Citations

Abstract Sex differences in brain tumor related epilepsy (BTE) as an initial symptom of glioma are rarely investigated. Sex differences are being explored with increased interest more recently. Epidemiological studies have generally indicated overall incidence of epilepsy to be slightly higher in males than females, but a higher incidence of idiopathic generalized epilepsy has been seen in females in some studies. Clinicians regularly face the challenge of anti-epileptic drug prescription determination in patients with newly identified brain mass and would greatly benefit from knowing clinical characteristics in BTE. We analyzed clinical characteristics in patients with pathologically-determined glioma with known seizure status at clinical presentation using non-parametric and Fisher’s Exact tests with the entire cohort and male and female separately. From our clinical data repository, we identified 223 patients (females, n=86 (39%); males, n=137 (61%)) divided by those that presented with seizure (SP, n=96, 43%; F, n= 28; M, n= 68) and those that presented without seizure (nSP, n=127, 57%, F n=58, M n=69). In sex-specific analysis males had a significantly (x2=6.28, p=0.01) higher proportion of SP (49.6%) than females (32.6%). There was a dependence between seizure presentation status and tumor grade in males (x2=5.94, p=0.015). Tumor kinetics in the female cohort showed significantly (p< 0.0001) more diffuse tumors in SP compared to nSP. Right-sided tumors were predominantly nSP, while left-sided tumors were split more evenly between SP and nSP. The predominance of nSP among right-sided tumors seems to be driven by females (74%), male right-sided tumors were split more evenly between SP and nSP. Seizure status is dependent on tumor location for the combined cohort, however not for males (x2=5.23, p=0.16) or females (x2=4.34, p=0.23). Clearly there are sex differences and similarities in clinical characteristics at glioma presentation. Further characterization could lead to improved adherence of national standards for AED prescription.

Abstract Glioblastoma (GBM) is the most aggressive primary brain tumor with an average survival of 15 months with standard of care treatment. GBM patients typically present with necrosis surrounded by enhancement on T1-weighted post gadolinium magnetic resonance imaging (T1gd MRI), however some patients present with a significant cystic component. Cysts are caused by different underlying biological mechanisms to necrosis and are important to identify for future clinical investigations. These cystic components can be manually identified through MRI but this process can be time consuming for large patient cohorts. Over the last two decades, our lab has collected serial MRI data of brain tumor patients. With over 70,000 images now in the database and that number increasing daily, it is clear that we have a unique resource for clinical investigation and a need to automate this process. To this end, the aim of this work was to develop and assess the performance of a convolution neural network (CNN) model for automatic detection of cystic GBMs. In this retrospective IRB-approved work, we collected pretreatment MRIs of a patient cohort consisting of 85 patients with a significant cystic component at presentation along with 400 non-cystic GBM, both identified manually through MRI. Image slices with a view of the cystic component were used as positive samples for training. Data were randomly split into training, validation, and test sets using a 70:15:15 ratio. The proportion of positive to negative cases was comparable between sets. Prior to training, we used image augmentation techniques to compensate for the class imbalance in our data. Our results showed that deep learning networks can automatically detect cystic GBMs on MRIs with high accuracy and thus illustrates the potential use of this technique in clinically relevant settings.

