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6. Assessment of immunological anti‐platelet factor 4 antibodies for vaccine‐induced thrombotic thrombocytopenia (VITT) in a large Australian cohort: A multicenter study comprising 1284 patients

Author

Favaloro, Emmanuel J., Clifford, Joanne, Leitinger, Emma, Parker, Michael, Sung, Pauline, Chunilal, Sanjeev, Tran, Huyen, Kershaw, Geoffrey, Fu, Suki, Passam, Freda, Ahuja, Monica, Ho, Shir Jing, Duncan, Elizabeth, Yacoub, Olivia, Tan, Chee Wee, Kaminskis, Lisa, Modica, Natasha, Pepperell, Dominic, Ballard, Leanne, Clarke, Lisa, Lee, Christine S.M., Gardiner, Elizabeth E., Young‐Ill Choi, Philip, Tohidi‐Esfahani, Ibrahim, Bird, Robert, Brighton, Timothy, and Chen, Vivien M.

Published
2022
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7. A novel flow cytometry procoagulant assay for diagnosis of vaccine-induced immune thrombotic thrombocytopenia

Author

Lee, Christine S.M., Liang, Hai Po Helena, Connor, David E., Dey, Agnibesh, Tohidi-Esfahani, Ibrahim, Campbell, Heather, Whittaker, Shane, Capraro, David, Favaloro, Emmanuel J., Donikian, Dea, Kondo, Mayuko, Hicks, Sarah M., Choi, Philip Y.-I., Gardiner, Elizabeth E., Clarke, Lisa Joanne, Tran, Huyen, Passam, Freda H., Brighton, Timothy Andrew, and Chen, Vivien M.

Published
2022
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12. 3178 – LONGITUDINAL DRUG INCORPORATION, CLONAL COMPOSITION, AND DNA METHYLATION DYNAMICS IN MDS/CMML PATIENTS TREATED WITH AZA

Author

Thoms, Julie, Hampton, Henry, Yan, Feng, Davidson, Sarah, Joshi, Swapna, Sarowar, Chowdhury, Lim, Xin Ying, Nunez, Andrea, Kakadia, Purvi, Saw, Jesslyn, Bhuyan, Golam Sarower, Zou, Xiaoheng, Ghodousi, Elaheh, Jolly, Christopher, Koch, Forrest, Vafaee, Fatemeh, Pickford, Russell, Raftery, Mark, Hough, Sally, Buckland, Griselda, Bailey, Michelle, Ghodke, Yuvaraj, Absar, Noorul, Vaughan, Lachlin, Pasalic, Leonardo, Fong, Chun, Kenealy, Melita, Hiwase, Devendra, Stoddart, Rohanna, Mohammed, Soma, Lee, Linda, Passam, Freda, Spring, Kevin, Skarratt, Kristen, Rebeiro, Patricia, Larsen, Stephen, Presgrave, Peter, Stevenson, William, Ling, Silvia, Tiley, Campbell, Fuller, Stephen, Roncolato, Fernando, Enjeti, Anoop, Hoenemann, Dirk, Lemech, Charlotte, Curtis, David, Bohlander, Stefan, Olivier, Jake, Hertzberg, Mark, Unnikrishnan, Ashwin, Polizotto, Mark, and Pimanda, John

Published
2024
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13. Erratum to ‘Illustrated State-of-the-Art Capsules of the ISTH 2024 Congress’ [Research and Practice in Thrombosis and Haemostasis Volume 8, Issue 4, May 2024, 102432]

Author

Ward, Chris, Curry, Nicola, El-Ekiaby, Magdy, Jurk, Kerstin, Versteeg, Henri H., Keragala, Charithani, Burstyn-Cohen, Tal, Antoniak, Silvio, Suzuki, Yuko, Baker, Ross I., Christophe, Olivier, Revel-Vilk, Shoshana, Hart, Alice, Deppermann, Carsten, Tran, Huyen, Pozzi, Nicola, Kahr, Walter H.A., Grover, Steven P., Wenzel, Philip, Brown, Ashley C., Oury, Cécile, Shea, Susan M., Fredenburgh, James, Passam, Freda H., Winearls, James, Moore, Hunter B., Tole, Soumitra, Merriman, Eileen, Barnes, Geoffrey D., Leonardo Liu, Z., Sholzberg, Michelle, Rivera, José, and Marín-Quilez, Ana

Published
2024
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15. Illustrated State-of-the-Art Capsules of the ISTH 2024 Congress

