Objectives:COVID-19 vaccination status varies widely among first responders. We sought to understand whether similar vaccination rates exist for first responders and healthcare providers (nurses/physicians) and if this rate changed over time. Methods:This is a secondary analysis of a prospective longitudinal study of first responders and healthcare providers recruited starting in January 2021 and followed until April 2024. Following enrollment, participants completed surveys concerning personal demographics (age, sex, race, professional role [first responder, healthcare worker], use of personal protective equipment (PPE), and number of household members under age 18), and medical history (COVID-19 vaccination status, previous COVID-19 infection, and history of comorbidities). Participant vaccination status was confirmed at least every 6 months. Descriptive statistics were calculated, followed by logistic regression models (OR, 95% CI) to describe the associations between vaccination, demographics, and work characteristics. The cumulative incidence was visually described using a Kaplan-Meier plot. Results:Across 190 study participants, 61.1% were first responders, and 38.9% were healthcare providers. First responders were older, predominantly male, and reported more prior exposure to COVID-19. Although the odds of vaccination varied greatly within healthcare providers (OR 8.26, 95% CI 2.42-28.18), their odds of vaccination were higher than those of first responders (referent). Kaplan-Meier plots demonstrated that vaccination rates for both groups plateaued after 1 year. Conclusions:This study noted differential rates of vaccination between first responders and healthcare professionals and that these rates plateaued, demonstrating fixed perspectives on vaccination. Focused efforts to understand diverse perspectives on vaccination concerns may enhance the protection and maintenance of these workforces.

Hairy cell leukemia is an uncommon B-cell malignancy with excellent response to purine analogs and to targeted therapies such as ibrutinib and vemurafenib. However, purine analogs are known to be highly immunosuppressive and the infection burden in this patient population with current therapies is unknown. We therefore conducted a retrospective cohort study following 149 patients. Median follow-up time was 6.9 years. Thirty-six percent developed an opportunistic or serious infection requiring hospitalization. Most cases were bacterial and most coincided with neutropenia and/or CD4 T-lymphopenia. No single treatment agent was significantly associated with increased or decreased incidence of infection. Reassuringly, the cumulative incidence of infections plateaued 2 months after initial treatment suggesting clinically significant immune recovery. Only one patient in our cohort passed away due to infection. Estimated 10-year overall survival was 99% suggesting that infections may not cause as much mortality as was seen prior to current therapies.

The impact of pre-existing common cold coronavirus (CCCoV) antibodies (Abs) on severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) immune responses and pathogenesis remains poorly defined. We evaluated these associations in a cohort of hospitalized patients with COVID-19 and respiratory failure of varying severity. Patients with respiratory failure from other causes (non-COVID-19) were evaluated as controls. We demonstrated a positive correlation between levels of CCCoV and SARS-CoV-2 Abs using CCCoV and SARS-CoV-2 N and S protein peptide-specific ELISA. Consistent with the above, moderately increased levels of CCCoV-specific Abs in non-COVID-19 vs. COVID-19 patients suggest potential protective effects. Further, higher SARS-CoV-2 N protein-specific and CCCoV Ab levels were observed among surviving vs. non-surviving COVID-19 positive patients. However, the highest SARS-CoV-2 N and S protein-specific IgG and IgA Ab levels were noted in the patients with the most severe clinical disease. Finally, advanced age, cancer and immunosuppression were associated with significantly higher mortality and reduced SARS-CoV-2 and CCCoV Ab levels. Thus, our data highlight that sufficient SARS-CoV-2 N protein-specific Ab responses improve clinical outcomes in severely ill COVID-19 patients. We also confirmed that pre-existing CCCoV-specific Abs do not inhibit the SARS-CoV-2 Ab response and may further reduce the prevalence and/or severity of COVID-19.

New Omicron subvariants continue to emerge throughout the world. In particular, the XBB subvariant, which is a recombinant virus between BA.2.10.1.1 and BA.2.75.3.1.1.1, as well as the BA.2.3.20 and BR.2 subvar-iants that contain mutations distinct from BA.2 and BA.2.75, are currently increasing in proportion of variants sequenced. Here we show that antibodies induced by 3-dose mRNA booster vaccination as well as BA.1-and BA.4/5-wave infection effectively neutralize BA.2, BR.2, and BA.2.3.20 but have significantly reduced effi-ciency against XBB. In addition, the BA.2.3.20 subvariant exhibits enhanced infectivity in the lung-derived CaLu-3 cells and in 293T-ACE2 cells. Overall, our results demonstrate that the XBB subvariant is highly neutralization resistant, which highlights the need for continued monitoring of the immune escape and tissue tropism of emerging Omicron subvariants.