AbstractBackgroundNutrient‐mediated release of cholecystokinin and glucagon‐like peptide‐1 (GLP‐1) regulates gastric emptying (GE) via duodenogastric feedback mechanisms; GLP‐1 also regulates postprandial insulin secretion. Some patients with functional upper gastrointestinal symptoms have impaired glucose tolerance during enteral dextrose infusion. Our hypothesis was that variants in CCK, GLP‐1, and TCF7L2 (transcription factor 7‐like 2 locus), which is associated with greatest genetic risk for development of type 2 diabetes mellitus, are associated with GE and independently with glucose tolerance. Our aims were to evaluate the associations between these GE, glucose tolerance, and these single nucleotide polymorphisms (SNPs).MethodsGenetic variants, scintigraphic GE of solids, plasma glucose, insulin, and GLP‐1 during enteral dextrose infusion (75gm over 2 hours) were measured. GE and enteral dextrose infusion were, respectively, evaluated in 44 (27 controls and 17 patients with functional dyspepsia or nausea) and 42 (28 controls, 14 patients) participants; of these, 51 participants consented to assessment of SNPs. Four functional SNPs were studied: rs6923761 and rs1042044 at GLP‐1 receptor, rs7903146 (TCF7L2), and rs1800857 (CCK receptor).Key ResultsGastric emptying was normal in 38, rapid in 4, and delayed in two participants; 38 had normal, and four had impaired glucose tolerance. The T allele at rs7903146 (TCF7L2) was non‐significantly associated (P = .14) with faster GE. The associations between SNPs and demographic variables, GE thalf, glucose tolerance and plasma GLP1 levels were not significant.Conclusions & InferencesThere is a trend toward an association between faster GE and the diabetes‐associated allele at rs7903146 in TCF7L2. However, these SNPs were not associated with plasma glucose or GLP1 concentrations during enteral dextrose infusion.

We report 21 cases of a distinctive and unique vascular tumor which we propose to be a pure lymphatic-type angiosarcoma characterized by architectural and growth characteristics of angiosarcoma, cytologic, and immunohistochemical features of lymphatic differentiation, a prominent lymphocytic infiltrate, and variable nuclear grade. Patients included 12 males and 9 females with a median age of 65 years (range: 32 to 95 y). Tumors involved the head and neck (n=11), lower extremities (n=5), trunk (n=4), and upper extremity (n=1) and were located superficially in the dermis and/or subcutis. Tumors were designated “low grade” (n=10) when the nuclear grade was low, and vascular channel formation was evident throughout but with multilayering of endothelium within the vessels. Cases were designated “high grade” (n=11) when nuclei appeared higher grade with more rounded contours and prominent nucleoli and when solid areas predominated over vascular channel formation. A striking feature of both groups was the presence of a dense, lymphocytic infiltrate with occasional germinal center formation. All cases strongly and diffusely expressed at least 1 lymphatic marker (21/21) with podoplanin (17/19) and Prox-1 (11/11) more commonly expressed than LYVE-1 (5/10). No consistent molecular alteration was identified. Follow-up on 17 patients (median: 41 mo, mean: 54 mo) showed 10 patients were alive without disease, 5 were alive with disease, 1 died of other cause, and 1 died of disease. Local recurrence developed in 9 cases and metastasis in 2 cases, although neither correlated with grade as defined. On the basis of clinical follow-up to date, the natural history of lymphatic-type angiosarcoma appears to be more favorable than other forms of cutaneous angiosarcoma.

Abstract Heritable mitochondrial DNA (mtDNA) mutations are common, yet only a few recurring pathogenic mtDNA variants account for the majority of known familial cases in humans. Purifying selection in the female germline is thought to be responsible for the elimination of most harmful mtDNA mutations during oogenesis. Here we show that deleterious mtDNA mutations are abundant in ovulated mature mouse oocytes and preimplantation embryos recovered from PolG mutator females but not in their live offspring. This implies that purifying selection acts not in the maternal germline per se, but during post-implantation development. We further show that oocyte mtDNA mutations can be captured and stably maintained in embryonic stem cells and then reintroduced into chimeras, thereby allowing examination of the effects of specific mutations on fetal and postnatal development.

