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Biological aging is associated with progressive damage accumulation, loss of organ reserves, and systemic inflammation ('inflammaging'), which predispose for a wide spectrum of chronic diseases, including several types of cancer. In contrast, aerobic exercise training (AET) reduces inflammation, lowers all-cause mortality, and enhances both health and lifespan. In this study, we examined the benefits of early-onset, lifelong AET on predictors of health, inflammation, and cancer incidence in a naturally aging mouse model (C57BL/J6). Lifelong, voluntary wheel-running (O-AET; 26-month-old) prevented age-related declines in aerobic fitness and motor coordination vs. age-matched, sedentary controls (O-SED). AET also provided partial protection against sarcopenia, dynapenia, testicular atrophy, and overall organ pathology, hence augmenting the 'physiologic reserve' of lifelong runners. Systemic inflammation, as evidenced by a chronic elevation in 17 of 18 pro- and anti-inflammatory cytokines and chemokines (P < 0.05 O-SED vs. 2-month-old Y-CON), was potently mitigated by lifelong AET (P < 0.05 O-AET vs. O-SED), including master regulators of the cytokine cascade and cancer progression (IL-1β, TNF-α, and IL-6). In addition, circulating SPARC, previously known to be upregulated in metabolic disease, was elevated in old, sedentary mice, but was normalized to young control levels in lifelong runners. Remarkably, malignant tumours were also completely absent in the O-AET group, whereas they were present in the brain (pituitary), liver, spleen, and intestines of sedentary mice. Collectively, our results indicate that early-onset, lifelong running dampens inflammaging, protects against multiple cancer types, and extends healthspan of naturally-aged mice.

BackgroundThe COVID-19 pandemic disrupted healthcare delivery worldwide, beginning in early 2020. While cardiac non-invasive testing (NIT) plays a critical role in the evaluation and management of cardiovascular disease, the population-level association of pandemic-related public health measures on cardiac diagnostics remains unclear.ObjectiveTo compare the rates and patterns of cardiac NIT before and after the implementation of the first and subsequent provincial COVID-19 lockdown measures.Design and settingA population-based and registry-based retrospective time series analysis conducted in Ontario, Canada, a single-payer healthcare system.ParticipantsAll individuals receiving transthoracic echocardiography, stress echocardiography, nuclear imaging, cardiac CT or cardiac MRI between 17 March 2018 and 16 March 2022.Outcome measuresStandardised weekly testing rates compared across pre-pandemic and pandemic intervals using ARIMA (autoregressive integrative moving average) modelling.ResultsAmong 5 269 897 cardiac tests performed, the cumulative rates decreased from 228.8 (95% CI 228.5 to 229.0) tests per 100 000 person-weeks in the pre-pandemic period to 204.3 (95% CI 204.0 to 204.5) tests per 100 000 person-weeks in the pandemic period (p<0.0001). The first lockdown led to the most significant decrease in cumulative testing rate (105.9 per 100 000 person-weeks, 95% CI 105.4 to 106.4, p<0.0001), with an incomplete recovery over time that varied based partially on NIT modality. Outpatient testing decreased more compared with inpatient testing. The rates of transthoracic echocardiography and nuclear imaging decreased, whereas cardiac MRI remained stable and cardiac CT increased.ConclusionsDuring the COVID-19 pandemic in Ontario, cumulative cardiac NIT rates declined significantly and did not fully recover by early 2022. The magnitude and patterns of these declines raise concerns about delayed cardiovascular diagnoses while also signalling a possible shift in diagnostic strategies. Efforts should prioritise preserving access to essential diagnostic testing during future health crises.

PurposeTo compare the imaging characteristics of intra-arterial cone-beam computed tomography during hepatic arteriography (CBCTHA) versus intra-arterial computed tomography during hepatic arteriography (CTHA) for intraprocedural transarterial chemoembolization (TACE) planning.Materials and MethodsThis single-institution retrospective study included 144 patients (96 men, mean age 67.9 years; 48 women, mean age 62.3 years) who underwent 181 TACE sessions between January 2015 and July 2017. Intraprocedural CBCTHA (111 procedures) or CTHA (70 procedures) was performed for TACE planning. Reformatted maximum intensity projection CBCTHA and CTHA images were reviewed by two radiologists and classified using an ordinal scoring system (for tumor identification, tumor feeder vessel identification, and streaking artifact) and a binary scoring system (for the presence of breathing motion artifact and field of view encompassing the entire liver). Data were analyzed using an F test and a z-score test.ResultsThere were no significant differences in demographic and tumor characteristics between the CBCTHA and CTHA patient cohorts. CTHA was superior to CBCTHA for tumor identification (P < .0001), tumor feeder vessel identification (P < .05), streaking artifact (P < .0001), and field of view encompassing the entire liver (P < .0001). There was a trend toward a lower frequency of breathing motion artifact with CTHA than with CBCTHA (1.4% vs. 10%; P = .057).ConclusionCTHA provides improved clinical relevant imaging information compared to CBCTHA for intraprocedural TACE planning.Level of EvidenceLevel III, retrospective comparative study.

