANT BALANCE , graduate , graduate in in patients. patients. by generated naturally Tcells anti-tumor reactive weakly of therapies such in use the expand further, and, therapies Tcell adoptive improve generally could suggest, they miR-155, of Overexpression Tcells. by recognized weakly antigen an express that tumors B16 of control the mice, in improves, and tumor the within functionality and fitness metabolic their bolsters cells T antigen-specific tumor in microRNA the of overexpression that showed They Tcells. transferred adoptively of functionality and persistence the improve pressures. and consequences of those selective nature the to identify attempts focus This, the researchers argue, should atumor. ultimately, and, cell cancer viable a to generate development cancer during pathways interacting of network avast of effects the balance pressures selective that implies This cancer. of emergence to the critical is pathways biochemical activated specific, of outputs multiple of modulation precise which in cancer, of model tuning” a“pathway support findings Their starvation. oxygen by activated—say, differently HIF is which in cancers other in and RCC in overlap that December their comparative analysis of published team his 9 in Scientific in Reports in in Ludwig Oxford Ratcliffe Peter Ludwig Lausanne Pedro Romero

LUDWIG LINK | APRIL 2020 News roundup News extending the lives of mice. of lives the extending further counterparts, ordinary their than cancer target better could CAR-T cells modified the that cancer, bone (solid) a even and leukemia, of models preclinical in demonstrated and activation, T-cell in involved aprotein c-Jun, to overexpress T-cells CAR engineered team The activity. T-cell of inhibition to the turn in led which cells, exhausted the in levels protein regulate that genes of aclass of activity the in imbalance an revealed This T cells. active and exhausted between genome the of activation the in differences Howard researchers Chang—the explored Professor Ludwig of laboratory the in technique ATAC-Seq—developed called a Using prevention. to its approach an exploration of the and phenomenon, their report Mackall Crystal Stanford’s Nature aDecember In activity. Tcell prolonged after in kicks naturally that exhaustion Tcell to the due often cancers, blood against even time some after wane can efficacy For its another, tumors. solid against effective to be shown been yet hasn’t it cancers, blood some against works it while thing, For one limitations. its have does it but wins, remarkable up racked has therapy T-cell CAR CAR-T REVIVAL paper , researchers led by Ludwig Ludwig by led , researchers Ludwig Stanford Howard Chang Ludwig Stanford Crystal Mackall Eynde den Van Benoît Ludwig Institute Ludwig 10

promise as a target for cancer therapy. cancer for atarget as promise some to hold appear does enzyme the case, either In vessels. blood feeding or theangiogenesis, generation of tumor- in as suppression immune in much so not involved to be seems TDO cancers, other many In cells. tumor in TDO expressed also cancers kidney of 10% and of 25% approximately that found They target. immunotherapeutic aprime be could it cancer—where liver primary of type common most carcinoma—the role in hepatocellular immunosuppressive an plays and cancers human of majority the by expressed is TDO that showed colleagues and Benoît biology. cancer in role TDO’s to explore antibody monoclonal TDO-specific anovel of use their reported Eynde den Van Benoît Ludwig’s by led Research Immunology Cancer in paper aDecember In system. immune the on effects its about other, or TDO, the of expression the about known is little But studied. exhaustively been has IDO, them, of one of expression The tryptophan. as known acid amino key a of them depriving by Tcells disable expressed by enzymes tumorsCertain TRACKING TDO , a team , ateam

LUDWIG LINK | APRIL 2020 TWO-HIT STRATEGYTWO-HIT SIGNALS TUNING AND DESIGNING News roundup News kills DMG cells, but the tumors tend to tend tumors the but cells, DMG kills panobinostat drug the that suggested these Previous incurable cancers. work treating for hope some offer could (amarizomib proteasome inhibitor)— and inhibitor) deacetylase (a histone combination—panobinostat drug a new reported preclinical results showing that colleagues and Monje Michelle researcher Translational Medicine paper aNovember In 4 to 12. of ages the between typically children, hundred afew in year every diagnosed others—are among glioma, cord spinal and (DIPG) pontine intrinsic glioma including (DMGs)— midline gliomas as diffuse known cancers brain childhood aggressive Highly abroad engineering by approach their of efficacy the proved colleagues his and Patrick allostery. via functions protein of re-purposing even and tuning accurate Biology Chemical Nature in December in Reported proteins. in functions allosteric such designing and predicting both for method acomputational developed have team his and Barth Patrick Lausanne’s Ludwig site to indirectly regulate its activity. active its than other site to aprotein bind molecules biological other and proteins which by amechanism is Allostery , their method , their permits the the permits , Ludwig Stanford Stanford , Ludwig in Science in marizomib alone. marizomib for and combination drug the for trial aclinical designing now are researchers The cells. cancer in only availability NAD affects selectively that away in synergize drugs two the cell, any of survival to the essential is NAD Though energetics. and metabolism cellular in role acentral plays which NAD, as known acompound make to ability cells’ cancer the with interfered also It samples. patient those from derived tumors with implanted mice in combination two-drug increased survival the that found and tumors patients’ from cultures cell in combinations 9,195 drug and compounds single 2,706 tested team The treatment. to the resistant become cell engineering. and biology synthetic in utility significant of to be likely is technology The serotonin. an entirely neurotransmitter, different to responsive was designed they D2 of variant One to GPCRs. mutations known 100 than more of effects signaling the predicted model Their designs. their in rate success 80% than agreater achieved and drugs antipsychotic of atarget is and cognition regulates which D2, receptor dopamine the of variants 36 made They (GPCRs). receptors Gprotein-coupled into functions signaling novel of spectrum 11 Ludwig Lausanne Barth Patrick Ludwig Stanford Monje Michelle