Abstract Introduction: Topoisomerase I is a nuclear enzyme that relaxes torsional strain in DNA by nicking one DNA strand, allowing rotation, then resealing the DNA backbone. This is an important enzyme in replication and transcription, and therefore has been targeted by anti-cancer agents such as camptothecins. These agents intercalate into DNA at the topoisomerase I active site and inhibit the religation step catalyzed by the enzyme, causing increased topoisomerase I-DNA complexes that impede advancing replication forks or transcription complexes, leading to DNA damage and cell death. Platinating agents also stabilize topoisomerase I-DNA covalent complexes. The topotecan/carboplatin combination has recently shown promise in combination with the PARP inhibitor veliparib in aggressive and transformed myeloproliferative neoplasms (MPNs) and chronic myelomonocytic leukemia (K Pratz et al., Clin Cancer Res. 23:899, 2017). Given that both classes of agents have a narrow therapeutic window, it is important to try to predict the sensitivity/resistance of these agents in malignancies such as acute myeloid leukemia (AML) and transformed MPNs. Some of mechanisms of drug resistance that have been described are decreased numbers of drug-stabilized topoisomerase I-DNA complexes due to drug efflux, diminished topoisomerase I expression or topoisomerase I mutation. Thus, being able to detect and quantify these DNA-protein complexes may provide insight into drug sensitivity. Methods: Using a unique monoclonal antibody that detects topoisomerase I-DNA covalent complexes (A. Patel et al., Nucleic Acids Res. 44:2816, 2016), immunofluorescence techniques were used to quantify these topoisomerase I-DNA complexes in AML cell lines (SET2, HEL, K562, U937, ML2, MV-4-11, THP1, HL60, ML1, and Molm13) and clinical AML samples. To verify the fidelity of the anti-topoisomerase I-DNA covalent complex antibody (TopIcc), siRNA knockdown methods were utilized with confirmatory immunofluorescence and Western blotting. Slot blots were additionally used to assess the presence of these complexes in AML cell lines. Western blots were performed to assess topoisomerase I levels in AML cell lines. Topotecan drug sensitivity analysis was performed by using an MTS assay. Results: With treatment of the topoisomerase I inhibitor, topotecan, there was an increase in the percentage of leukemia cells positive for the topoisomerase I-DNA covalent complexes. The degree of increase in complexes varied across cell lines and patient samples. To ensure we were detecting TopIcc by immunofluorescence, we performed a topoisomerase-I siRNA knockdown to confirm the specificity of the antibody for TopIcc's. Slot blots on multiple AML cell lines confirmed the presence of topoisomerase-DNA covalent complexes. The Western blot of all the AML cell lines, ordered from low to high TopIcc revealed increasing amounts of topoisomerase I. The MTS assay revealed lower topotecan IC50 values in three of the cell lines with higher complex formation, including Molm13, ML1 and ML2 (IC50 6-8 nM compared to 13-46 nM in the other cell lines). Conclusions: Based on recent clinical results, there has been renewed interested in topoisomerase I inhibitors, especially for aggressive and transformed MPNs. Topoisomerase I-DNA complex repair/downregulation has been a hallmark of drug resistance to topoisomerase I inhibitors. Therefore, detecting and quantifying these complexes in treated samples has been hypothesized to provide insight into the drug sensitivity, which is particularly important in camptothecins and platinating agents given their narrow therapeutic windows. Immunodetection techniques using an anti-TopIcc antibody may help predict sensitivity of AML to topoisomerase I inhibitors and will be used as a correlative biomarker study in an upcoming phase II randomized study of topotecan/carboplatin with or without veliparib or placebo in advanced myeloproliferative disorders and chronic myelomonocytic leukemia (ClinicalTrials.gov NCT03289910). Disclosures Pratz: AbbVie: Consultancy, Research Funding; Agios: Research Funding; Astellas: Consultancy, Research Funding; Boston Scientific: Consultancy; Millenium/Takeda: Research Funding. Kaufmann:Mayo Clinic: Patents & Royalties: Co-inventor on a patent held by Mayo Clinic for the use of the anti-TOP1cc antibody as a diagnostic reagent.

