Transplantation Immunology and Tolerance Induction, Bone Marrow Chimerism, Innate and Adaptive Immunity, and Lung Cancer
Congratulations to Dr. Colson, recipient of the 2006 Johnson & Johnson Young Clinician Research award. Read more about her Special Study Award for lung cancer research here.
Research Profile
Dr. Colson's primary research focus centers on the understanding of the immune system as it relates to 1) the induction of transplantation tolerance for lung allografts, 2) the roles of adaptive and innate immunity in the development of chronic rejection in lung transplant recipients, and 3) the targeting of lung cancer using minimally invasive approaches.
Induction of transplantation tolerance
Induction of transplantation tolerance: Engraftment of both donor and recipient hematopoietic stem cells (SC) results in mixed bone marrow (BM) chimerism, induces donor-specific tolerance for allogeneic and xenogeneic solid organ grafts, preserves recipient immunocompetence, and is not associated with chronic rejection. We have been extensively involved in the characterization of a rare BM-derived cell population known as the facilitating cell (FC), that “facilitates” engraftment of highly purified murine SC in completely MHC-disparate recipients and induce transplantation tolerance without evidence of graft vs. host disease. Our laboratory has identified a novel member of the T cell receptor β (TCRβ) heterodimer family. The TCRβ-FCp33 receptor has been shown to be responsible for the unique properties of allogeneic SC facilitation and donor-specific tolerance induction exhibited by the FC in vivo. Isolation, purification, and characterization of this FCp33 receptor and the signaling pathways utilized for tolerance induction form a major research focus of the current NIH funded laboratory. Recent studies have demonstrated that FC-mediated SC alloengraftment results from the invivo induction of a regulatory T cell network. Understanding the mechanism by which FC induce regulatory T cells in vivo is a current area of intense interest.
Roles of Adaptive and Innate Immunity in Chronic Rejection
Compared with the other conventional solid organ allografts, lung transplant patients have the worst outcome, the most rejections, more graft infections and the most aggressive and lethal form of chronic rejection, known as bronchiolitis obliterans syndrome (BOS). As a result, less than half of all lung transplant patients survive more than 5 years. Why? It is our hypothesis that these outcomes are a result of unique demands involved in transplanting an organ that is environmentally exposed and continually immune challenged, such as the lung, into an immunocompromised patient. Unlike the more successful cardiac, liver and renal solid organ transplants, the transplanted lung is inherently exposed to the environment and infectious agents, both by the transplantation of pathogens contained in the donor lung and the continual exposure to new pathogens. Both the T cells of the adaptive immune system and the alveolar macrophages of the innate immune system play critical roles in cellular host defenses in the normal lung. The contributions of innate immune stimulation, common in an infection-prone organ such as the lung, are being investigated in the setting of an immunocompromised adaptive response as is present following lung transplantation. Identification of post-transplant kinetic changes within the immune system of the transplanted lung and a profile of the innate immune response during rejection and infection are the focus of this project, with the aim of identifying predictors and potential treatments of BOS.
Targeting of Lung Cancer Using Minimally Invasive Approaches
Lung Cancer is the number one cancer killer of both men and women. Surgical resection offers the best hope for cure, yet an estimated 9% to 16% of patients will have a local recurrence. Higher recurrence rates are associated with more localized resections, often performed in patients with limited lung function. The current therapy for tumor recurrence is re-resection but due to tumor location and patient morbidity, only 1/3 of these recurrences can be resected. The goal of this project, is to design a delivery device to distribute anti-neoplastic agents at the surgical resection line in order to prevent local recurrence. We currently have manufactured drug eluting microspheres with reagents targeted against non small cell lung cancer and mesothelioma.
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Ongoing Research Projects
Pre-Clinical Study of Drug Delivery Microsphere Incorporation at Surgical Resection Margins
(CIMIT/Johnson and Johnson, PI: Yolonda Colson, M.D., PhD.)