Author

Ward, Chris, Curry, Nicola, El-Ekiaby, Magdy, Jurk, Kerstin, Versteeg, Henri H., Keragala, Charithani, Burstyn-Cohen, Tal, Antoniak, Silvio, Suzuki, Yuko, Baker, Ross I., Christophe, Olivier, Revel-Vilk, Shoshana, Hart, Alice, Deppermann, Carsten, Tran, Huyen, Pozzi, Nicola, Kahr, Walter H.A., Grover, Steven P., Wenzel, Philip, Brown, Ashley C., Oury, Cécile, Shea, Susan M., Fredenburgh, James, Passam, Freda H., Winearls, James, Moore, Hunter B., Tole, Soumitra, Merriman, Eileen, Barnes, Geoffrey D., Liu, Z. Leonardo, and Sholzberg, Michelle

Published
2024
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17. Thrombo‐inflammatory response in hospitalised patients with COVID‐19: a single institution experience.

Author

Sultan, Muhammad Ahmed, Kong, Yvonne, Story, Chloe, Caterson, Harriet, Dix, Caroline, Gad, Fady, Dhaliwal, Jagpreet Singh, Dunkley, Scott, Jo, Helen, van Hal, Sebastian, and Passam, Freda

Subjects
BIOMARKERS, PARTIAL thromboplastin time, C-reactive protein, INTENSIVE care units, COVID-19, VEINS, BLOOD coagulation tests, INFLAMMATION, ANTI-inflammatory agents, ANTICOAGULANTS, RETROSPECTIVE studies, ACQUISITION of data, NEUTROPHILS, COMPARATIVE studies, HOSPITAL care, THROMBOEMBOLISM, MEDICAL records, ELECTRONIC health records, LONGITUDINAL method
Abstract

Background: Severe COVID‐19 causes acute inflammation, which is complicated by venous thromboembolism events (VTE). However, it is unclear if VTE risk has evolved over time since the COVID‐19 outbreak. Aims: To determine markers of thrombo‐inflammation and rates of symptomatic VTE in patients hospitalised for COVID‐19 in a metropolitan hospital in Sydney, Australia. Methods: A retrospective, single‐centre, cohort study was performed by reviewing electronic medical records of consecutive patients admitted to Royal Prince Alfred Hospital between March 2020 and September 2021. This period included three waves of COVID‐19 outbreaks in Australia with the ancestral, alpha and delta variants. Standard coagulation assays and inflammatory markers were recorded over 4 weeks. Results: A total of 205 patients were consecutively admitted during the study period. Activated partial thromboplastin time, neutrophil count and C‐reactive protein (CRP) were significantly increased in patients hospitalised in the intensive care unit (ICU) compared with non‐ICU patients. The use of anti‐inflammatory medication increased in 2021 compared with 2020. The mortality rate was 7.3% in our cohort. Ninety‐four per cent of patients received anticoagulation with 6.3% of patients developing VTE. Conclusion: We observed lower rates of VTE compared to the internationally reported rate for the same period. We conclude that in the setting of controlled hospital admission rate and standard anticoagulation guidelines, COVID‐19 resulted in similar thrombo‐inflammatory response and VTE rates over the first 1.5 years of the pandemic. [ABSTRACT FROM AUTHOR]

Published
2024
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18. Sex, Endothelial Cell Functions, and Peripheral Artery Disease.

Author

Cartland, Siân P., Stanley, Christopher P., Bursill, Christina, Passam, Freda, Figtree, Gemma A., Patel, Sanjay, Loa, Jacky, Golledge, Jonathan, Robinson, David A., Aitken, Sarah J., and Kavurma, Mary M.

Subjects
PERIPHERAL vascular diseases, CELL physiology, ENDOTHELIAL cells, GENDER differences (Psychology), INDIVIDUALIZED medicine
Abstract

Peripheral artery disease (PAD) is caused by blocked arteries due to atherosclerosis and/or thrombosis which reduce blood flow to the lower limbs. It results in major morbidity, including ischemic limb, claudication, and amputation, with patients also suffering a heightened risk of heart attack, stroke, and death. Recent studies suggest women have a higher prevalence of PAD than men, and with worse outcomes after intervention. In addition to a potential unconscious bias faced by women with PAD in the health system, with underdiagnosis, and lower rates of guideline-based therapy, fundamental biological differences between men and women may be important. In this review, we highlight sexual dimorphisms in endothelial cell functions and how they may impact PAD pathophysiology in women. Understanding sex-specific mechanisms in PAD is essential for the development of new therapies and personalized care for patients with PAD. [ABSTRACT FROM AUTHOR]

Published
2023
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19. Movable typing of full‐lumen personalized Vein‐Chips to model cerebral venous sinus thrombosis.