Abstract Obinutuzumab-Gazyva (G) is an anti-CD20 monoclonal antibody that has shown better outcomes in patients (pts) with chronic lymphocytic leukemia and low-grade lymphoma (Goede 2014, Marcus 2017). However, one limitation for its use when compared to Rituximab is the presence of significantly more frequent and more severe infusion related reactions (IRR). Strategies to mitigate this significant adverse event are needed particularly to allow a safer administration of this antibody to elderly pts or those with existing comorbidities. We have observed a reduction of G-induced IRR in previously untreated CLL pts that are enrolled on a phase Ib/II clinical trial (NCT02315768) that combines G with the Bruton's tyrosine kinase inhibitor, ibrutinib (Ibr). Only 5 out of 23 pts treated have developed IRR (Grade 1-2, 17% and Grade 3, 4%). This rate of IRR is much lower as compared with rates previously reported (all grades: 65%, grade 3-4: 20% - Goede 2014), (all grades: 92%, grade 3-4: 26.3% - Freeman,2015). Moreover, there were no pts that require permanent discontinuation of G due to IRR. To understand the biology of this beneficial effect of Ibr, we performed serial cytokine measurements on plasma samples from 23 pts enrolled in this study at different time points during the first week of combined treatment (Cycle 1 prior to the first infusion of G and post G infusion on Day 1, Day 2 and Day 8) - Figure 1. We developed a multiplex assay (Luminex) to measure 7 different cytokines previously reported to be involved in IRR (IFN-g, IL-10, IL6, IL8, CCL3/MIP1-a, CCL4/MIP1-band TNF-a). Standards were set up in duplicate yielding curves from 3.2 pg/ml to 10.000 pg/ml. Assays were performed according to manufacturer's instructions, with undiluted samples and overnight agitated incubation at 4 °C. We identified the maximum peak of cytokine levels post G infusion and compared those values with the baseline cytokine profile obtained prior to the first G infusion on Cycle 1 Day 1. The majority of pts (22 out of 23) showed cytokines maximum peaks in the middle of G-infusion during Cycle 1 Day 1 and this correlated with the onset of IRR associated symptoms in those pts that reacted to G. With the exception of IL-6, we observed statistically higher post vs. pre G infusion levels of TNF-a(p=0.0012), IFN-g(p=<0.0001), CCL3 (p=0.0458), CCL4 (p=<0.0001), IL-8 (p=<0.0001), and IL-10 (p=<0.0001) even in pts that did not develop IRR. However, the post infusion peak levels of TNF-a(p=0.0043), IFN-g(p=0.0457) and CCL3 (p=0.0460) were significantly higher in pts with IRR compared to those that had no IRR. Baseline levels prior to G infusion of TNF-a(p=0.0495) and IFN-g(p=0.0301) were higher in IRR pts, suggesting a possible predictive role in the development of IRR. Figure 1. Our study shows that concurrent administration of Ibr (Initiated on Cycle 1 Day 1 with pre-medications) and G shows a beneficial effect decreasing the rates of IRR (Amaya-Chanaga, 2016). All pts showed a significant increase of cytokine levels post G infusion with IL-6 levels being the exception. When we compared post G infusion cytokine levels, we observed that IRR-pts had a significant increase in TNF-a, IFN-g, and CCL3 suggesting a role of these cytokines in the clinical manifestations associated with IRR. In addition, higher levels of TNF-a and IFN-g, at baseline prior to G infusion appear to be predictive of the development of IRR. Even though our sample size is small, our observations provide additional insights into the biology of G associated IRR and how to decrease effectively those adverse events using Ibr while preserving the immune function needed for the activity of this monoclonal antibody. In addition, Ibr induced modulation of signaling through the B cell receptor and patterns of cytokine release might be efficacious in preventing other monoclonal antibody IRR as well as those reactions observed in pts that receive adoptive cellular therapy (i.e. CART cell treatment). Disclosures Choi: AbbVie, Inc: Consultancy, Speakers Bureau; Gilead: Speakers Bureau; Genentech: Speakers Bureau; Pharmacyclics: Consultancy, Research Funding, Speakers Bureau; Rigel: Consultancy. Amaya-Chanaga:AbbVie: Equity Ownership, Other: Research performed while employed as an investigator of this study at UCSD. Review and approval of abstract performed while employed at Pharmacyclics, LLC, an AbbVie Company.; Pharmacyclics, an AbbVie Company: Employment, Other: Research performed while employed as an investigator of this study at UCSD. Review and approval of abstract performed while employed at Pharmacyclics, LLC, an AbbVie Company.. Kipps:Celgene: Consultancy; F. Hoffmann-La Roche Ltd: Consultancy, Research