Omicron subvariants continuingly challenge current vaccination strategies. Here, we demonstrate nearly complete escape of the XBB.1.5, CH.1.1, and CA.3.1 variants from neutralizing antibodies stimulated by three doses of mRNA vaccine or by BA.4/5 wave infection, but neutralization is rescued by a BA.5-containing bivalent booster. CH.1.1 and CA.3.1 show strong immune escape from monoclonal antibody S309. Additionally, XBB.1.5, CH.1.1, and CA.3.1 spike proteins exhibit increased fusogenicity and enhanced processing compared with BA.2. Homology modeling reveals the key roles of G252V and F486P in the neutralization resistance of XBB.1.5, with F486P also enhancing receptor binding. Further, K444T/M and L452R in CH.1.1 and CA.3.1 likely drive escape from class II neutralizing antibodies, whereas R346T and G339H mutations could confer the strong neutralization resistance of these two subvariants to S309-like antibodies. Overall, our results support the need for administration of the bivalent mRNA vaccine and continued surveillance of Omicron subvariants.

7577 Background: HCL is a rare indolent leukemia that is more common in men, with a 4:1 male predominance. To date, no studies have characterized the potential difference in outcomes of HCL between male and female patients. Hence, we sought to evaluate the outcomes of female HCL patients using the HCL-PDR. Methods: The HCL Foundation sponsored the development of HCL-PDR to characterize the clinical features and outcomes of this rare leukemia. HCL-PDR is an international multicenter PDR that includes patient, disease and treatment information abstracted from medical records. Adult patients enrolled in the HCL-PDR were included in the study. Female patients with HCL were the study population, with males as the comparator. The primary endpoint was the time to next treatment (TTNT) in females compared to males. Secondary endpoints included response rates (RR) and predictors of TTNT. Responses were categorized as: complete response (CR) including CR/CRu (CR unconfirmed)/HR (hematologic response), and partial response (PR), which included PR/PRu (PR unconfirmed)/pHR (partial HR). CRu was defined as no disease in bone marrow (BM) without available blood counts and HR as blood counts meeting criteria for HR, but no available BM. Cox proportional hazard models were used to estimate the hazard ratios for TTNT risk. Results: 357 patients were included: 265 males and 92 females. Table shows baseline characteristics stratified by sex. Among the patients who had disease status assessed after first treatment (n=224, males 169 and females 55), there was no significant difference in RR. However, females had significantly longer median TTNT (17.6 years) relative to males (8 years, HR 0.54, 95% CI 0.32-0.91, p=0.02) that remained significant after adjusting for other variables (RR and BRAF mutation) in multivariable analysis (HR 0.32, 95% CI 0.11-0.97, p=0.04). Factors predictive of longer TTNT include female sex and CR (HR.0.26, 95% CI 0.11-0.57, p=0.001). Conclusions: This is the first study to date reporting the clinical characteristics and outcomes in female HCL patients. The significantly longer TTNT in females compared to males may be related to factors such as underlying molecular features or hormonal influences. This finding needs to be explored further. [Table: see text]