Author

Zhao, Yunduo Charles, Zhang, Yingqi, Nasser, Arian, Hong, Tianbo, Wang, Zihao, Sun, Allan, Moldovan, Laura, Edwards, Leon S, Passam, Freda, Butcher, Ken S, Ang, Timothy, and Ju, Lining Arnold

Subjects
SINUS thrombosis, VENOUS thrombosis, CRANIAL sinuses, ENDOTHELIUM diseases, IDIOPATHIC thrombocytopenic purpura
Abstract

Cerebral venous sinus thrombosis (CVST) is a type of stroke associated with COVID‐19 vaccine‐induced immune thrombotic thrombocytopenia. The precise etiology of CVST often remains elusive due to the highly heterogeneous nature of its governing mechanisms, specifically, Virchow's triad that involves altered blood flow, endothelial dysfunction, and hypercoagulability, which varies substantially amongst individuals. Existing diagnostic and monitoring approaches lack the capability to reflect the combination of these patient‐specific thrombotic determinants. In response to this challenge, we introduce a Vein‐Chip platform that recapitulates the CVST vascular anatomy from magnetic resonance venography and the associated hemodynamic flow profile using the "Chinese Movable Type‐like" soft stereolithography technique. The resultant full‐lumen personalized Vein‐Chips, functionalized with endothelial cells, enable in‐vitro thrombosis assays that can elucidate distinct thrombogenic scenarios between normal vascular conditions and those of endothelial dysfunction. The former displayed minimal platelet aggregation and negligible fibrin deposition, while the latter presented significant fibrin extrusion from platelet aggregations. The low‐cost movable typing technique further enhances the potential for commercialization and broader utilization of personalized Vein‐Chips in surgical labs and at‐home monitoring. Future research and development in this direction will pave the way for improved management and prevention of CVST, ultimately benefiting both patients and healthcare systems. [ABSTRACT FROM AUTHOR]

Published
2023
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21. Microvasculature‐on‐a‐Post Chip That Recapitulates Prothrombotic Vascular Geometries and 3D Flow Disturbance.

Author

Zhang, Yingqi, Aye, San‐Seint‐Seint, Cheng, Vivian, Nasser, Arian, Hong, Tianbo, Vatankhah, Parham, Jiang, Fengtao, Zhao, Yunduo Charles, Moldovan, Laura, Sun, Allan, Dupuy, Alexander, Wang, Yao, Li, Zhiyong, Ang, Timothy, Passam, Freda, Yong, Ken‐Tye, and Ju, Lining Arnold

Subjects
MICROFLUIDICS, ENDOTHELIAL cells, CARDIOVASCULAR diseases risk factors, GEOMETRY, HEMODYNAMICS, THROMBOSIS
Abstract

Stenosis, characterized by partial vessel narrowing, alters blood hemodynamics and can lead to unpredictable thrombosis. Existing models struggle to accurately represent the complex vascular geometries and hemodynamics involved in such conditions. To address this challenge, a microvasculature‐on‐a‐post chip is developed to mimic partially stenotic vascular geometries and thrombogenicity, featuring isolated 3D micropost structures with variable sizes that recreate disturbed flow profiles. To emulate the diseased vessel wall, the post microfluidics are vascularized with a confluent layer of endothelial cells. Subsequently, human blood is perfused through the endothelialized post microfluidics, observing the temporal and spatial thrombotic response governed by Virchow's triad, including vessel wall injury, hemodynamic disturbance, and hypercoagulability. The innovative model offers valuable insights into stenosis‐induced thrombosis and endothelial behavior, paving the way for improved assessment of thrombotic risks associated with stenotic vessels. This advanced microfluidic platform also offers new approaches for evaluation of prothrombotic phenotypes and cardiovascular risk assessment in the future. [ABSTRACT FROM AUTHOR]

Published
2023
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23. Novel Movable Typing for Personalized Vein‐Chips in Large Scale: Recapitulate Patient‐Specific Virchow's Triad and its Contribution to Cerebral Venous Sinus Thrombosis.