LUDWIG LINK | APRIL 2020 News roundup News across a large variety of cancers. In their their In cancers. of variety alarge across heterogeneity cellular and progression tumor in role akey plays ecDNA that uncovered the phenomenon and revealed lab Paul’s in work Previous cells. cancer in found exclusively almost are ecDNAs genes, growth-driving of copies multiple encode and chromosomes outside exist that DNA of Circles resistance. drug and heterogeneity growth, tumor drives (ecDNA) DNA extrachromosomal how into dive adeep took Chang Howard Stanford’s Ludwig with Ren Bing and Mischel A study HOOPS NUCLEAR HYPERACTIVE Diego San Ludwig Paul Mischel led by Ludwig San Diego’s Paul Paul Diego’s San Ludwig by led

Ludwig San Diego San Ludwig Ren Bing cancer therapy.cancer like threats and environments changing to nimbly more respond and quickly more evolve cells tumor helps turn in oncogenes of expression pitched The expression. of levels high extraordinarily to prone and accessible highly genes cancer-driving its makes that a manner in structured is it cores, protein around tightly wound is ecDNA though that Nature in reported They tools. analysis genomic of avariety using ecDNAs of patterns expression gene and structure molecular the between link the investigated team the study, recent most 12 Ludwig Stanford Howard Chang in November November in

LUDWIG LINK | APRIL 2020 News roundup News clock holds true in fruit flies as firmly firmly as flies fruit in true holds clock biological to the metabolism linking in role Myc’s that showed colleagues and Segal November, Chi, his Amita collaborator astudyIn cells. cancer of rhythms circadian the on impact aprofound has also and growth tumor to fuel metabolism cellular alters previously shown that Myc dysfunction have Dang Chi Van Director Scientific Ludwig by led Studies cancer. in genes overexpressed or otherwise dysregulated among the most frequently mutated, also is It to metabolism. essential expression gene the orchestrates broadly that aprotein encodes gene Myc The LINK CLOCK colorectal advanced that November in ofCancer ImmunoTherapy for Journal the They inhibitors. MEK or gamma could be reversed by treatment with IFN- resistance whether to determine sought also team her and Michal resistance. this for reason the to explore lab the in grown organoids, or tumors, derived patient- to small immunopeptidomics as known atechnology applied Sternberg Lausanne investigator Michal Bassani- Ludwig by part in led researchers of Ateam immunotherapies. to these resistant highly proved have most inhibitors, to checkpoint briskly respond DNA mutated highly have that cancers colorectal of subset asmall Although DEADLY LOW PROFILE in in Reports Cell in published reported in in and the circadian clock. circadian the and metabolism linking in role Myc’s of roots evolutionary deep the expose findings The activity. dMyc suppresses which dMnt, as known aprotein of loss the by reversed be could these but behaviors, circadian drosophila influenced similarly activity cwo rhythms— in circadian involved genes of expression heightened the by accompanied was disruption latter The well. as behavior circadian their but flies, fruit of metabolism the only not disrupted (dMyc) significantly protein ofOverexpression the cancers. their and humans in does it as organoids. the in improved the presentation of neoepitopes inhibitors MEK nor IFN-gamma Neither predicted by computational methods. number the of afraction detected—just were neoantigens three Only neoantigen. a generate potentially could that mutations gene 612 contained together which samples, patient from grown mini-tumors five at looked researchers The CRCs. advanced of majority the in well worked not have attack aTcell stimulate that immunotherapies why explain helps This surface. their Tcells—on patrolling by detected fragments protein mutated neoantigens— few very display cancers . Mutations that dialed down Myc Myc down dialed that . Mutations 13 Drosophila and and cry tim, cyc, Myc Myc Ludwig Lausanne Michal Bassani-Sternberg Ludwig Institute Ludwig Dang Van Chi