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) continues to impact patients globally, especially patients with hematologic malignancies [1-3]. Several studies have demonstrated that patients with hematological malignancies and COVID-19 are at greater risk for mortality [4-6]. Patients with hairy cell leukemia (HCL) in particular are inherently at risk for profound neutropenia and monocytopenia and treatment-associated severe T-cell dysfunction [7, 8]. In conjunction with the myelosuppressive treatment options available for HCL (i.e., nucleoside analogs, cladribine, and pentostatin), patients with active HCL are susceptible to poor outcomes associated with severe infections [9], including COVID-19. The incorporation of targeted agents into active HCL therapy, including BRAF inhibitors (e.g., vemurafenib), Bruton tyrosine kinase inhibitors (e.g., ibrutinib), and anti-CD20 monoclonal antibodies (e.g., rituximab and obinutuzumab), adds another variable of uncertainty as to the immune dysregulation in HCL patients affected with COVID-19. The implications and efficacy of mRNA vaccinations, COVID-19-targeted monoclonal antibody treatments, and antiviral treatments (e.g., remdesivir) are also unknown in patients with HCL. We thus report the experience of 14 HCL patients who contracted SARS-CoV-2 between September 1, 2020, and January 24, 2022, to provide better guidance to treating hematologists. This is a single institution retrospective cohort study that included adult patients with a diagnosis of HCL who tested positive for SARS-CoV-2 during 2020–2022. The study was conducted after approval by the Institution Review Board. Descriptive statistics were used to summarize and present data for this cohort. Of the 14 patients reviewed, the median age at HCL diagnosis was 47 years (Table 1). All but one patient was diagnosed with classical HCL, with only one patient having the variant. The majority of patients were male (n = 10, 71.4%). Eleven (78.6%) patients had received HCL-directed treatment prior to COVID-19 infection, with a median of two lines of prior treatment (range 1–4). In patients not on active HCL treatment the median time since last treatment was 52.6 months (range 5.5–103.4 months). Two patients were on HCL therapy when diagnosed with COVID-19. Of these, one patient treated with both rituximab and ibrutinib discontinued rituximab and remained on ibrutinib. The other continued ibrutinib throughout the COVID-19 infection course. All treated patients had prior purine analog therapy. The most common method of diagnosis of SARS-CoV-2 infection was polymerase chain reaction testing (n = 8, 66.7%), followed by antigen (n = 2, 16.7%) and rapid antigen (n = 2, 16.7%) testing. The median time from onset of symptoms to resolution was 13 days (range 5–32 days), with one patient asymptomatic and three in which duration of symptoms was unknown. The most common symptoms were cough (n = 11, 78.6%), nasal congestion (n = 10, 71.46%), and fatigue (n = 7, 50%). Two patients were hospitalized due to COVID-19, with median length of stay of 4 days (range 3–5 days). Of the two hospitalized patients, one had SARS-CoV-2 antibodies detected several months prior to hospitalization, presumed to be from previous vaccination. The other patient was not vaccinated prior to infection. No patients required intensive care unit level of care, and none died due to complications of COVID-19 infection. Ten (71.4%) patients received treatment, seven (50%) of whom received monoclonal antibodies, and the remaining three received remdesivir (n = 1), Paxlovid (n = 1), and antibiotics (n = 1). No patients were diagnosed with arterial or venous thrombosis during or after active COVID-19 infection, and two patients were put on prophylactic anticoagulation. Regarding vaccination status, only five out of the 14 patients received at least one dose of a vaccine before testing positive for COVID-19. Of these, two received Pfizer and three received Moderna. Six patients received vaccinations after COVID-19 diagnosis. In total, six patients received Moderna (one received one dose, three received two doses, and two received three doses), four received Pfizer (three received two doses and one received three doses), and one received Janssen (two doses). Only four patients underwent spike antibody testing, with two patients having detectable antibodies after the first vaccine but prior to COVID-19 infection, one after COVID-19 diagnosis and before first vaccine, and the last having positive antibodies after both infection and first vaccine (Figure 1). This is a case series describing the treatment and outcomes of HCL patients who contracted COVID-19. It is notable that most patients had relatively mild COVID-19 symptoms, with only two admitted due to infection and no deaths. The majority of patients were able to receive COVID-19-specific treatments such as monoclonal antibodies and Paxlovid, which may have contributed to their recovery. It is interesting that cases were mild even though 64% of patients were unvaccinated at the time they tested positive. As the SARS-CoV-2 virus continues to mutate, patients with hematological malignancies remain at risk for infection. This limited series demonstrates that HCL patients are able to recover from SARS-CoV-2 infection even when unvaccinated. However, patients are still at risk for infections, especially as new variants emerge, and should remain vigilant. As this only describes a group of 14 patients, larger studies are needed to confirm these results. It is also not known what variant was involved in each of these patients, as patients infected with delta variant would be expected to have worse outcomes than those infected with omicron. Providers should continue to encourage vaccination of HCL patients against COVID-19 as well as advocate for continued safety measures, especially for those receiving immunosuppressive treatment. It is notable that no patients in our series were receiving treatment with purine analogs at the time of SARS-CoV-2 infection. The majority of patients in our cohort received COVID-19-directed treatment, which likely improved outcomes. Therefore, physicians should consider early treatment of COVID-19 with the best available therapies in HCL patients. Kaitlin Annunzio and Michael Ozga performed the data collection. Ying Huang analyzed the data. Mirela Anghelina and Jasmine Neal provided patient support. Seema Bhat, James Blachly, Michael Grever, and Kerry Rogers cared for the patients included in this correspondence. Gerard Lozanski contributed essential reagents or tools. Polina Shindiapina designed the research study. All authors participated in the writing of this correspondence. N/A. James Blachly: AbbVie, AstraZeneca, Astellas, MingSight, patent on a leukemia diagnostic device, patent pending on a leukemia classification scheme. Ying Huang: Statistical consulting for AstraZeneca. Kerry Rogers: Research funding Genentech, AbbVie, and Novartis.Consulting AbbVie, Genentech, AstraZeneca, Janssen, Pharmacyclics, LOXO@lilly, and Beigene. Other authors declare they have no conflicts of interest. The authors received no specific funding for this work. This study was reviewed and approved by the Institutional Review Board. Waiver of consent obtained as this was a non-interventional study. Research involved no more than minimal risk to the patients. The authors have confirmed clinical trial registration is not needed for this submission. No material from other sources was used in this correspondence. For original data, please contact [email protected].