Background To evaluate the feasibility of a novel approach for predicting hepatocellular carcinoma (HCC) response to drug-eluting beads transarterial chemoembolization (DEB-TACE) using computed tomography hepatic arteriography enhancement mapping (CTHA-EM) method. Methods This three-institution retrospective study included 29 patients with 46 HCCs treated with DEB-TACE between 2017 and 2020. Pre- and posttreatment CTHA-EM images were generated using a prototype deformable registration and subtraction software. Relative tumor enhancement ( T Post/pre-RE ) defined as the ratio of tumor enhancement to normal liver tissue was calculated to categorize tumor response as residual ( T Post-RE > 1) versus non-residual ( T Post-RE ≤ 1) enhancement, which was blinded compared to the response assessment on first follow-up imaging using modified RECIST criteria. Additionally, for tumors with residual enhancement, CTHA-EM was evaluated to identify its potential feeding arteries. Results CTHA-EM showed residual enhancement in 18/46 (39.1%) and non-residual enhancement in 28/46 (60.9%) HCCs, with significant differences on T Post-RE (3.05 ± 2.4 versus 0.48 ± 0.23, respectively; p < 0.001). The first follow-up imaging showed non-complete response (partial response or stable disease) in 19/46 (41.3%) and complete response in 27/46 (58.7%) HCCs. CTHA-EM had a response prediction sensitivity of 94.7% (95% CI, 74.0–99.9) and specificity of 100% (95% CI, 87.2–100). Feeding arteries to the residual enhancement areas were demonstrated in all 18 HCCs (20 arteries where DEB-TACE was delivered, 2 newly developed collaterals following DEB-TACE). Conclusion CTHA-EM method was highly accurate in predicting initial HCC response to DEB-TACE and identifying feeding arteries to the areas of residual arterial enhancement.

S9 Table is omitted from the list of Supporting Information. Supporting information LifeLong I Heart mRNA. Skip to file navigationSkip to generic navigation A B C D E F G H I J K L M N O P Q R S T U V W X Y Z AA AB AC AD AE AF AG AH AI AJ AK AL AM AN AO AP AQ AR AS AT AU AV AW AX 1 Plate 1 Raw CT values Average delta CT ΔCT 2 Gene ↓ Subject → S8.1 S24 S9.3 S6.4 S9.1 Y18 Y25 Y19 Y9 Gene ↓ S8.1 S24 S9.3 S6.4 S9.1 Y18 Y25 Y19 Y9 S8.1 S24 S9.3 S6.4 S9.1 Y18 Y25 3 GAPDH A 17.2227584197101 17.0960169111601 17.1450399266626 17.2261195007261 17.2124745053596 16.9728519295508 17.3746878619056 17.4504414950499 17.1233350547625 17.0068797617316 17.1670375618892 17.0066086089542 17.2249380779292 16.9480574830836 16.143782730167 16.2069201529908 16.8567610725968 16.3439680391188 GAPDH 17.159387665435098 17.185579713694352 17.0926632174552 17.41256467847775 17.06510740824705 17.0868230854217 17.0864977805064 16.1753514415789 16.6003645558578 Housekeeper GAPDH 4 IL-6 B 31.2832774422591 31.235382455168 30.2525150817788 29.9037571204569 31.6058739365401 31.9775533045845 27.9692968107875 27.9982552939548 32.7702831691699 33.7756423941107 28.2279066586806 28.0454943907626 31.386558277345 31.7741916616727 30.3798453818442 30.3087536324683 32.9874743823418 32.8994165659944 IL-6 31.25932994871355 30.07813610111785 31.791713620562298 27.983776052371148 33.2729627816403 28.136700524721597 31.58037496950885 30.34429950715625 32.9434454741681 14.099942283278452 12.892556387423497 14.699050403107098 10.571211373893398 16.20785537339325 11.049877439299898 14.49387718900245 5 IL-1b C 27.7607610399024 28.0818057660842 29.2743824258867 29.0258717700794 29.4553611635112 29.2098723094273 28.6113257800381 28.9045331522702 30.7655600970071 31.0763075351084 30.0488085335771 29.7378195063969 28.3498373549533 28.3655445868964 30.4028544981929 30.2303532089152 30.4824451280281 30.562068913743 IL-1b 27.9212834029933 29.150127097983052 29.332616736469248 28.757929466154152 30.920933816057747 29.893314019987 28.35769097092485 30.31660385355405 30.52225702088555 10.761895737558202 11.9645473842887 12.239953519014048 11.345364787676402 13.855826407810696 