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Lung Cancer is the number one cause of cancer deaths in both men and women. Despite what appears to be successful surgical resection, tumor recurrence at the site of the prior surgery (i.e. surgical resection margins) occurs in an estimated 9% to 16% of patients 1,2 . Higher recurrence rates are associated with more localized resections and therefore most patients with even small surgically resections tumors have ~1/2 of an entire lung removed, thus sacrificing a large amount of "good" lung in order to decrease the risk of recurrence. The current therapy for tumor recurrence is re-resection. However, due to tumor location and patient morbidity, only 1/3 of these recurrences can be resected, and the majority of the remaining patients die as a consequence of their recurrent disease. The overall objective of this study is to design a practical delivery platform and perform a preclinical study to assess the safety and feasibility invivo of the local delivery of anti-neoplastic agents (chemotherapeutic drugs that inhibit the growth of malignant cells) by microsphere incorporation at surgical resection margins using a minimally invasive surgical approach in a large animal model.
1. Jemal, Ahmedin et al. Cancer statistics, Cancer J Clin 2004; 54:8-29
2. Landreneau, RJ, Sugarbaker, DJ et al. Wedge resection versus lobectomy for stage 1 (TINOMO) non-small cell lung cancer. JTCVS. 1997, 691-699 |
Mechanism of Facilitating Cell-Mediated Tx Tolerance
(NIH, 1 R01 HL074150-01, PI: Yolonda L. Colson, M.D., Ph.D.)
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1. FCp33 Signaling And The Mechanism Of Allogeneic Stem Cell Facilitation.
The incidence and severity of graft vs. host disease (GVHD) is directly related to the degree of antigenic disparity between donor and recipient and is attributed to donor T cells in the BM inoculum. Clinical trials depleting these primary GVHD effector cells, although successful in reducing GVHD, resulted in concurrent rise in the incidence of engraftment failure. A rare donor BM-derived cell population called the facilitating cell (FC) is necessary and sufficient to permit engraftment of purified murine SC in completely MHC-disparate recipients, without GVHD. In vivo experiments demonstrated that mice deficient in T-cell receptor beta chain (TCRβ) and Fc receptor gamma chain (FcRy) expression, fail to facilitate engraftment of purified allogeneic SC. We have shown that the dependence of TCRβ in FC-mediated SC engraftment and transplantation tolerance is associated with the functional expression of a unique TCRβ-FCp33 heterodimer that co-precipitates with FcRy - suggesting that FC function is in part dependent on a non-conventional TCRβ-FcRy signaling pathway. Our goal is to elucidate the signaling mechanisms associated with FC function in vivo.
Schuchert, M. J.,Wright, R. D., Colson, Y. L. Characterization of a newly discovered T-cell receptor beta-chain heterodimer expressed on a CD8+ bone marrow subpopulation that promotes allogeneic stem cell engraftment. Nat Med. Volume 6 (8); 904-9.
Taylor, K. Shinde-Patil, V. Colson, Y.L. Reconstitution of Allegeneic Hematopoietic Stem Cells: The essential role of FcRg and the TCRb-RCp33 comples. (Submitted)
2. The Induction of Regulatory T cells After FC Transplantation Results in Long Term Survival.
(Principal Investigator, George H.A. Clowes, JR. MD, FACS, Memorial Research Career Development Award, American College of Surgeons, The Mechanism of Facilitating Cell Induced Regulatory T Cell Networks.)
Engraftment of purified allogeneic hematopoietic stem cells (HSC) has been increased in various BMT models by including donor BM-derived CD8+/αβγδTCR- facilitating cells (FC). We have demonstrated through an aggressive semiallogeneic parent → F1 model of GVHD that recipients of donor HSC+FC inocula did not exhibit significant clinical or histologic evidence of GVHD. We have now demonstrated similar findings and show the same in a fully allogeneic model despite the presence of both class I and class II MHC disparities. HSC+FC recipients are characterized by increased numbers of CD4+25+ Tregs in spleen and BM with splenocyte expression of TGFβ the regulatory T cell genes CTLA4, GITR and FoxP3+. These findings suggest that the FC, which express a unique FCp33-TCRβ heterodimer in place of αβTCR, mediates HSC alloengraftment, induces donor-specific tolerance without GVHD in fully allogeneic SC+FC recipients as a result of the induction of functional regulatory T cells in vivo. These findings are the first description of a naïve cell population able to induce tregs in vivo as a means to extablish transplantation tolerance. It is our goal to further understand this mechanism of FC-mediated alloengraftment in order to develop clinically relevant tolerance incutsion strategies in the future.