LUDWIG LINK | APRIL 2020 News roundup News the amino acid sequences of more than than more of sequences acid amino the determined and spectrometry mass their model, the researchers applied To Tcells. develop to helper presented to be likely cancer of signs molecular the to identify method accurate more and anew reported Gfeller David and Bassani-Sternberg Michal Racle, Julien researchers Lausanne Ludwig October paper an In vaccines. cancer by responses immune anti-tumor therapeutic of elicitation to the essential to be studies recent in shown been have and responses immune adaptive orchestrating in role acentral play Tcells Helper PREDICTIONS EMPOWERING Ludwig Lausanne Julien Racle

in Nature Biotechnology in Ludwig Lausanne Michal Bassani-Sternberg , for cancer. for immunotherapies develop individualized to efforts Lausanne’s Ludwig in employed being is and techniques previous as good as twice least at is method their of power predictive The pathogens. and tumors of avariety from peptides of capability to predict the HLA-II presentation algorithm an to train used were results The motifs. binding consensus HLA-II defined accurately deconvolution), motif (for MoDec called learning, machine on based tool computational novel their data, this With tissues. and cells from eluted peptides binding HLA-II 99,000

14 Ludwig Lausanne David Gfeller

LUDWIG LINK | APRIL 2020 News roundup News the design of new immunotherapies. to adoor opens work The patients. from taken tumors melanoma in out hiding cells cDC2A found researchers the possibility, this of support In cells. cancer targeting be could cDC2B while growth, tumor nurturing be could example, for cells, cancer—cDC2A of development the in roles opposing play could clans cDC2 two the that suggest findings The divisions. same these shared cells cDC2 human that found team his and Alexander responses. cell T inflammatory to direct tends latter concerned with wound-healing; the primarily and anti-inflammatory seems former The B. and cDC2A named now clans, distinct two of consists tribe DC this that found and mice from cells cDC2 individual of thousands in expression gene profiled team his and Alexander that. Cell in published and Rudensky Alexander Director MSK Astudy understood. well less were cells cDC2 But responses. Tcell killer to provoke known are and characterized well been have uniform, to be appear cells cDC1 responses. cell T distinct of priming their and markers molecular on based cDC2, and cDC1 tribes, two into divided been traditionally have They cells. cancerous or pathogens to system immune adaptive the alert and body the (DCs) patrol cells Dendritic THE TRIBES OF DC in October just changed changed just October in led by Ludwig Ludwig by led Ludwig MSK Ludwig Alexander Rudensky Bradley Bernstein Ludwig Harvard Ludwig Harvard George Demetri 15

Nature work The sunitinib. called GIST for therapy inhibitor kinase astandard with combination in or alone either inhibitors, receptor FGF with xenografts in mice could be suppressed patient-derived as GISTs growing human that demonstrated They patients. GIST of majority the in mutations somatic by activated is that gene KIT the and on-switch an between contacts aberrant causes similarly epigenetic abnormality researchers also showed how another The expression. gene for switch “on” an as serves that DNA of astretch contacting FGF4, from gene, factor growth promoting acancer- prevents that (an insulator) an element structure of chromosomal dismantles abnormality epigenetic An cancers. GISTs of other and development leadsequences to themselves—can the gene the in abnormalities not read, are genes how alter that packaging protein its and DNA to modifications changes—chemical epigenetic how reveal findings Their treated. be might they how studies, preclinical in shown, and cancers these drives what identified have Bernstein Bradley investigator and Demetri George Co-director Harvard genome. Researchers led by Ludwig their in mutations driver no have tumors such of to 20% 10% But growth. their driving enzymes mutated the target that to therapies respond cancer, tissue connective (GISTs), of atype Most gastrointestinal stromal tumors ALTERNATIVES ONCOGENIC . was published in October in in October in published was