12.8064909345653 11.271193190418451 6 IL-18 D 31.0242427859449 30.8631544198324 30.6976407996928 29.8345660968711 30.32994861068 30.3145546343817 27.7622969217847 27.6972954924814 30.5621005433449 30.718048359783 29.7132291328988 29.8871056810122 30.4645477381786 30.5593651611927 29.1422958771514 29.0787128186274 31.8903661393288 32.0048169676586 IL-18 30.943698602888652 30.26610344828195 30.32225162253085 27.72979620713305 30.64007445156395 29.800167406955502 30.51195644968565 29.110504347889403 31.9475915534937 13.784310937453554 13.080523734587597 13.22958840507565 10.317231528655299 13.5749670433169 12.713344321533803 13.42545866917925 7 NFKb-1 E 24.8254567305921 25.1348088185582 25.0062082930937 24.5186512654426 24.8872569734572 24.779394225765 24.1319627569722 24.0011813531246 24.4887046419295 24.6995725596868 24.3820148457641 24.3865172414558 24.5644210615383 24.6691290358862 24.2274232660528 24.0889242450612 25.0731850378707 24.6953365937736 NFKb-1 24.98013277457515 24.76242977926815 24.8333255996111 24.0665720550484 24.59413860080815 24.384266043609948 24.61677504871225 24.158173755557 24.884260815822152 7.820745109140052 7.576850065573797 7.7406623821559 6.65400737657065 7.529031192561099 7.297442958188249 7.53027726820585 8 NFkb-2 F 26.7045516920118 26.6757345804755 26.7646421207714 26.8003272797153 26.6759706329691 27.0759950868447 25.8618089955849 26.1801295324672 27.1202851729312 27.0835233764581 26.2010221629559 26.2986877952507 26.3336393871413 26.4945753531329 25.7828308451832 25.9383731474701 27.3708254452238 26.9787996700945 NFkb-2 26.69014313624365 26.78248470024335 26.875982859906898 26.02096926402605 27.10190427469465 26.2498549791033 26.4141073701371 25.86060199632665 27.174812557659152 9.53075547080855 9.596904986549 9.783319642451698 8.6084045855483 10.036796866447599 9.163031893681602 9.3276095896307 9 Cdkn1a G 24.5507361616066 25.3559147556468 24.6079147431688 25.1782502986826 25.2563040633391 25.1598136456992 24.4294896036426 24.5228059376776 26.4031158122344 26.1242908123156 24.5802551734152 24.6413624043314 24.4282269326323 24.1965984515812 25.2088295538285 25.0528520694569 25.3329599581332 24.8160728889468 Cdkn1a 24.9533254586267 24.8930825209257 25.20805885451915 24.4761477706601 26.263703312275 24.6108087888733 24.312412692106747 25.1308408116427 25.074516423539997 7.793937793191603 7.7075028072313465 8.115395637063951 7.063583092182348 9.198595904027947 7.523985703451601 7.2259149116003485 10 CDKn2a H 31.4164200969947 31.0429903524676 31.2079072243556 31.4143918034498 31.934769607 32.5200067014273 30.9810559840924 31.187906600095 31.5622914271198 31.6594025383255 33.7404204593239 33.0560980126742 33.3737262937795 33.5228506413887 32.6502542170308 33.0616429880405 34.722677748124 35.0908853816313 CDKn2a 31.22970522473115 31.3111495139027 32.22738815421365 31.0844812920937 31.61084698272265 33.39825923599905 33.4482884675841 32.85594860253565 34.90678156487765 14.07031755929605 14.125569800208346 15.134724936758449 13.671916613615949 14.545739574475597 16.31143615057735 16.3617906870777 11 CXCL1 I 28.7206322985985 28.9339128995328 28.3298871415528 28.0462166079446 29.1076582245152 29.2643337952645 29.6820397705059 29.3485383661744 29.6849346064857 29.9287287583586 29.3483864108378 29.3275096675003 29.0009619306224 29.3668816551351 29.2808715089445 29.327670178107 30.649263415718 30.4691555624855 CXCL1 28.82727259906565 28.1880518747487 29.18599600988985 29.51528906834015 29.80683168242215 29.33794803916905 29.18392179287875 29.30427084352575 30.55920948910175 11.667884933630553 11.00247216105435 12.093332792434648 12.102724389862399 12.741724274175098 12.25112495374735 12.09742401237235 12 Stat3 J 26.0904890379949 25.9328304379032 25.9063931310091 26.1329342458923 26.4609068410479 26.4297398050048 25.7018593565636 24.9656464528592 26.0560010797303 25.8896903923348 25.1840850843387 25.3433284943611 25.7927734157918 25.6862456816375 24.7283906358084 25.0138247366201 