Colson, Y. L., Christopher, K., Glickman, J., Taylor, K. N., Wright, R., Perkins, D. Absence of clinical GVHD and the in vivo induction of regulatory T cells after transplantation of facilitating cells. Blood. 104 (12); 3829-35.
Shinde-Patil, V. Taylor, KN. Glickman JN. Liang Y. Khatri A. Colson Y.L. In Vivo Induction of Regulatory T-cells Following Allotransplantation of a Unique Bone-Marrow Derived Facilitating Cell Population. (Submitted). |
Local Incorporation of Neoplastic Agents Into Surgical Resection Margins Using A Minimally Invasive Delivery System (Principal Investigator, CIMIT Proof of Principle Grant, Local Incorporation of Anti-Neoplastic Agents Into Surgical Resection Margins using a Minimally Invasive Delivery System)
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Lung Cancer, the most lethal of all cancers, shows recurrence at surgical resection margins (the boundary where tissue is removed) in an estimated 9% to 16% of patients. Higher recurrence rates are associated with more localized resections. The current therapy for tumor recurrence is re-resection. However, due to tumor location and patient morbidity, only 1/3 of these recurrences can be resected. The goal of this project, is to design a delivery device to distribute anti-neoplastic agents (drugs or chemicals that inhibit the growth of malignant cells) at resection lines in order to prevent local recurrence. To date, as part of our initial “New Concept CIMIT Award”, bioabsorbable poly D,L-lactide-co-glycolide (PLGA) microspheres have been loaded with Paclitaxel, an effective anti-tumor drug in lung cancer. These microspheres have been examined for size and porosity (figure 1), and have demonstrated effective anti-tumor activity in in vitro cell proliferation assays.
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Figure 1: SEM of chemotherapy loaded microspheres. Microspheres loaded with Paclitaxel, a highly effective chemotherapy agent, have been synthesized in our lab. | In addition, other agents have been shown to permit microsphere adherence to lung tissue under dynamic flow conditions. Preliminary findings suggest that drug delivery microspheres could be used in combination with an adherent gel system to promote the prevention of local cancer cell growth on the lung. We currently are working to extend these results with the design of a prototype device for the delivery of anti-neoplastic activity in vivo. |
Assessment of Innate Immune Activation & Toll-like Receptor Function Within Lung Transplant Patients
(International Society for Heart & Lung Transplantation, Fellowship Award, PI: Kendra N. Taylor, Ph.D. / Yolonda L. Colson, M.D., Ph.D.)