LUDWIG LINK | APRIL 2020 News roundup News glioma (DIPG), among others. Michelle and and Michelle others. among (DIPG), glioma pontine intrinsic diffuse , pediatric aggressive highly the and tumor, brain adult common most the High-grade gliomas include glioblastoma, impulses. amplify and transmit help which junctions, gap as known connections electrical cell-to-cell contain also tumors brain the within cells cancer the of many Nature in September in Reported growth. own their to drive neurons healthy from signals electrical tap neurons—and with connections synapses—or form gliomas high-grade as known tumors brain that discovered has Stanford at Center Ludwig the of Monje Michelle by led A team DISCOVERY ELECTRIC 80s. and 20s their in patients 300 than other medical procedures from more and biopsies during collected tissues self-renewing healthy, of samples in cell replication rates analyzed colleagues their and Bert Cristian, old. very the in the accumulation of mutations slows indicated that data of areview from came study the for clue Amajor 80. of age the over people in declines then but 65 of age the after precipitously climbs incidence cancer why exploring astudy led Tomasetti Cristian colleague VogelsteinBert and and Johns Hopkins Ludwig Johns Hopkins Co-director THE ADVANTAGE OF SLOWING DOWN , the study , the further revealed that that revealed further help people with HGGs. could tumors within signaling electrical blocking whether investigating is team The mice. in gliomas human of growth the reduced greatly drug anti-epilepsy existing an with signals these interrupting seizures. Experiments demonstrated that suffer patients HGG many why explain could which hyperexcitable, to be tend tumors near neurons healthy that noticed also researchers The growth. their accelerated tumors into signals electrical Boosting junctions. gap via amplified are that currents potassium-evoked prolonged exhibit 40% about and signals, synaptic receive tumor each within cells glioma of 5-10% that showed team her aging and cancer. stem relationship cells, normal between the understanding for implications significant have results These incidence. cancer in decline asimilar experience not do which mice, in seen not was slowdown Aparallel nose. the near found tissue in 83% by and duodenum the in 26% by 25%, about by slowed rate division the tissue, esophageal In 20s. their in those with compared 80s their in people from samples tissue colon in 40% by slowed rates division cell that of Sciences Academy National ofthe Proceedings the paper aSeptember in reported They 16 in in Ludwig Johns Hopkins Johns Ludwig Bert Vogelstein Ludwig Stanford Monje Michelle

LUDWIG LINK | APRIL 2020 News roundup News depletion too aids immune escape. immune aids too depletion whether tumor-mediated alanine seen to be remains It surveillance. immune to suppress glucose, like nutrients, vital many of T cells to deprive known Tumors are purposes. metabolic other for down broken being than rather synthesis protein toward directed quickly is Tcells by in brought alanine the all that revealed tracing pools. Radioisotope nutrient extracellular from acid amino the to import obliged thus are and biosynthesis to alanine essential enzyme an of levels low produce which Tcells, by not cells—but most by easily rather manufactured is This acid amino acid,amino alanine. asimple of import the on dependent is Tcells, memory of reactivation the and Tcells, naïve of activation the that found Reports Cell in September in published astudy In transition. state cell this promoting for necessary is that acid amino new a identified now has colleagues their and Sharpe Arlene Haigis, Marcia Harvard’s Ludwig by effort Acollaborative glutamine. acid amino the and glucose including nutrients, several of availability the on depends and taxing metabolically be can process The one. active an into state aquiescent from switch they cell, cancer a or apathogen detect Tcells When NEEDS SIMPLE , Marcia’s team team , Marcia’s

Ludwig Harvard Arlene Sharpe Ludwig Harvard Marcia Haigis 17

across multiple clinical sites in the UK. the in sites clinical multiple across year this later to begin slated is trial The benefit. of likelihood the to maximize NY-ESO-1 and MAGE-A3 of expression tumors’ their for screened be will Patients NSCLC. with patients 80 approximately in response immune anti-cancer effective and asafe to provoke ability its assess and immunotherapy anti-PD-1 and chemotherapy first-line standard with combination in vaccine the test will CRUK by managed and sponsored trial I/IIa Phase The cells. cancer on attack a Tcell boost then and prime to first designed is platform delivery aVaccitech ESO-1—on NY- and scientists—MAGE-A3 Ludwig by discovered antigens two carrying vaccine, The 17%. is cancer lung for rate survival 5-year overall the as needed, urgently are treatments New NSCLC. to be expected are cases those of 85% approximately and US the in deaths 142,670 for accounted cancer lung 2019, In (NSCLC). cancer lung cell non-small with patients for option atreatment as immunotherapy VOLT’s VTP-600 (CRUK) to develop UK Research Cancer with partnership aclinical into entered Vaccitech, biotech the and Research Cancer for Institute Ludwig the of collaboration strategic a (VOLT), Limited Oncology Vaccitech PRIME AND BOOST AND PRIME Clinical trials Clinical

LUDWIG LINK | APRIL 2020 FOR ONCOLOGY MOLECULAR AT MIT DIRECTOR OF THE LUDWIG CENTER WEINBERG ROBERT Q&A 18 question. particular that on energy of alot focusing been has group lab my and obscure, a bit still is it do they How succeed. rarely only and challenge adifficult face They living? a make how to out figure tissue, distant a in land and tumor aprimary leave they once cells, cancer disseminated do How research? lab’s your drive questions central What arise. cancers human how of principles mechanistic basic the to understand Trying atweet? in research your summarize you would How