26.1147216604091 25.8976191416658 Stat3 26.01165973794905 26.0196636884507 26.44532332302635 25.3337529047114 25.97284573603255 25.2637067893499 25.73950954871465 24.871107686214252 26.00617040103745 8.852272072513951 8.834083974756346 9.35266010557115 7.9211882262336495 8.907738327785498 8.176883703928201 8.653011768208252 13 TNF-a K 30.1073341921065 30.5360636345848 30.2260615221732 29.9559067650374 29.2464199480057 29.1643666740457 28.6089768107746 28.79978930134 29.6793392945751 29.1310263213341 29.9822045453806 29.6659316486985 30.7461596433001 30.2097075953468 29.6386111561683 29.709346427943 30.1151871528581 29.8693295774509 TNF-a 30.32169891334565 30.0909841436053 29.2053933110257 28.7043830560573 29.405182807954603 29.82406809703955 30.47793361932345 29.67397879205565 29.9922583651545 13.162311247910552 12.905404429910948 12.112730093570498 11.291818377579549 12.340075399707551 12.737245011617851 13.391435838817053 14 Casp1 L 27.2033919131097 27.6744363531269 26.5802828002749 26.2281642714393 26.4250342743884 26.7102082676285 25.6336464042801 25.5547383413519 27.0678362649028 27.0065083778922 27.2463448661041 27.1608443954414 27.35798527279 27.3796265798296 26.627225712546 26.8875428314112 27.5112526099685 27.5986345348855 Casp1 27.438914133118303 26.4042235358571 26.56762127100845 25.594192372816 27.0371723213975 27.20359463077275 27.3688059263098 26.7573842719786 27.554943572427 10.279526467683205 9.218643822162747 9.474958053553248 8.18162769433825 9.972064913150447 10.11677154535105 10.282308145803402 15 NEK7 M 23.9685847278823 24.5433164196844 23.43572321289 23.9081916995917 23.5086828809897 23.5270279353252 23.2133882975186 23.2757457924196 23.3805267633634 23.5192038087196 23.1886907682083 23.4814557673291 23.358820269235 24.1215698673907 22.9541524276427 22.8534133014146 23.7893714938226 23.5573365389361 NEK7 24.25595057378335 23.67195745624085 23.517855408157452 23.2445670449691 23.4498652860415 23.3350732677687 23.74019506831285 22.90378286452865 23.67335401637935 7.09656290834825 6.486377742546498 6.425192190702251 5.8320023664913485 6.384757877794449 6.248250182347 6.653697287806452 16 NLRP3 N 30.244118458751 29.5369897211229 30.3603582591055 30.2503268831856 29.4758591262319 29.4736269640112 29.3352875367771 29.320653238761 30.26 30.1814655814764 31.146281441585 30.6535936006003 29.45 29.6706759432538 29.7277413856785 29.6453588719767 32.0548305999839 31.4854419974249 NLRP3 29.89055408993695 30.30534257114555 29.47474304512155 29.32797038776905 30.2207327907382 30.89993752109265 29.5603379716269 29.686550128827598 31.7701362987044 12.73116642450185 13.1197628574512 12.382079827666349 11.9154057092913 13.155625382491149 13.81311443567095 12.473840191120502 17 ASC O 26.9861347390865 27.0521925568865 27.534747032205 26.6997139959596 27.0828035675481 27.0235988480711 25.8575043892974 26.0087951630763 26.696034618544 27.1135738040462 26.1538464899565 26.0982055323081 26.9292364798881 26.7892820090882 25.841950717191 25.4027055290128 27.1753237657249 27.1722998114956 ASC 27.0191636479865 27.1172305140823 27.0532012078096 25.933149776186852 26.9048042112951 26.1260260111323 26.85925924448815 25.6223281231019 27.17381178861025 9.859775982551401 9.93165080038795 9.9605379903544 8.520585097709102 9.83969680304805 9.039202925710601 9.772761463981752 18 SPARC P 22.4062672259926 22.5213462994263 22.1406264428644 22.1952706102821 22.3852686414166 23.3004426221895 20.7103936770761 21.0545135691509 22.0901620956444 22.4793107093598 22.6866619438751 21.6821678981581 22.3 21.6934115711809 21.0815559489363 21.0559757672406 22.1297187073265 21.8817057286147 SPARC 22.46380676270945 22.167948526573248 22.84285563180305 20.8824536231135 22.284736402502098 22.1844149210166 21.99670578559045 21.068765858088447 22.0057122179706 5.3044190972743515 4.982368812878896 5.7501924143478504 3.4698889446357484 5.21962899425