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Lung transplantation is currently the only available option for end-stage lung disease once limited medical therapy has failed. Despite the significant clinical improvements that have resulted in the performance of over 15,000 lung transplants in the world to date, long-term survival and quality of life for lung allografts has not reached the levels enjoyed by recipients of other solid organ transplants. Attempts to decrease rejection with additional immunosuppression have been met with marked increases in infectious complications that are often fatal. Despite progress in the areas of acute rejection and infection, the major obstacle to long-term success in Lung Transplantation remains unchanged as patients develop evidence of bronchiolitis obliterans syndrome (BOS). Studies suggest that the risk is increased with repeated episodes of graft injury, either as acute rejection or infections, particularly with viral pathogens The first line of cellular host defense in the normal lung is the epithelial surface of the airway and the alveolar macrophages (AM). The innate macrophage requires “recognition” of microbes by a family of cell surface receptors referred to as Toll-like receptors or TLRs. The activated macrophage releases several immune factors that can recruit other non-antigen specific (i.e. innate) immune cells, such as neutrophils, natural killer cells, dendritic cells and eosinophils that can effectively remove the “invader”. It is our hypothesis that the likely continuous activation of alveolar macrophage of the innate immune system by exogeneous stimuli encountered by the transplanted lung is critical to the development of BOS. The goal of this project is to explore the relationship between TLR expression on alveolar macrophage within the allograft, the resultant cytokines induced and the development of BOS. |
Past Research -- Last 3 Years
Facilitating Cell Induced Tolerance in Organ Transplants
(NIH-NIAID, R29 AI40933 Year 1-5, PI: Yolonda L. Colson, M.D., Ph.D., 4/1/97-3/31/02)
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The major goals of this project are: 1) Characterize the CD3 associated molecules (CD3AMs) present on the facilitating cell (FC) population and determine if CD3AM expression is independent of the T cell receptor; 2) Determine the mechanistic role of CD3AM on the ability of the FC population to facilitate engraftment of the allogeneic stem cell (SC); and 3) Identify the mechanism by which the FC facilitates SC survival. |
Nonablative Approaches to Chimerism - Induced Transplantation Tolerance
(American Association for Thoracic Surgery, Second Alton Ochsner Research Scholarship, PI: Yolonda L. Colson, M.D., Ph.D., 7/1/02-6/30/04)
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The major goals of this project are: 1) Identify the recipient factors that constitute a competitive disadvantage to the donor SC in nonmyeloblated environment and 2) Determine whether the donor FC confers the competitive advantage to the donor SC in a nonablated host. |
Identifying the Tumor Stem Cell in Malignant Mesothelioma
(The Thoracic Surgery Foundation for Research and Education, Research Award / Grant, PI: Yolonda L. Colson, M.D., Ph.D., 7/1/02-6/30/04)
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The major goal is to identify and characterize the tumor stem cell of human malignant mesothelioma. |
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Funding
Present
Past (Last 3 Years)
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Selected Publications
For the latest articles by Dr. Yolonda Colson, please visit 
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1. Markus BH, Colson YL, Fung JJ, Zeevi A, Duquesnoy RJ. HLA antigen expression on cultured human arterial endothelial cells. Tissue Antigens 1988; 32:241-253.
2. Zerbe TR, Kaufman C, Colson Y, Duquesnoy R. Associations of HLA-A, B, DR antigens with primary disease in cardiac allograft recipients. Am J Cardiol 1988; 61:1359-1361.
3. Colson YL, Markus BH, Zeevi A, Duquesnoy RJ. Adherence of alloreactive lymphocytes to human arterial endothelial cell monolayers. Clin Exp Immunol 1989; 77:206-210.
4. Colson YL, Markus BH, Zeevi A, Duquesnoy RJ. Increased lymphocyte adherence to human arterial endothelial cell monolayers in the context of allorecognition. J Immunol 1990; 144:2975-2984.
5. Colson YL, Carty SE. Medullary thyroid carcinoma. Am J Otolaryngol 1993; 14:73-81.
6. Colson YL, Cooper MH, Ildstad ST. Cross species bone marrow transplantation: an approach to donor-specific transplantation tolerance for xenografts. Transplant Sci 1993; 3:61-65.
7. Kaufman CL, Colson YL, Wren SM, Watkins S, Simmons RL, Ildstad ST. Phenotypic characterization of a novel bone marrow-derived cell that facilitates engraftment of allogeneic bone marrow stem cells. Blood 1994; 84:2436-2446.
8. Colson YL, Wren SM, Schuchert MJ, Patrene KD, Johnson PC, Boggs SS, Ildstad ST. A nonlethal conditioning approach to achieve durable multilineage mixed chimerism and tolerance across major, minor, and hematopoietic histocompatibility barriers. J Immunol 1995; 155:4179-4188.