Author

Zhao, Yunduo Charles, Zhang, Yingqi, Wang, Zihao, Jiang, Fengtao, Kyanian, Kiarash, Aye, San‐Seint‐Seint, Hong, Tianbo, Vatankhah, Parham, Nasser, Arian, Sun, Allan, Moldovan, Laura, Su, Qian P., Cho, Ann‐Na, Wang, Yao, Passam, Freda, Ang, Timothy, and Ju, Lining Arnold

Subjects
SINUS thrombosis, VENOUS thrombosis, CRANIAL sinuses, FIBRIN, SHEARING force
Abstract

The Vein‐Chip recapitulates CVST Virchow's triad and enables systematic characterization of venous thrombogenesis with respect to fibrin formation and platelet aggregation. Distinct from the arterial setting, platelets universally adhere across the entire CVS Vein‐Chip independent of stenotic geometry and flow disturbance. Intriguingly, fibrin propagates along with the flow direction, but exclusively deposits to the inner vessel wall. Upon inflammatory endothelial injury, fibrin deposition mirrors to the outer vessel wall, but still not in the lumen. Together, the Vein‐Chip promises future applications for personalized thrombotic assessment and monitoring. [ABSTRACT FROM AUTHOR]

Published
2023
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24. In Vivo Drug Incorporation and Intracellular Dynamics of Injectable Versus Oral Azacytidine: A Phase II Open Label Multicentre Trial

Author

Pimanda, John E., Thoms, Julie A.I., Hampton, Henry R., Davidson, Sarah, Joshi, Swapna, Sarowar, Chowdhury H., Lim, Xin Ying, Nunez, Andrea C., Kakadia, Purvi M., Pickford, Russell, Raftery, Mark, Hough, Sally, Buckland, Griselda, Bailey, Michelle, Ghodke, Yuvaraj, Absar, Noorul, Vaughan, Lachlin, Pasalic, Leonardo, Fong, Chun Yew, Kenealy, Melita, Hiwase, Devendra, Stoddart, Rohanna, Mohammed, Soma, Lee, Linda, Passam, Freda H., Spring, Kevin, Skarratt, Kristy K., Rebeiro, Patricia, Larsen, Stephen R, Presgrave, Peter, Stevenson, William S, Ling, Silvia, Tiley, Campbell, Fuller, Stephen, Roncolato, Fernando, Enjeti, Anoop Kumar, Hoenemann, Dirk, Lemech, Charlotte, Bohlander, Stefan K., Olivier, Jake, Hertzberg, Mark, Unnikrishnan, Ashwin, and Polizzotto, Mark N.

Published
2022
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30. Protein disulfide isomerase inhibitors constitute a new class of antithrombotic agents

Author

Jasuja, Reema, Passam, Freda H., Kennedy, Daniel R., Kim, Sarah H., van Hessem, Lotte, Lin, Lin, Bowley, Sheryl R., Joshi, Sucharit S., Dilks, James R., Furie, Bruce, Furie, Barbara C., and Flaumenhaft, Robert

Subjects
Enzyme inhibitors -- Identification and classification, Thrombolytic drugs -- Identification and classification, Health care industry
Abstract

Thrombosis, or blood clot formation, and its sequelae remain a leading cause of morbidity and mortality, and recurrent thrombosis is common despite current optimal therapy. Protein disulfide isomerase (PDI) is an oxidoreductase that has recently been shown to participate in thrombus formation. While currently avail-able antithrombotic agents inhibit either platelet aggregation or fibrin generation, inhibition of secreted PDI blocks the earliest stages of thrombus formation, suppressing both pathways. Here, we explored extracellular PDI as an alternative target of antithrombotic therapy. A high-throughput screen identified quercetin-3-rutinoside as an inhibitor of PDI reductase activity in vitro. Inhibition of PDI was selective, as quercetin-3-rutinoside failed to inhibit the reductase activity of several other thiol isomerases found in the vasculature. Cellular assays showed that quercetin-3-rutinoside inhibited aggregation of human and mouse platelets and endothelial cell-mediated fibrin generation in human endothelial cells. Using intravital microscopy in mice, we demonstrated that quercetin-3-rutinoside blocks thrombus formation in vivo by inhibiting PDI. Infusion of recombinant PDI reversed the antithrombotic effect of quercetin-3-rutinoside. Thus, PDI is a viable target for small molecule inhibition of thrombus formation, and its inhibition may prove to be a useful adjunct in refractory thrombotic diseases that are not controlled with conventional antithrombotic agents., Introduction Protein disulfide isomerase (PDI) is the prototypical member of an extended family of oxidoreductases, best known as endoplasmic reticulum-resident enzymes. These enzymes catalyze posttranslational disulfide bond formation and exchange [...]