(1) Background: COVID-19 vaccination status varies widely among law enforcement and emergency medical services professionals. Though at high risk of exposure, these first responders have demonstrated significant vaccine hesitancy, with only 70% reportedly vaccinated. We sought to understand whether similar vaccine hesitancy exists for first responders and their household contacts around COVID-19 boosters. (2) Methods: In a prospective longitudinal cohort of first responders and their household contacts, survey data was collected, including demographics, medical history, COVID-19 exposure risks, and vaccination and/or booster status. The statistical analysis focused on primary vaccination and booster rates of both the first responders and their household contacts. (3) Results: Across 119 study participants, 73% reported having received some combination of vaccine and/or booster, and 26% were unvaccinated. Vaccinated individuals were older, reported less prior exposure to COVID-19 and had more comorbidities. Only 23% reported having received a COVID-19 booster. Pairing of the data for household contacts demonstrated a 60% agreement to receive primary vaccination but only a 20% agreement for boosters within households. (4) Conclusions: This study provides insight into the vaccination and booster rates of first responders and household contacts. Focused efforts to enhance vaccinations is essential for the protection and maintenance of this critical workforce.

Continued evolution of SARS-CoV-2 has led to the emergence of several new Omicron subvariants, including BQ.1, BQ. 1.1, BA.4.6, BF.7 and BA.2.75.2. Here we examine the neutralization resistance of these subvariants, as well as their ancestral BA.4/5, BA.2.75 and D614G variants, against sera from 3-dose vaccinated health care workers, hospitalized BA.1-wave patients, and BA.5-wave patients. We found enhanced neutralization resistance in all new subvariants, especially the BQ.1 and BQ.1.1 subvariants driven by a key N460K mutation, and to a lesser extent, R346T and K444T mutations, as well as the BA.2.75.2 subvariant driven largely by its F486S mutation. The BQ.1 and BQ.1.1 subvariants also exhibited enhanced fusogenicity and S processing dictated by the N460K mutation. Interestingly, the BA.2.75.2 subvariant saw an enhancement by the F486S mutation and a reduction by the D1199N mutation to its fusogenicity and S processing, resulting in minimal overall change. Molecular modelling revealed the mechanisms of receptor-binding and non-receptor binding monoclonal antibody-mediated immune evasion by R346T, K444T, F486S and D1199N mutations. Altogether, these findings shed light on the concerning evolution of newly emerging SARS-CoV-2 Omicron subvariants.

The continued evolution of SARS-CoV-2 has led to the emergence of several new Omicron subvariants, including BQ.1, BQ.1.1, BA.4.6, BF.7, and BA.2.75.2. Here, we examine the neutralization resistance of these subvariants against sera from 3-dose vaccinated healthcare workers, hospitalized BA.1-wave patients, and BA.4/5-wave patients. We found enhanced neutralization resistance in all new subvariants, especially in the BQ.1 and BQ.1.1 subvariants driven by N460K and K444T mutations, as well as the BA.2.75.2 subvariant driven largely by its F486S mutation. All Omicron subvariants maintained their weakened infectivity in Calu-3 cells, with the F486S mutation driving further diminished titer for the BA.2.75.2 subvariant. Molecular modeling revealed the mechanisms of antibody-mediated immune evasion by R346T, K444T, F486S, and D1199N mutations. Altogether, these findings shed light on the evolution of newly emerging SARS-CoV-2 Omicron subvariants.