Funding; Pharmacyclics: Consultancy, Honoraria, Membership on an entity's Board of Directors or advisory committees, Research Funding; Verastem: Membership on an entity's Board of Directors or advisory committees; Janssen: Honoraria, Membership on an entity's Board of Directors or advisory committees; Gilead: Consultancy, Honoraria, Research Funding; AbbVie: Consultancy, Honoraria, Membership on an entity's Board of Directors or advisory committees, Research Funding; Genentech Inc: Consultancy, Research Funding; Janssen: Honoraria, Membership on an entity's Board of Directors or advisory committees; Verastem: Membership on an entity's Board of Directors or advisory committees. Castro:F. Hoffmann-La Roche: Consultancy; Genentech, Inc: Consultancy; Pharmacyclics, LLC, an AbbVie Company:: Consultancy.

Abstract Introduction Multiple myeloma (MM) has characteristics that influence the prognosis and are useful to make decisions regarding treatment. Diagnosis and treatment patterns of hematological malignancies have not been described in Colombia and having access to this regional information could guide public health policies and help design clinical trials. The Colombian Association of Hematology and Oncology (ACHO) designed a registry for Hemato-Oncological diseases to fill this information gap. This is the first report of RENEHOC focusing on MM. Methods We conducted an ambispective multi-centric cohort study of clinical records available from patients with MM that were diagnosed in the most populated regions of Colombia. We collected demographic, diagnostic, clinical and treatment data at different time points from diagnosis to the most current follow up. The computerized de-identified data was consolidated and analyzed using basic statistical measures of central tendency and dispersion. The most current follow up included data available from last clinic visit, loss of follow up, death or withdrawal of consent. This study was approved by local and centralized institutional review board. Results We analyzed data from 206 MM patients (pts). Average age at diagnosis was 62.9 (SD 10.2) years and 51.4% of pts were male. Most common symptoms at diagnosis were bone pain (74.2%), anemia related (58.2%) and pathological fractures (45.1%). Mean time from symptoms to diagnosis was 7.3 (Range 1-44) months. Baseline mean hemoglobin, creatinine and calcium serum levels were 10.5 g/dL, 1.58 mg/dL and 9.2 mg/dL respectively. At diagnosis, 22% of patients presented with renal failure and 30% required dialysis. Immunoglobulin (Ig) subtype distribution was: IgG 50.6%, IgA 20.6%, only light chain secretion (61% Kappa) and IgM 1.1%. In 11.6% all Igs were low. Most pts were diagnosed at advanced stages (64.5% Durie-Salmon III, and 37% and 47% International Staging System II and III respectively). Molecular prognostic characterization was performed only in 39 patients (18.4%). Four patients were considered too fragile for active treatment. The most common initial treatment was triple combinations that included Bortezomib (84% of patients). Among those, CyBorD was the most frequently used first line therapy (58.3%), followed by VTD (14.6%). Mean number of cycles was 4.8 (SD 2.5). Overall Response Rate (ORR) 74.7% was observed. Only 40% of patients treated with intense induction therapy received autologous transplant. Response to treatment including transplant are shown in table 1. Second and further lines of treatment were highly variable. 18 patients were treated with a second autologous transplantation consolidating 2nd line therapy. 12 patients received Carfilzomib combinations, all of them in 2nd line. 5 patients were treated with Daratumumab, all >2nd line. Mean follow-up time was 33.53 (SD 3.6) months. After a median follow up of 27 months we observed in our cohort an overall survival of 82% and 68% of patients progression-free. . Conclusions This first report focusing on MM highlights important differences on patient's characteristics and treatment in Colombian patients. This includes and treatment initiation due to insurance barriers; high risk clinical characteristics and complications upon diagnosis and low rate of transplantation in patients otherwise eligible for this procedure. Rates of response to induction seem slightly lower than reported (CB Reeder 2009). However, overall survival and progression-free survival met the expectations for this type of patients. The development of country specific databases may influence the design of policies, allocation and use of resources and improve patient outcomes. Only cooperative efforts like the one spearheaded by RENEHOC can achieve those goals. Disclosures No relevant conflicts of interest to declare.