Published
2012
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32. Monocyte tissue factor-dependent activation of coagulation in hypercholesterolemic mice and monkeys is inhibited by simvastatin

Author

Owens, III, A. Phillip, Passam, Freda H., Antoniak, Silvio, Marshall, Stephanie M., McDaniel, Allison L., Rudel, Lawrence, Williams, Julie C., Hubbard, Brian K., Dutton, Julie-Ann, Wang, Jianguo, Tobias, Peter S., Curtiss, Linda K., Daugherty, Alan, Kirchhofer, Daniel, Luyendyk, James P., Moriarty, Patrick M., Nagarajan, Shanmugam, Furie, Barbara C., Furie, Bruce, Johns, Douglas G., Temel, Ryan E., and Mackman, Nigel

Subjects
Simvastatin -- Usage -- Health aspects, Coronary heart disease -- Risk factors -- Health aspects -- Research, Monocytes -- Physiological aspects -- Research, Hypercholesterolemia -- Risk factors -- Drug therapy -- Research, Health care industry
Abstract

Hypercholesterolemia is a major risk factor for atherosclerosis. It also is associated with platelet hyperactivity, which increases morbidity and mortality from cardiovascular disease. However, the mechanisms by which hypercholesterolemia produces a procoagulant state remain undefined. Atherosclerosis is associated with accumulation of oxidized lipoproteins within atherosclerotic lesions. Small quantities of oxidized lipoproteins are also present in the circulation of patients with coronary artery disease. We therefore hypothesized that hypercholesterolemia leads to elevated levels of oxidized LDL (oxLDL) in plasma and that this induces expression of the procoagulant protein tissue factor (TF) in monocytes. In support of this hypothesis, we report here that oxLDL induced TF expression in human monocytic cells and monocytes. In addition, patients with familial hypercholesterolemia had elevated levels of plasma microparticle (MP) TF activity. Furthermore, a high-fat diet induced a time-dependent increase in plasma MP TF activity and activation of coagulation in both LDL receptor-deficient mice and African green monkeys. Genetic deficiency of TF in bone marrow cells reduced coagulation in hypercholesterolemic mice, consistent with a major role for monocyte-derived TF in the activation of coagulation. Similarly, a deficiency of either TLR4 or TLR6 reduced levels of MP TF activity. Simvastatin treatment of hypercholesterolemic mice and monkeys reduced oxLDL, monocyte TF expression, MP TF activity, activation of coagulation, and inflammation, without affecting total cholesterol levels. Our results suggest that the prothrombotic state associated with hypercholesterolemia is caused by oxLDL-mediated induction of TF expression in monocytes via engagement of a TLR4/TLR6 complex., Introduction Hypercholesterolemia describes the presence of increased lipids in blood that is caused either by a predisposed genetic condition, such as a mutation of the LDL receptor (LDLR), or by [...]

Published
2012
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35. Diffuse alveolar haemorrhage as a rare complication of antiphospholipid syndrome.

Author

Seth, Ishith, Bhagavata Srinivasan, Shyam Prakaash, Bulloch, Gabriella, Yi, Dong Seok, Frankel, Anthony, Hsu, Kelvin, Passam, Freda, Garsia, Roger, and Corte, Tamera J.

Subjects
HEMORRHAGE, ANTIPHOSPHOLIPID syndrome, PHOSPHOLIPID antibodies, DEATH rate, RITUXIMAB, EARLY diagnosis
Abstract

Diffuse alveolar haemorrhage (DAH) is a rare complication of antiphospholipid syndrome. With a mortality rate of 46%, early diagnosis and management remain an ongoing challenge. Case reports are limited, and management guidelines are not yet definitive. In this case report, we present a 43‐year‐old male with DAH who required high‐dose oral steroids, intravenous methylprednisolone cyclophosphamide and rituximab over 18 months to control life‐threatening episodes of pulmonary bleeding. [ABSTRACT FROM AUTHOR]

Published
2022
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43. Determining the Rate of Anti-PF4 Antibody Positive Results in Patients Presenting with Venous Thrombosis but a Normal Platelet Count Following ChAdOx1 Ncov-19 Astrazeneca Vaccination: An Australian Combined State Testing Centre Experience

Author

Leitinger, Emma J, Clifford, Joanne, Parker, Michael, Iacobelli, Amanda, Sung, Pauline, Chen, Vivien, Brighton, Timothy A., Lee, Christine Shu Mei, Clarke, Lisa, Malan, Erica, Kershaw, Geoffrey, Shadood, Noor, Passam, Freda H., Favaloro, Emmanuel J, Tran, Huyen A, and Chunilal, Sanjeev D

Published
2021
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46. Front Cover: Movable typing of full‐lumen personalized Vein‐Chips to model cerebral venous sinus thrombosis.