Hairy cell leukemia (HCL) is a rare lymphoproliferative disorder, comprising only 2% of all leukemias. The Hairy Cell Leukemia Foundation (HCLF) has developed a patient data registry to enable investigators to better study the clinical features, treatment outcomes, and complications of patients with HCL. This system utilizes a centralized registry architecture. Patients are enrolled at HCL Centers of Excellence (COE) or via a web-based portal. All data are de-identified, which reduces regulatory burden and increases opportunities for data access and re-use. To date, 579 patients have been enrolled in the registry. Efforts are underway to engage additional COE’s to expand access to patients across the globe. This international PDR will enable researchers to study outcomes in HCL in ways not previously possible due to the rarity of the disease and will serve as a platform for future prospective research.

A diagnosis of leukemia can have a profound effect on patients' health-related quality of life (HRQoL), however this has not been measured prospectively in patients with hairy cell leukemia (HCL). At the request of patients living with HCL who had identified this gap in knowledge about the disease, we conducted a longitudinal study of HRQoL among patients enrolled in the HCL Patient Data Registry (PDR). From September 1, 2018 to September 1, 2020, 165 patients were enrolled in the study and completed the baseline survey. The Functional Assessment of Cancer Therapy - Leukemia (FACT-Leu) was used to measure patients' HRQoL. Results show that newly diagnosed HCL patients reported the lowest HRQoL, followed by patients in relapse and those on "watch and wait." Factors associated with higher (better) FACT-Leu total scores in the multivariable analysis included older age, higher social support, and greater physical activity. These same factors were associated with lower levels of fatigue. In rare diseases where it is difficult to perform large prospective studies, patient/researcher collaborations are critical for the identification of studies that are of importance to patients and their families in order to maximize the benefits of the research and improve the lives of patients living with HCL.

Key Points Infections are a major cause of morbidity and mortality in HCL patients, and myelosuppressive therapies increase the risk of poor outcomes. Vemurafenib achieves rapid hematologic improvement in HCL and may facilitate management during life-threatening infection.

The objective of this study was to explore the mechanisms through which water may contribute to the structural integration of the cells and to their mechanical failure at large cellular deformations. To this end, we performed acute substitution of H2O with D2O in THP-1 myeloid leukocytes, then forced them at constant flow rates through filter pores smaller than their average resting diameter and analyzed the resulting fragments by flow cytometry and confocal microscopy. We found that this solvent replacement in culture media maintained the THP-1 cells viability, as shown by maintained plasma membrane integrity and a preserved cell response to a physiological agonist, while increasing their volume and actin polymerization. However, D2O exposure dramatically reduced filterability of cells and amplified their overall fragmentation. At the same time, size distribution of cytoplasmic fragments remained larger in D2O than in water, unlike those derived from the nuclei, which remained unchanged. Our data suggests that water as biological solvent is ‘gluing’ not only on the plasma membrane through hydrophobic effects, but also the cytoplasm, via the reciprocal influence between actin polymerization and the solvent’s molecular network.