LUDWIG LINK | APRIL 2020 that, in turn, provokes these cells to begin to begin cells these provokes turn, in that, them around environment tissue inflamed an create increasingly cells carcinoma the when happens that accident an is body the in sites to distant site tumor primary a from cells cancer of dissemination To metastatic mind, my spreading? on intent they is—are question the body, the in sites different in begin tumors When bigger? get and grow they as put to stay content just tumors malignant aren’t Why cells. altered genetically of growth the forward to push genes suppressor tumor inactivated or oncogenes activated allowed that mechanisms the to reveal order in developing rapidly then were that biology molecular of tools the use really could one that proof direct no was there is, that speculation, of matters simply were mechanisms these then Until genes. or oncogenes inactive tumor suppressor hyperactive either of actions the through pathogenesis cancer human understand principle, in could, one how for blueprint, or atemplate, out laid discoveries two These Bernards. René and Friend Stephen post-docs of to work thanks lap my into fell it since run,” unearned “an was 1986 in Rb gene suppressor tumor first the of discovery However, subsequent the identifying, isolating and cloning it. in involved work the of because run” earned “an as discovery to this to refer like I 1979. in Ras cellular first the of discovery to the led which 1977, in oncogenes viral studying We began suppressor gene? tumor first the and gene causing cancer- human first the of discoveries your of impact greatest the was What Q&A

playing hooky one afternoon from a one afternoon hooky playing Iwere and Hanahan Doug accident. an was ofCancer Hallmarks The Writing come about? Cancer of Hallmarks The of writing the did How malignancies. high-grade of cells cancer to the ascribe we that attributes the of all virtually cells to carcinoma mesenchymal transition—that imparts EMT—epithelial-to- the called often the program complex cell-biological understanding of context the in solved basically is carcinomas, of case the in least at tissue, to adistant tumor primary a from move cells cancer mechanistically how of question the contrast, In unsolved. essentially is that problem this of aspect one remains That tissues. distant these in aliving to make going are they how of problem the confront they there, are they Once tissues. to distant physically to disseminate ultimately and to invade improvements in the we way treat cancer. preventing that are profound obstacles the how all know to through break really We don’t mud. in stuck the is a whole I think bit as a the field 19

LUDWIG LINK | APRIL 2020 Q&A cancer research to be just a collection of of acollection just to be research cancer perceived we indeed, And phenomena. of kinds all to explain principles fundamental of powers the in faith great had we so education, MIT an of products I were and he Both conceptualized. clearly not and messy quite were biology cancer of laws the physics, of laws the unlike that, fact the about to talk began we when avolcano of mouth the down walking were we and Hawaii, in conference 20 . I knew him when he when him Iknew Baltimore. David was career my during most the me supported who person the Arguably supported you throughout your career? have who mentors the of some are Who cells. cancer of genomes the sequencing by understood be cannot that consequence of cell-biological programs the largely is after comes that spread metastatic the whereas cells, cancer of genomes the strike that mutations genetic of responsibility the largely is tumor primary the of formation the that argued often I’ve because thinking, my influenced strongly has dichotomy That responsible for its metastatic spread? are mechanisms or principles what other, the On tumor? aprimary forming cells the of creation for responsible principles the are what hand, one the On progression. cancer about thinking my in adichotomy to create able I was research? personal own your influence Cancer of Hallmarks The did How principles. mechanistic underlying of number small a relatively of terms in cancer of complexities the to understand people allowing in helpful very to be out turned it astonishment, total indeed surprise, our of Cell issue first the in appeared It pond. aquiet into thrown astone like sink would it reviews, most like that, expecting fully 1999 in review the We wrote tumors. of kinds different between comparisons to undertake principles that might enable people underlying of aset articulate could we whether to discuss We began phenomena. in January 2000. To 2000. January in

LUDWIG LINK | APRIL 2020 regard that as a failure on my part. part. my on afailure as that regard I so, doing in unsuccessful are they If lab. my left have they after careers research independent own their launch and feet two own their on to stand able be should lab the through pass who trainees the that is lab my of goal stated explicitly the case, own my In investigators. independent as to thrive how learn and conducted is research cancer how to see achance have people young where meetings of a series greater in organizing community the in and MIT at both active very been also Ihave lab. my in people the mentoring in active very been actually I’ve decades four or three for so, And forward. to move ensure that research cancer continues what They’re work. our from produce we that results the as important as are lab my in mentorship and training that required to teach. on, Early I realized is department biology the in member At faculty MIT, every research. doing as important as are mentoring Teaching and generation of scientists? next the support and mentor you do How him. from inspiration and support continuing Ihad that fact to the due is Iam what of much respects, many in So, board. on me brought 1982 in and Institute Whitehead the of director founding the was David member. faculty ajunior as me to hire Research, Cancer for Center MIT the of director first and founder the was who Luria, Salvador of ear the in whispered who he was It 1970-71. in Institute Salk the at apostdoc get Icould that so connections necessary the make helped who he was it and 1963-64, was a graduate student at MIT in MIT at student agraduate was Q&A