Author

Zhao, Yunduo Charles, Zhang, Yingqi, Nasser, Arian, Hong, Tianbo, Wang, Zihao, Sun, Allan, Moldovan, Laura, Edwards, Leon S, Passam, Freda, Butcher, Ken S, Ang, Timothy, and Ju, Lining Arnold

Subjects
SINUS thrombosis, CRANIAL sinuses, VENOUS thrombosis, ENDOTHELIUM diseases, OCCLUSION (Chemistry), BLOOD flow
Abstract

Researchers Zhao et al. have developed a patient-specific Vein-Chip inspired by traditional Chinese Movable Typing. This innovative platform utilizes injection soft-lithography and assembly techniques to create a cost-efficient tool for analyzing cerebral venous sinus thrombosis. The Vein-Chips have the potential to serve as pre-clinical diagnostic tools, allowing for a thorough assessment of personalized Virchow's triad, which includes hyper-coagulation, altered blood flow, and endothelial dysfunction. The study was conducted by a diverse team of authors and provides valuable insights into the field of personalized medicine. [Extracted from the article]

Published
2023
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47. In Vivo Assessment of Intracellular Dynamics Comparing Injection Versus Oral Azacitidine in a Phase IIb Investigator Initiated Clinical Trial

Author

Unnikrishnan, Ashwin, Lim, Xin Ying, Joshi, Swapna, Nunez, Andrea C., Vaughan, Lachlin, Pickford, Russell, Hough, Sally, Davidson, Sarah, Fong, Chun, Kenealy, Melita, Hiwase, Devendra K, Pasalic, Leonardo, Mohammed, Soma, Lee, Linda, Passam, Freda H., Spring, Kevin, Rebeiro, Patricia, Ling, Silvia, Fuller, Stephen, Presgrave, Peter, Roncolato, Fernando, Larsen, Stephen, Enjeti, Anoop K, Stevenson, William S., Tiley, Campbell, Campbell, Peter J, Lemech, Charlotte, Olivier, Jake, Hertzberg, Mark, Polizzotto, Mark N., and Pimanda, John

Published
2019
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49. Histological expression of angiogenic factors: VEGF, PDGFR alpha, and HIF-1 alpha in Hodgkin lymphoma

Author

Passam, Freda H. Alexandrakis, Michael G. Kafousi, Maria and Fotinou, Marianthi Darivianaki, Katerina Tsirakis, George and Roussou, Paraskevi A. Stathopoulos, Efstathios N. Siafakas, Nikolaos M.

Abstract

Angiogenesis is a prerequisite for solid tumor growth, but there is relatively limited data regarding Hodgkin lymphoma. The purpose of this study was to examine the immunohistochemical expression of angiogenic and proliferation markers in Hodgkin biopsies in relation to clinical parameters. Immunostaining was performed on 65 Hodgkin biopsies with vascular endothelial growth factor (VEGF), hypoxia inducible factor-1 alpha (HIF-1 alpha), platelet-derived growth factor receptor alpha (PDGFR alpha), Ki-67, and p53. Microvessel density (MVD) was determined by CD31 staining. In all cases, neoplastic cells and reactive background cells were evaluated. The neoplastic population expressed VEGF in 48% of the cases, HIF-1 alpha in 54% of the cases, and PDGFR alpha in 95% of the cases. Both Ki-67 and p53 were positive in neoplastic cells in over 60% of the cases. The MVD had a median of 2.6/0.0625 mm(2) which was not different from normal lymph nodes. VEGF in the non-neoplastic compartment showed increased staining in Ann Arbor stage I-II versus III-IV. In conclusion, VEGF, HIF-1 alpha, and predominantly PDGFRa are expressed in neoplastic cells in the majority of Hodgkin lymphomas. As microvessel formation is not increased in Hodgkin, additional functions of these angiogenic molecules should be investigated. (C) 2008 Elsevier GmbH. All rights reserved.

Published
2009

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