Early neurosyphilis can occur in an immunocompromised host. It has a widely varied presentation. Isolated CN6 as presenting symptom has not been described. Early neurosyphilis can occur in an immunocompromised host. It has a widely varied presentation. Isolated CN6 as presenting symptom has not been described.

BackgroundPancreas ductal adenocarcinoma (PDAC) is highly resistant to most therapies, including immunotherapy. PDAC create highly immunosuppressive tumor microenvironments, yet also contain infiltrates of exhausted gamma delta T cells (gDTs). We sought to determine how PDAC suppresses gDT activation within the tumor-immune microenvironment through production of secreted factors. Using RNAseq we identify dysregulated cholesterol metabolism as a potential mechanism induced by PDAC in gDT which may impair gDT anti-tumor cytotoxicity.MethodsPDAC organoids were developed from patient biopsies. Media in which PDAC organoids were cultured were harvested (conditioned media), modelling secreted factors produced by PDAC. Circulating gDTs were isolated from the peripheral blood of healthy allogeneic donors using negative selection (StemCell Tech) after gradient centrifugation, and expanded with IL-2, IL-15, and zoledronic acid. Healthy gDTs were then exposed to PDAC-conditioned media for 72 hours to simulate the in vivo PDAC secretome and incubated with PDAC organoids at an effector:target ratio of 5:1. After 48 hours, a fluorescent cleaved caspase 3/7 dye was added. Live cell imaging was performed (BioTek) to assess organoid area stained positive for cleaved caspase 3/7.ResultsCulture of healthy donor gDTs with PDAC secretome is associated with decreased gDT killing of PDAC organoids across 2 separate patient PDAC organoid lines. Greater than 50% reduction in total cleaved caspase 3/7 area of organoids was seen with PDAC-conditioned gDTs versus gDTs in base media (figure 1A; each data point represents a separate measured organoid). Bulk RNAseq of gDTs (n= 3 biological replicates of 3 separate conditioned media exposed and control media exposed gDT) following conditioning with PDAC secreted factors results in increased cholesterol efflux (ABCG1 upregulated by 16 fold vs control, p<0.0001), decreased cholesterol uptake (LDLR downregulated 4 fold vs control, p<0.0001), and downregulation of cholesterol biosynthesis in gDTs (HMGCR downregulated 2.7 fold vs control, p<0.0001) (figure 1B). Preliminarily, addition of 10ug/mL of low-density lipoprotein (LDL) to gDTs exposed to PDAC conditioned media increased overall gDT mediated PDAC killing (n= 236 organoids evaluated across 8 technical replicates of conditioned media; figure 1C).ConclusionsgDTs are functionally suppressed by PDAC secretome, potentially driven by decreased uptake, increased efflux, and decreased biosynthesis of cholesterol in gDTs (figure 1D). In a preliminary experiment, supplementation of the tumor microenvironment with LDL appears to restore gDT cytotoxicity against PDAC. Modulation of cholesterol handling in the tumor-immune microenvironment may enhance immune cell effector therapy for patients with PDAC.AcknowledgementsThis work was supported by a NCI/NIH T32 CA009135, as well as a University of Wisconsin Trainee Pilot Award (Department of Medicine; JDE), University of Wisconsin Carbone Cancer Center (UWCCC) pilot grant (Project AAK9374 from the UWCCC Pancreatic Cancer Task Force; JDE, JDK, CMC), St. Baldrick’s Empowering Pediatric Immunotherapies for Childhood Cancer Team Grant, and the MACC Fund (C.M.C). We would like to thank the UWCCC core facilities, who are supported in part through NCI/NIH P30 CA014520.Ethics ApprovalOrganoids used in the course of this work were developed under an IRB approved by the University of Wisconsin-Madison (Protocol B00000976, PI Dr. Jeremy Kratz, MD), with all patient tissue collected and used with informed consent.Abstract 1471 Figure 1(A,C) gDT ware pre-conditioned with either organold growth media or media conditioned by organoids from Patient A or B for 72 hours. gDT were then exposed to PDAC organoids for 48 hours: caspase 3/7 activity as a% of the total area of the measured organoids was determined by live cell imaging, Each dot represents one separate organoid, (B) Schematic of key RNAseq results superimposed on cholesterol handling pathways. (D) Graphical schematic of potential impact of PDAC factors on key elements of cholesterol handling that may impact gDT activation