the behavior of the genetic alterations alterations genetic the of behavior the to integrate how is second The skeptical. very Iremain but problem, entire the solve will intelligence artificial and bioinformatics that claim Many them. from lessons take-home biological simple some glean and sets data complex analyze how to is first The horizon. the on challenges big two I envision field? research cancer the facing challenges greatest the are What resentment.” and envy breeds “success people, my told often I’ve as because, aggrandizing self- too to be not tried I’ve mind. my of front the at much very remained has advice door. That your on knocking come would shirts brown the in guys the night one visible, too or successful too were you if where, 1930s the in Germany fled having his from stemmed This visible. too be don’t but successful, to be right all occasions—it’s of anumber on me to said who father my from came It amentor? from received ever have you advice of piece best the is What research funding. of plight the bewails that one than rather message apositive of more it’s say would I So, most. doing enjoy they what and at best they’re what out to figure them tuned-up,brain. Once it’s I encourage their to tune-up is mentor their as job only my that them Itell law, the or pharma big biotech, academia, into go they Whether incareer science? a to pursue trainees your encourage you do how scientists, for challenging more is funding where climate, this In 21

work. from our produce that we results the as important as are lab mentorship in my and that training on, Irealized Early

LUDWIG LINK | APRIL 2020 Q&A preventing profound improvements in the the in improvements profound preventing are that obstacles the all through break to how know really We don’t mud. the in stuck bit is a whole as a field the I think today? research cancer in opportunities greatest the are think you do What of research. cancer success future to the critical is problems cell. Understanding and solving those two cancer the of phenotype biological final the create to ultimately another one with interact programs epigenetic the and changes genetic the how about picture clear avery have We don’t cell. particular that in transcribed being are that genes of with the transcriptomes—the repertoire genomes cell cancer the in ensconced 22 overshadow any other human problem. problem. human other any overshadow humanity. and breadth gravity It’s of all threatens that challenge greatest the It’s change. Climate solve? to choose you would what cancer, than other problem world any to eradicate power the and resources the had you If cells. carcinoma undifferentiated tumor-initiating or differentiating aggressive, eradicating by state aggressive a less into cells carcinoma aggressive switch to able being fourth, and, them hit to selectively order in cells cancer of aberrations metabolic the into insights our to harness how Third, applicability. quite limited in terms of its widespread is present at which immunotherapy, checkpoint of efficacy the potentiate to how Second, combination. in treatments existing various the to use how is First opportunity. of areas four about optimistic I’m cancer patients?cancer for promise greatest the hold that research cancer of areas the are What tumors. human solid of series awhole treat to successfully applicable widely be can it that so immunotherapy checkpoint of efficacy the to improve is opportunity greatest the that argue Iwould So, that. to do how know really don’t we present, At tumors. of kinds most in work it make how to out figure could we only represent an enormous opportunity, if might it and attractive, very seems Immunotherapy cancer. treat we way

LUDWIG LINK | APRIL 2020 a sense of humor. If a person wasn’t too too wasn’t aperson humor. If of a sense secondly, and, intelligence firstly, were, aperson in most valued grandparents and parents my characteristics the that clear was it refugees, European of afamily in up Growing up? espoused in your household growing were that values the were What cell. acancer into cell anormal convert could that information genetic carried actually cell transformed chemically a of DNA the that demonstrated paper 1979 The of? proud most you are what career, on your reflect you When ofAccidents. Concatenation AWhole Another: After Step One be? it would what life, your of story the of title the write could you If the bunker. Berlin in suicide committed Hitler moment The witnessed? to have liked most have you would history in moment What to. aspired I’ve agoal been always has Nathan Dan For emulating me, effacing. self- and humble extraordinarily was who someone yet and intellect great success, great of aman was He Hopkins. Johns at Nathan Dan Laureate Nobel The that you admire most? dead or living scientists the are Who grandchildren. and children our for consequences catastrophic be will there successfully, problem this to address fail we If Q&A

in which we we which in

workers are doing. are workers the what study Ican so stop family my that Iinsist site, aconstruction by go we To day, when this structures. complex of design the and connected get things how by fascinated endlessly I’m and a beam, to ajoist to attach Iuse will bolt size what like problems simple to ponder Ilike lab, the of Outside things. repairing relish and gardener afanatic I’m summer, the In aporch. and wings more two added years the over and Hampshire New in cabin our Ibuilt and wife my 1976, in Starting hands. my with working about satisfying very something is There A carpenter. taken? have might you think you do paths career other what researcher, acancer become not had you If beings. human other valued they how of terms in success material or financial mentioning their recall Iever do Never humor! of sense agood had they if it for up make could person that bright, how to dothat. know really At of present, we tumors. don’t kinds how out most in makeit figure to work we could only if opportunity, enormous might an represent it and attractive, very seems Immunotherapy 23