Abstract Despite recent advances and improvement in treatment options, chronic lymphocytic leukemia (CLL) is still an incurable disease. Recent advancement in parallel sequencing technology has provided better understanding of genetic landscape and clonal architecture underlying disease course. Furthermore, mutation status of TP53, SF3B1, NOTCH1, and BIRC3 has improved current CLL risk stratification. In order to better understand the genetic basis and clonal evolution underlying disease progression we analyzed a homogeneously treated cohort of CLL cases at multiple time points before and after therapy. We performed WES in 30 sequential samples from 12 CLL cases. All 12 cases received PCR (pentostatin, cyclophosphamide and rituximab) based chemoimmunotherapy as initial treatment. Of these 12 cases, two had samples available both >6 months prior to enrollment and at treatment initiation, seven patients who experienced relapse had samples available at both treatment initiation and at and the time of relapse, and three patients had samples >6 months prior to enrollment, at treatment initiation, and at relapse. These cases were previously characterized by aCGH/FISH. R function Mclust and kernel density estimate (KDE) plots were used to identify subclonal heterogeneity. An average of 102-fold depth coverage was obtained with an average of 80% of the targeted regions being covered by at least 30X. Overall, we detected a total of 219 nonsynonymous Single Nucleotide Variants (SNV) and indels (average 19, range 11-33). Del13q (42%) was identified as most prevalent copy number abnormality followed by trisomy 12 (33%), del11q and del17p (17% each). Recurrent mutations were identified in NOTCH1 (33%), DDX3X (25%), TP53, SF3B1 XPO1 and MED12 (17% each). Other tumor implicated genes such as CARD11, NOTCH2, NOTCH4, DIS3, TRAF2, NFKBID, CHK2 and RB1 were found mutated in individual cases. In all 12 cases we identified at least one relevant cytogenetic abnormalities (del11q32, del13q14, del17p13, trisomy 12) and/or a mutated driver gene. Interestingly we found NOTCH1, DDX3X and XPO1 mutated at a significantly higher prevalence than previous studies (10%, 2% and 4%, respectively). Since all cases in our cohort correspond to individuals with progressive disease, a plausible explanation for the higher prevalence of mutations in our cohort is that these mutations are associated with disease progression. By WES we identified multiple subclones in 58% of cases (7 of 12 cases), as compared to previously identified 33% (4 of 12 cases) by CGH/FISH. In 5 chemotherapy naïve cases, no significant increase in genomic complexity was detected with disease progression. In contrast, 5 out of 10 cases with samples analyzed before CIT and at the time of relapse had changes in clonal dynamics, with initially dominant subclones diminishing in response to therapy and the available empty niche being occupied by expansion of another “fitter” subclone at the time of relapse. No acquisition of tumor associated gene mutations was seen post therapy or associated with relapse in 9 of 10 cases. In the remaining case we identified an interesting example of convergent evolution. The pre-therapy sample was comprised of a unique clone characterized with del11q13, mutations in SF3B1 (G742D) and DDX3X (pE196fs). After therapy that clone was either eradicated or reduced to below detection level. Interestingly another clone emerged after relapse that harbored an independent del11q22 and mutations affecting different aminoacids of SF3B1 (K700E) and DDX3X (pL21fs). The strong selection of impairment in these genes during disease progression suggests a key role of these pathways/genes in the pathogenesis of this patient. In conclusion, these studies provide additional insight into the genomic landscape and clonal architecture in a cohort of homogeneously treated CLL cases before and after therapy. Stable clonal architecture was seen in prior to treatment, whereas