Pancreatic and ampullary cancers remain highly morbid diseases for which accurate clinical predictions are needed for precise therapeutic predictions. Patient-derived cancer organoids have been widely adopted; however, prior work has focused on well-level therapeutic sensitivity. To characterize individual oligoclonal units of therapeutic response, we introduce a low-volume screening assay, including an automated alignment algorithm. The oligoclonal growth response was compared against validated markers of response, including well-level viability and markers of single-cell viability. Line-specific sensitivities were compared with clinical outcomes. Automated alignment algorithms were generated to match organoids across time using coordinates across a single projection of Z-stacked images. After screening for baseline size (50 μm) and circularity (>0.4), the match efficiency was found to be optimized by accepting the diffusion thresholded with the root mean standard deviation of 75 μm. Validated well-level viability showed a limited correlation with the mean organoid size (R = 0.408), and a normalized growth assayed by normalized changes in area (R = 0.474) and area (R = 0.486). Subclonal populations were defined by both residual growth and the failure to induce apoptosis and necrosis. For a culture with clinical resistance to gemcitabine and nab-paclitaxel, while a therapeutic challenge induced a robust effect in inhibiting cell growth (GΔ = 1.53), residual oligoclonal populations were able to limit the effect on the ability to induce apoptosis (GΔ = 0.52) and cell necrosis (GΔ = 1.07). Bioengineered approaches are feasible to capture oligoclonal heterogeneity in organotypic cultures, integrating ongoing efforts for utilizing organoids across cancer types as integral biomarkers and in novel therapeutic development.

Background Liver venous deprivation (LVD) is known to induce better future liver remnant (FLR) hypertrophy than portal vein embolization (PVE). The role of LVD, compared with PVE, in inducing FLR hypertrophy and allowing safe hepatectomy for patients with extensive colorectal liver metastases (CLM) and high-risk factors for inadequate hypertrophy remains unclear. Methods Patients undergoing LVD ( n  = 22) were matched to patients undergoing PVE ( n  = 279) in a 1:3 ratio based on propensity scores, prior to planned hepatectomy for CLM at a single center (1998–2023). The propensity scores accounted for high-risk factors for inadequate hypertrophy, namely pre-procedure standardized FLR (sFLR), body mass index, number of systemic therapy cycles, an extension of PVE to segment IV portal vein branches, prior resection, and chemotherapy-associated liver injury. Results The matched cohort included 78 patients (LVD, n  = 22; PVE, n  = 56). Baseline characteristics were comparable. The number of tumors in the whole liver was similar but more LVD patients had five or more tumors in the left liver (32% vs. 11%; p =  0.024). Post-procedure sFLR was similar but LVD patients had a significantly higher degree of hypertrophy (16% vs. 11%; p =  0.017) and kinetic growth rate (3.9 vs. 2.4% per week; p =  0.006). More LVD patients underwent extended right hepatectomy (93% vs. 55%; p =  0.008). Only one patient had postoperative hepatic insufficiency after PVE, and no patients died within 90 days of hepatectomy. Conclusion In patients with extensive CLM and high-risk factors, LVD is associated with better FLR hypertrophy compared with PVE and allows for safely performing curative-intent extended major hepatectomy.