Abstract Background: Hairy Cell Leukemia (HCL) is a rare hematological malignancy, comprising only of 2% of all leukemias, with an estimated 900 new cases diagnosed each year in the United States. HCL displays a characteristic immunophenotypic profile that include pan-B cell markers including CD103, CD11c, and CD25. World Health Organization guidelines defines two forms of HCL, classic HCL (cHCL) and variant HCL (HCLv) as two distinct clinical entities. Patients with cHCL have a distinct immunophenotypic profile on their malignant leukemic cells including CD20+, CD19+, CD11c+, CD25+, CD103+, and CD123+, while the leukemic cells from patients with HCLv show CD11c+, CD20+ and CD19+, while lacking CD25 and CD123 expression. Some patients with cHCL will retain CD25 positivity while demonstrating negativity for other typical markers, herein termed atypical HCL (aHCL). Presence or absence of CD25 is an important determinant in classifying patients into cHCL and HCLv. Although it has previously been reported that CD25 expression may be lost during treatment with the targeted agent vemurafenib, we sought to identify whether this immunophenotypic change occurs following other treatment types, including standard purine nucleoside analog therapy and with targeted BTK inhibition. Methods: Adult patients (≥18 years) with a diagnosis of HCL whom had immunophenotype data collected before and after treatment between 2010 and 2018 were included in the study. Immunophenotype and morphological characteristics of initial and follow-up peripheral blood, bone marrow aspirate, and core biopsy specimens were reviewed and correlated with the treatment received. Results: We evaluated 30 HCL patients who underwent different therapies. All available specimens were reviewed and showed morphologic features characteristic for cHCL (n=26, 86.7%), and aHCL (n=4, 13.3%). The median age at HCL diagnosis was 50 years (44-76 years) with male predominance (76%). Patients with aHCL were treated with ibrutinib (n=2) and pentostatin (n=2). Patients with cHCL were treated with pentostatin (n=12), ibrutinib (n=8), vemurafenib (n=4), dabrafenib (n=1), and cladribine (n=1). Bone marrow analyses showed that all the patients had leukemic B-lymphocyte co-expression of CD19, CD20, CD103, CD11c, CD25, and CD123 prior to treatment. Some patients also had a smaller percentage of lymphocytes lacking CD25 expression along with the CD25 positive lymphocytes. Follow-up bone marrow and peripheral blood analysis showed that almost half (n=14, 46%) of treated patients had a partial or complete loss of CD25 expression regardless of the treatment type. Leukemic cells continued to express other HCL signature markers. Conclusion: Our study indicates that during the course of disease some patients display a loss of CD25 expression after therapy. This phenomenon was observed across different therapies and is not specific to the type of treatment. This is the first study to show treatment-dependent CD25 variability with pentostatin, ibrutinib and dabrafenib. Our results advocate for caution when using CD25 for the differential diagnosis of cHCL versus HCLv in treated patients. Future studies are needed in larger patient cohorts to determine the overall role and utility of CD25 in the diagnosis of cHCL and HCLv. Disclosures Lozanski: Genentech: Research Funding; Stem Line: Research Funding; BI: Research Funding; Novartis: Research Funding; Beckman: Research Funding; Coulter: Research Funding. Andritsos:Astra Zeneca: Consultancy; HCLF: Membership on an entity's Board of Directors or advisory committees.

Increasing evidence suggests that asymptomatic carriers are an important source of healthcare-associated Clostridium difficile infection. However, it is not known which test for the detection of C. difficile colonization is most sensitive in patients with haematological malignancies. We performed a prospective cohort study of 101 patients with haematological malignancies who had been admitted to the hospital for scheduled chemotherapy or haematopoietic cell transplantation. Each patient provided a formed stool sample. We compared the performance of five different commercially available assays, using toxigenic culture as the reference method. The prevalence of toxigenic C. difficile colonization as determined by toxigenic culture was 14/101 (14 %). The Cepheid Xpert PCR C. difficile/Epi was the most sensitive test for the detection of toxigenic C. difficile colonization, with 93% sensitivity and 99% negative predictive value. Our findings suggest that the Xpert PCR C. difficile/Epi could be used to rule out toxigenic C. difficile colonization in this population.

Attachment of magnetic particles to cells is needed for a variety of applications but is not always possible or efficient. Simpler and more convenient methods are thus desirable. In this study, we tested the hypothesis that endothelial cells (EC) can be loaded with micron-size magnetic beads by the phagocytosis-like mechanism ‘angiophagy’. To this end, human umbilical vein EC (HUVEC) were incubated with magnetic beads conjugated or not (control) with an anti-VEGF receptor 2 antibody, either in suspension, or in culture followed by re-suspension using trypsinization. In all conditions tested, HUVEC incubation with beads induced their uptake by angiophagy, which was confirmed by (i) increased cell granularity assessed by flow cytometry, and (ii) the presence of an F-actin rich layer around many of the intracellular beads, visualized by confocal microscopy. For confluent cultures, the average number of beads per cell was 4.4 and 4.2, with and without the presence of the anti-VEGFR2 antibody, respectively. However, while the actively dividing cells took up 2.9 unconjugated beads on average, this number increased to 5.2 if binding was mediated by the antibody. Magnetic pulldown increased the cell density of beads-loaded cells in porous electrospun poly-capro-lactone scaffolds by a factor of 4.5 after 5 min, as compared to gravitational settling (p < 0.0001). We demonstrated that EC can be readily loaded by angiophagy with micron-sized beads while attached in monolayer culture, then dispersed in single-cell suspensions for pulldown in porous scaffolds and for other applications.