clonal evolution leading to increased tumor heterogeneity occurred after the under selection selective pressure of therapy in relapsed cases. Early identification of tumoral heterogeneity and underlying genetic abnormalities might provide better targets for therapy to decrease the likelihood of relapse. Disclosures: Fonseca: Medtronic: Consultancy; Otsuka: Consultancy; Celgene: Consultancy; Genzyme: Consultancy; BMS: Consultancy; Lilly: Consultancy; Onyx: Consultancy, Research Funding; Binding Site: Consultancy; Millennium: Consultancy; AMGEN: Consultancy; Cylene: Research Funding; Prognostication of MM based on genetic categorization of the disease: Prognostication of MM based on genetic categorization of the disease, Prognostication of MM based on genetic categorization of the disease Patents & Royalties. Shanafelt:Genentech: Research Funding; Glaxo-Smith-Kline: Research Funding; Cephalon: Research Funding; Hospira: Research Funding; Celgene: Research Funding; Polyphenon E International: Research Funding.

Abstract Background: Compared to Whites, Black-Americans may have a 40% higher incidence of idiopathic VTE. However, whether other VTE characteristics vary by race is uncertain. Objective: To compare demographic and baseline characteristics among White- and Black-Americans with VTE. Methods: Using a standardized data-collection form, demographic and baseline characteristics were prospectively collected from consecutive consenting patients enrolled in seven Thrombosis and Hemostasis Centers from August 2003 to March 2008. For patients with objectively diagnosed VTE, demographic and baseline characteristics were compared among White- and Black-American VTE patients, both overall, and by age and gender. Results: Among 1960 White- and 368 Black-Americans with VTE, compared to Whites, Blacks had significantly less isolated DVT (73.9% vs. 86.5%, p<0.001) and significantly more PE ± DVT (45.1 vs. 39.6%, p=0.05). Blacks and Whites did not differ in mean age (43.4 vs. 44.3 years), but a significantly higher proportion of Black men VTE patients were in age groups 20–39 and 80+ years. Blacks and Whites differed significantly by gender, with a significantly higher proportion of Black women with VTE (69.8% vs. 59.1%, p=0.0001). Blacks had a significantly higher mean BMI (32.3 vs. 29.4 kg/m2, p<0.0001), a significantly lower proportion with recent surgery or trauma, active cancer and infection, and a significantly lower proportion with a family history of VTE or documented thrombophilia (solely due to reduced Factor V Leiden and Prothrombin G20210A prevalence). Conversely, Blacks had a significantly higher proportion with hypertension, hyperlipidemia, diabetes mellitus, chronic renal disease and dialysis, HIV and sickle cell disease. The two races did not differ significantly regarding the proportion with idiopathic VTE, CHF, CAD/MI, peripheral artery disease, stroke or other chronic neurological disease (i.e., cerebral palsy), chronic liver disease or autoimmune disease, including antiphospholipid syndrome. Compared to White women VTE patients, Black women VTE patients had a significantly lower proportion with recent surgery, trauma, infection, oral contraceptive use and possibly hormone therapy; and a significantly higher proportion with idiopathic VTE, hypertension, diabetes mellitus, chronic renal disease, HIV and sickle cell disease. Compared to White men VTE patients, Black men VTE patients did not differ significantly regarding recent surgery, trauma, cancer, infection or autoimmune disease, but Black men had a significantly higher proportion with hypertension, diabetes mellitus, HIV and sickle cell disease. Black and White men with VTE did not differ significantly regarding idiopathic VTE, CHF, CAD/MI, stroke, peripheral arterial disease and chronic renal disease. Conclusion: White- and Black-Americans with VTE differ significantly regarding demographic and baseline characteristics that may be risk factors for VTE.