9. Colson YL, Zadach K, Nalesnik M, Ildstad ST. Mixed allogeneic chimerism in the rat. Donor-specific transplantation tolerance without chronic rejection for primarily vascularized cardiac allografts. Transplantation 1995; 60:971-980.
10. Li H, Colson YL, Ildstad ST. Mixed allogeneic chimerism achieved by lethal and nonlethal conditioning approaches induces donor-specific tolerance to simultaneous islet allografts. Transplantation 1995; 60:523-529.
11. Colson YL, Lange J, Fowler K, Ildstad ST. Mechanism for co-tolerance in nonlethally conditioned mixed chimeras: negative selection of the Vb-TCR repertoire by both host and donor bone marrow-derived cells. Blood 1996; 88:4601-4610.
12. Colson YL, Li H, Boggs SS, Patrene KD, Johnson PC, Ildstad ST. Durable mixed allogeneic chimerism and tolerance by a nonlethal radiation-based cytoreductive approach. J Immunol 1996; 157:2820-2829.
13. Gaines BA, Colson YL, Kaufman CL, Ildstad S. Facilitating cells enable engraftment of purified fetal liver stem cells in allogeneic recipients. Exp Hematol 1996; 24:902-913.
14. Exner BG, Colson YL, Li H, Ildstad ST. Chimerism with partial recipient conditioning: targeting of CD4 sup + and CD8 sup + cells in the recipient marrow space permits chimerism with reduced conditioning. Br J Sur 1997; 84:1610-1611.
15. Exner BG, Colson YL, Li H, Ildstad ST. In vivo depletion of host CD4+ and CD8+ cells permits engraftment of bone marrow stem cells and tolerance induction with minimal conditioning. Surgery 1997; 122:221-7.
16. Gammie JS, Pham SM, Colson YL, Kawai A, Keenan RJ, Weyant RJ, Griffith BP. Influence of panel-reactive antibody on survival and rejection after lung transplantation. J Heart Lung Transplant 1997; 16:408-415.
17. Colson YL, Tripp RA, Doherty PC, Wren SM, Neipp M, Abou El-Ezz AY, Ildstad ST. Antiviral cytotoxic activity across a species barrier in mixed xenogeneic chimeras: functional restriction to host MHC. J Immunol 1998; 160:3790-3796.
18. Yaroslavskiy B, Colson YL, Parrish D, Ildstad ST, Parrish D, Boggs SS. Addition of a bone marrow "facilitating cell" population increases stem cell-derived cobblestone area formation in impaired long-term bone marrow culture stroma. Exp Hematol 1998; 26:604-611.
19. Gammie JS, Li S, Colson YL, Demetris AJ, Neipp M, Ildstad ST, Pham SM. A partial conditioning strategy for achieving mixed chimerism in the rat: tacrolimus and anti-lymphocyte serum substantially reduce the minimum radiation dose for engraftment. Exp Hematol 1998; 2 (10):927-935.
20. Gammie JS, Li S, Kawaharada N, Colson YL, Yousem S, Ildstad ST, Pham SM. Mixed allogeneic chimerism prevents obstructive airway disease in a rat heterotopic tracheal transplant model. J Heart Lung Transplant. 1998; 17 (8): 801-8.
21. Colson YL, El-Ezz A, Ashraf YA, Gaines BA, Ildstad T. Positive and negative selection of abTCR+ T cells in thymectomized adult radiation bone marrow chimeras. Transplantation 1999; 68(3):403-410.
22. Pham SM, Mitruka SN, Youm W, Li S, Kawaharada N, Yousem SA, Colson YL, Ildstad ST. Mixed hematopoietic chimerism induces donor-specific tolerance for lung allografts in rodents. Am J Resp Crit Care 1999; 159 (1):199-205.
23. Colson YL, Schuchert MJ and Ildstad ST. The abrogation of allosensitization following the induction of mixed allogeneic chimerism. J Immunol 2000; 165 (2): 637-644.