LUDWIG LINK | APRIL 2020 Ask a scientist a Ask from amentor? What is the piece best ofWhat you advice ever received Ludwig Diego San DAVIS ROBERT . at again back and settings, to industrial academic from work, my influenced always tractable. That advice has experimentally were questions important as long so next, on Iworked problem particular it really didn’t matter what that me told Weintraub, Hal research, my thesis advisor, graduate finishing Iwas As Oxford Ludwig PEDRO MOURA-ALVES to knowledge. advance to take these results positively able be will you controls, right the do you as long as ideas, your with flexible more be can you However, if hypothesis. original your against go that “negative so-called results” with struggling spent be will days your of 90% research, In

24 Ludwig Lausanne CRIBIOLI ELISABETTA personal and unique. into something it transform and others from get you inspiration to apply the and knowledge means ascientist Being others. with it compare to not and scientist as a path own my find to was amentor from received Ihave advice of piece best The Ludwig Wistar BROOKS REBEKAH this delays the inevitable. ultimately but question, your that may not directly answer experiments easier on time to spend tempted be might You hypothesis. your disprove definitively will that experiment the challenging Prioritize

LUDWIG LINK | APRIL 2020 Required reading PK. Sorger NS, Gray JM, Asara C, Yapp JY, Chen Q, Liu SC, Sivakumaren C, Mills M, Chung M, Niepel A, Palmer A, Jenney SS, Chopra cells. cancer breast triple-negative PI3K-activated of death cause to vulnerabilities checkpoint and replication exploits Torin2 print] of ahead [Epub 2019 December 2 Cell Systems JK. Harrison DA, Mitchell RK, Jain M, TJ, Datta Schall R, IF, Singh Charo JJ, Campbell MR, Sarkisian A, Gopinath D, Luo JA, Flores-Toro murine gliomas. resistant of progression slow to effect inhibitor checkpoint a unmasks and cells myeloid CCR2 inhibition reduces tumor print] of ahead [Epub 26 December 2019 Academy of Sciences USA National the of Proceedings Ludwig Harvard BJ. Eynde den Van E, Marbaix BJ. Eynde den Van E, Marbaix J, Lelotte N, Baren van JC, Renauld Solvay M, S, Klaessens Letellier MC, A, Daumerie C, V, Bouzin Stroobant T, Dvorakova D, Hoffmann most cancers. of pericytes intratumoral in and hepatocellular carcinoma cells human in identified expression Tryptophan 2,3-dioxygenase print] of ahead [Epub 5 December 2019 Cancer Immunology Research Ludwig

Dang CV. Dang A, Sehgal RN, Eisenman AM, Weljie R, Brooks SD, Rhoades A, Mancuso ZE, Stine Z, Yue X, Zheng AL, Hsieh metabolism. and behavior circadian disrupts Myc Drosophila of Misregulation 2019 November 12 Reports Cell Institute Ludwig Rabinowitz JD, Haigis MC. Rabinowitz JD, Haigis MC. AH, Y, Sharpe MW, Tsubosaka LaFleur G, Notarangelo JM, Ron-Harel N, Ghergurovich extracellular alanine. on depends activation T cell 2019 September 17 Reports Cell BE. Bernstein GD, BE. Bernstein GD, JL, ET,Hornick Sicinska Demetri PC, Gokhale BK, CP, Eschle Raut NM, Javed SJ, Shareef E, Hegazi DR, Tarjan ML, Hemming SE, Y, Johnstone Drier WA, Flavahan GISTs. SDH-deficient in programs oncogenic drives Altered chromosomal topology print] of ahead [Epub 2019 October 16 Nature

25 Vogelstein B. Vogelstein CA, RH, Iacobuzio-Donahue Hruban AK, Meeker CM, Heaphy A, Kim B, Karim A, Baras A, Rizzo MC, Haffner ME, Jr, NR Pittman London NJ, J, Roberts Poling C, Tomasetti cancer incidence. dependent deceleration in age- the for explanation apotential providing age, with decrease rates division Cell print] of ahead [Epub 23 Sep 2019 Academy of Sciences USA National the of Proceedings Ludwig Johns Hopkins Romero P. A, Donda G, Coukos M, Irving P-C, Ho W-C, SF, Cheng Lopes E, Lanitis A, Martinez-Usatorre GC, Monnot antigen. tumor affinity tumour activity against low anti- improves Tcells CD8+ OT-1 in overexpression MIR-155 2019 December 24 Molecular Therapy Oncolytics P. Barth D, Keri KM, Chen allosteric signal transductions. receptor protein-coupled G of design Computational print] of ahead [Epub 2019 December 2 Nature Chemical Biology Ludwig Lausanne