24. Schuchert MJ, Wright RD and Colson YL. Characterization of a newly discovered T-cell receptor b-chain heterodimer expressed on a CD8(+) bone marrow subpopulation that promotes allogeneic stem cell engraftment. Nat Med 2000; 6 (8): 904-909.
25. Schuchert MJ, Wright RD, Colson YL. The CD3/TCRb/FCp33 complex on the facilitating cell is capable of receptor signaling and is required for the facilitation of allogeneic stem cell engraftment. Transplantation 2000; 69(8):654 Suppl.
26. Byrne JG, Karavas, AN, Colson YL, Bueno R, Richards, WG, Sugarbaker DJ, Goldhaber SZ. Cardiac Decortication (Epicardiectomy) for Occult Constrictive Cardiac Physiology After Left Extrapleural Pneumonectomy. Chest 2002; (6): 2256-9.
27. Carty SE, Colson YL, Garvey LS, Schuchert VD, Schwentker A, Tzeng E, Corcoran NA, Simmons RL, Webster MW, Billiar TR. Maternity Policy and Practice During Surgery Residency: How We Do It. Surgery 2002; 132 (4): 682-7.
28. Colson YL, Jaklitsch M, Neragi-Miandoab S, Sugarbaker, D. The Role of Minimally Invasive Surgery in Lung Cancer. American Society of Clinical Oncology, Educational Book 2003; 153.
29. Sugarbaker DJ, Jaklitsch MT, Bueno, R, Richards W, Lukanich J, Mentzer SJ, Colson YL, Linden P, Chang M, Capalbo L, Oldread E, Neragi-Miandoab S, Swanson SJ, Zellos LS. Prevention, Early Detection, and Management of Complications Following 328 Consecutive Extrapleural Pneumonectomies. Journal of Thoracic and Cardiovascular Surgery, 2004;128:138-146.
30. Tatli S, M.D., Couper GS, M.D., Henderson JM, M.D., Ph.D, Yucel EK M.D. Colson YL, M.D. Aneurysm of an Aberrant Systemic Artery to the lung. May, 2004. American Journal of Roentgenology. In Press.
31. Linden, PA, Jaklitsch MT, Bueno R, Chang MY, Colson YL, Lukanich JM, Mentzer SJ, Sugarbaker DJ. Lung Tumor Resection in Patients with Severely Compromised Lung Function with Low Mortality or Major Morbidity. American Journal of Respiratory and Critical Care Medicine. 2004;7:169.
32. Colson YL, Xu H, Huang Y, Ildstad ST. Mixed xenogeneic chimerism induces donor-specific humoral and cellular immune tolerance for cardiac xenografts. The Journal of Immunology. 2004; 173 (9):5827-34.
33. Colson YL, Christopher K, Glickman J, Taylor KN, Wright R, Perkins DL. Absence of Clinical GVHD and the In Vivo Induction of Regulatory T cells following Facilitating Cell Transplantation. Blood. 2004; 104 (12):3829-35.
34. Parungo CP, Ohnishi S, Kim SW, Kim S, Laurence RG, Soltesz EG, Chen FY, Colson YL, Cohn LH, Bawendi MG, Frangioni JV. Intraoperative identification of esophageal sentinel lymph nodes with near-infrared fluorescence imaging. J Thorac Cardiovasc Surg. 2005 Apr;129(4):844-50.
35. Parungo CP, Ohnishi S, De Grand AM, Laurence RG, Soltesz EG, Colson YL, Kang PM, Mihaljevic T, Cohn LH, Frangioni JV. In vivo optical imaging of pleural space drainage to lymph nodes of prognostic significance. Ann Surg Oncol. 2004 Dec;11(12):1085-92. Epub 2004 Nov 15.
36. Parungo CP, Colson YL, Kim SW, Kim S, Cohn LH, Bawendi MG, Frangioni JV. Sentinel lymph node mapping of the pleural space. Chest. 2005 May;127(5):1799-804.
37. Linden PA, Bueno R, Colson YL, Jaklitsch MT, Lukanich J, Mentzer S, Sugarbaker DJ. Lung resection in patients with preoperative FEV1 < 35% predicted. Chest. 2005 Jun;127(6):1984-90.