Gfeller D. Jandus C, Bassani-Sternberg M, A, Harari G, P, Coukos Guillaume C, Chong S, Bobisse M, Arnaud GA, J, Rockinger J, Michaux Racle immunopeptidomes. of deconvolution motif deep by epitopes II class HLA of prediction Robust print] of ahead [Epub 2019 October 14 Nature Biotechnology M, Gerlinger M. Bassani-Sternberg D, Cunningham N, Starling D, J, Gfeller Racle G, Coukos I, Chau D, Watkins S, Rao N, Matthews LJ, Journal of Motzer R, Voss MH, Hakimi AA. Hakimi MH, Voss R, Motzer TA, Chan AJ, Dannenberg CH, Liu P, J, Russo Coleman P, R, Mano Patel A, Reising S, Petruzella I, Ostrovnaya S, Y, Ged Patil L, Vuong F, Kuo H, Furberg A, Sanchez carcinoma: a cohort study. cell renal cell clear with patients in paradox obesity the to related Transcriptomic signatures print] of ahead [Epub 2019 December 20 Oncology Lancet MSK Ludwig Barber G, Spain M, Semiannikova A, Woolston BJ, Stevenson HS, Pak J, Michaux B, Griffiths A, Newey treatment. interferon or MEK-inhibitor increase in neoantigens with no and landscape neoantigen I class HLA asparse reveals organoids Immunopeptidomics of 2019 November 18 ImmunoTherapy Cancer

LUDWIG LINK | APRIL 2020 Required reading Chanock S, Ratcliffe PJ, Mole DR. PJ, Mole Ratcliffe S, Chanock H, Choudhry L, Colli R, Salama R, Li O, Lombardi VN, V, Lafleur Schmid cancer. of model tuning apathway supports with HIF cis-acting sequences polymorphisms susceptibility ofCo-incidence RCC- 2019 December 10 Scientific Reports X. Lu D, Ebner C, Royer B, Sgromo RP, Owen RC, Brewer TM, Leissing D, Sangberg C, Ruiz-Puig L, Buti organoids. gastric H. pylori colonization of human favors and polarity cell of loss mediates complex CagA-ASPP2 print] of ahead [Epub 21 2020 January Academy of Sciences USA National the of Proceedings Oxford Ludwig AY. Rudensky D, Pe’er C, Leslie C, Ariyan L, Mazutis R, Fromme A, VP, Mendoza Lavallée D, Y, Deep Pritykin H, Gudjonson CC, Brown heterogeneity. cell dendritic human and Transcriptional basis of mouse print] of ahead [Epub 2019 October 24 Cell

Mackall CL. Mackall HY, Chang M, Monje AT, SR, Quake Satpathy R, Majzner CFA, Bourcy J, de Granja S, V, Nagaraja Tieu R, J, Jones Lattin H, Anbunathan P, Xu Z, D, Good Gennert E, Sotillo EW, Weber RC, Lynn resistance. exhaustion induces T cells CAR in overexpression c-Jun print] of ahead [Epub 2019 December 4 Nature Stanford Ludwig PS. V, Mischel Bafna HY, B, Ren Chang FB, Furnari M, Hu RGW, Verhaak JA, Law H, Yu Kim M, J, R, Ye Hu Z, Houston A, Abnousi C, Coruh X, Chen JM, Granja MR, Corces N, W, Jameson Zhang B, Y, Li U, Diao J, Rajkumar Luebeck J, Santini M, Erb R, Raviram N, Nguyen KM, Turner S, Wu oncogene expression. high and chromatin accessible promotes ecDNA Circular print] of ahead [Epub 2019 November 20 Nature Diego San Ludwig

26 Malenka RC, Monje M. Monje RC, Malenka ML, Suvà DE, Bergles S, Jumper Hervey- H, Vogel D, Brang A, Regev A, Agarwal KR, PJ, Taylor Woo L, Ni A, Ponnuswami C, Espenel Tam M, LT, Arzt SM, Gillespie D, Silverbush AC, Geraghty Venkatesh HS, Morishita W, circuits. neural into glioma of integration synaptic and Electrical print] of ahead [Epub 2019 September 18 Nature M. Monje CJ, Thomas KE, Andreasson KI, NA, Vitanza Warren L, Ni AC, Geraghty R, Ghanem L, Chen EH, Raabe P, Z, Itkin Minhas C, McKnight S, Michael C, Thomas Klumpp- M, Ferrer P, R, Shinn Guha AM, DY, Michalowski Duveau SM, Gillespie M, PJ, Quezada Morris S, J, Nagaraja Lennon X, EY, Zhang Qin S, PJ, Kreimer Woo BZ, Stanton M, Ceribelli KM, Wilson GL, Lin drug screening. high-throughput combination from glioma midline diffuse Therapeutic strategies for 2019 November 20 Medicine Translational Science

LUDWIG LINK | APRIL 2020 27

LUDWIG LINK | APRIL 2020 LUDWIGCANCERRESEARCH.ORG