38. Mery CM, Pappas AN, Bueno R, Colson YL, Linden P, Sugarbaker DJ, Jaklitsch MT. Similar Long-term Survival of Elderly Patients With Non-small Cell Lung Cancer Treated With Lobectomy or Wedge Resection Within the Surveillance, Epidemiology, and End Results Database. Chest. 2005 Jul;128(1):237-245.
39. Modi BP, Owens C, Ashley SW, Colson YL. Bouveret meets Boerhaave. Ann Thorac Surg. 2006 Apr;81(4):1493-5.
40. Paul S, Marty FM, Colson YL. Treatment of cavitary pulmonary zygomycosis with surgical resection and posaconazole. Ann Thorac Surg. 2006 Jul;82(1):338-40.
41. Taylor KN, Shinde Patil VR, Colson YL. Reconstitution of allogeneic hemopoietic stem cells: the essential role of FcR gamma and the TCR beta-chain-FCp33 complex. J Immunol. 2006 Aug 1;177(3):1444-50.
42. Ozols RF, Herbst RS, Colson YL, Gralow J, Bonner J, Curran WJ Jr, Eisenberg BL, Ganz PA, Kramer BS, Kris MG, Markman M, Mayer RJ, Raghavan D, Reaman GH, Sawaya R, Schilsky RL, Schuchter LM, Sweetenham JW, Vahdat LT, Winn RJ; American Society of Clinical Oncology. Clinical cancer advances 2006: major research advances in cancer treatment, prevention, and screening--a report from the American Society of Clinical Oncology. J Clin Oncol. 2007 Jan 1;25(1):146-62. Epub 2006 Dec 8.
43. Colson YL, Shinde Patil VR, Ildstad ST. Facilitating cells: Novel promoters of stem cell alloengraftment and donor-specific transplantation tolerance in the absence of GVHD. Crit Rev Oncol Hematol. 2007 Jan;61(1):26-43. Epub 2006 Dec 5.
44. Parungo CP, Soybel DI, Colson YL, Kim SW, Ohnishi S, De Grand AM, Laurence RG, Soltesz EG, Chen FY, Cohn LH, Bawendi MG, Frangioni JV. Lymphatic Drainage of the Peritoneal Space: A Pattern Dependent on Bowel Lymphatics. Ann Surg Oncol. 2007 Feb;14(2):286-298.
45. Linden PA, Bueno R, Mentzer SJ, Zellos L, Lebenthal A, Colson YL, Sugarbaker DJ, Jaklitsch MT. Modified T-tube repair of delayed esophageal perforation results in a low mortality rate similar to that seen with acute perforations. Ann Thorac Surg. 2007 Mar;83(3):1129-33.
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Inventions and Patents
Invention Disclosures
“Local Incorporation of anti-neoplastic agents into surgical resection margins using a minimally invasive delivery system”
File Date: 2/2003
“Minimally invasive targeted delivery of anti-neoplastic agents to the tumor-draining lymph nodes”
File Date: 9/2004
Patent Disclosure
Stem Cell Engraftment Enhancing Cellular Proteins and Their Uses (No. 60,121,108)
Non-provisional Application
File Date: 10/00
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Current Laboratory Members
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Yolonda L. Colson, M.D., Ph.D., Principal Investigator
Kendra N. Taylor, Ph.D., Postdoctoral Fellow
Vivek R. Shinde-Patel Ph.D., Postdoctoral Fellow
Meredith Chittenden, Technical Research Assistant
Evan Cohick, Technical Research Assistant
Solomon Azouz, Graduate Student
Sarah Lucier, Undergraduate Student
Sepideh Amirifeli, M.D., Postdoctoral Fellow |
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Contact
For more information or to inquire about any research opportunities, contact Yolonda Colson c/o Cari Donnelly (Administrative Assistant) at cdonnelly1@partners.org or via telephone at 617-732-6648.
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