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Herman Yeger

Herman Yeger, PhD
Department of Paediatric Laboratory Medicine
Division of Pathology
The Hospital for Sick Children
555 University Avenue
Toronto, Ontario M5G 1X8
Tel: 1 416-813-5958
Fax:1 416-813-5974

Present Positions

  • Professor, Department of Laboratory Medicine & Pathobiology, University of Toronto
  • Cross-appointed to graduate faculty of Institute of Medical Science, University of Toronto
  • Senior Scientist, Research Institute, The Hospital for Sick Children, Program in Developmental & Stem Cell Biology
  • Member on the University of Toronto Department of Laboratory Medicine & Pathobiology Promotions & Appointments Committee
  • Member on the University of Toronto Department of Laboratory Medicine & Pathobiology Research Committee


  • Canadian Society of Biochemistry, Molecular & Cellular Biology
  • American Association of Cancer Research
  • International CCN Society

Editorial Boards

  • Editorial Board, Journal of Cell Communication & Signaling (Springer) 2007-2010
  • Editorial Board, Cell Communication and Signaling [BioMed Central] 2003-2006
  • Editorial Board, Molecular Pathology (Journal of Clinical Pathology). 1999-2003


  • Dept Paediatric Laboratory Medicine Teaching Award, 2009
  • Visiting Professor, May-July, Universite Paris 7-Denis Diderot, Laboratoire d'Oncologie Virale et Moleculaire, 2004
  • Visiting Professor, May-July, Universite Paris 7-Denis, Diderot, Laboratoire d'Oncologie Virale et Moleculaire, 2001
  • Visiting Professor, May-July, Universite Paris 7-Denis Diderot, Laboratoire d'Oncologie Virale et Moleculaire, 2001

Research Themes

  • The main focus of my laboratory since the 1980’s has been on the pathobiology of human disease and modalities of therapy.
    The following outlines our research interests and accomplishments.
  • 1. Pediatric Cancer Research
    Our research on pediatric cancers has followed 3 lines of investigation: a] identification and validation of new therapeutic agents of dietary origin; b] identification of the tumor stem cell fraction in neuroblastoma and characterization of the TSC niche; and c] development of neuroblastoma in vivo models for drug evaluation.
    A] New Therapeutic Approaches: Prior to 2004 our focus on pediatric cancer research was on phenotypic characterization of the heterogeneity in these cancers in particular their differentiated states. We studies both neuroblastoma and Wilms tumor and reported on correlations between differentiation and the metastatic phenotype. In collaboration with Dr. Bryan Williams (Monash) we described a gene signature for relapsed Wilms tumor [Li et al, 2005]. We also isolated and characterized key cell line models, one of which, WiT49 a Wilms tumor line is being consistently requested by labs in many countries for studies on Wilms tumor. This cell line is only one of very few derived from Wilms tumor and in fact the only one recognized thus far. We continue to exploit WiT49 for new ideas on aging and cancer.
    Our attention was turned to identifying dietary agents with anti-tumor properties for neuroblastoma since this pediatric cancer has a poor prognosis and current treatments have not increased survival beyond 60% for advanced stage neuroblastoma. We also sought agents that would have minimal side effects for the pediatric population. We reported that curcumin, resveratrol and apigenin (polyphenolic compounds) possessed significant anti-neuroblastoma and apoptosis inducing properties both in vitro and in a xenograft model [Liontas and Yeger, Anticancer Res, 2004; Torkin et al, Cancer Res 2005]. Our most recent work focuses on the isothiocyanates, in particular sulforaphane (prevalent in broccoli) with potent anti-neuroblastoma activity at physiological concentrations [Mokhtari et al, conference presentations, 2009]. In additional studies we are studying epigenetic modulators such as HDAC inhibitors as potent inhibitors of neuroblastoma growth, apoptosis inducers and inducers of differentiation. Thus epigenetic modulation of the neuroblastoma phenotype has become a rich source of new ideas for research on neuroblastoma and we are exploring combination therapeutic approaches. We are developing new approaches to capitalize on the potential of dietary compounds for chemopotentiation, chemosensitization and chemoprotection of drug treated tumors to reduce use of cytotoxic chemotherapeutics while protecting normal tissues, a desirable objective for the treatment of developing children.
    B] Tumor Stem Cell (TSC) Identification and the TSC Niche:
    We have made significant advances in this focus due to the efforts of a PDF, Dr. B. Das [now at Stanford]. We first described an autocrine growth mechanism, VEGF/Flt-1 that drives neuroblastoma growth [Das et al, Cancer Res, 2005] under the hypoxic conditions found in all cancers. Importantly, we found a small fraction of cells within a broad range of pediatric tumor cell lines, the side population (SP), that harbors the tumorigenic potential and is increased under hypoxia. The SP fraction expressed stem cell markers and stemness was maintained through the VEGF/Flt-1 pathway. In fact, using neuroblastoma and an osteogenic cancer cell line model we showed that hypoxia upregulated the tumorigenic capacity, also correlating with increased invasiveness [Das et al, Stem Cells, 2008; Tsuchida et al, Oncogene, 2008]. The stemness idea in cancer has been elaborated on in an invited review [Das et al, Regulatory Networks in Stem Cells, Humana Press, 2009]. We developed a novel method for isolation of the very small fraction of tumor cells that survives under hypoxia and possesses invasive properties allowing metastatic dissemination. We showed that this tagged cell subfraction, designated SPmHox could migrate into the hypoxic niche of established xenografts and could form tumors with as low as 100 cells [Das et al, Stem Cells, 2008]. Thus we have identified the hypoxic niche as a source for sequestration of the putative TSC. Using a different tact, based on growth of stem cells under defined culture conditions, a tumor initiating cell phenotype was isolated and characterized from patient material, bone marrow isolates which are favored for early metastasis by neuroblastoma. This tumor initiating cell (TIC) population reported in Cancer Res [Hansford et al, Cancer Res, 2007] has become an important model for studies on neuroblastoma and for the work on development of new therapeutics identified in large chemical screens [Smith et al, 2010].
    C] In vivo models for drug evaluation: We have been exploiting the potential of immunocompromised mice for development of pediatric cancer xenograft models for the past 30 years. Initially we used these models to study differentiation of these cancers.
    For our work on polyphenolic and other types of dietary derived compounds and to validate the anti-tumor properties of drugs identified in chemical screens [collaborations with Drs Baruchel and Kaplan] we have developed several variations, primary tumor growths in the subcutaneous and inguinal fat pad sites, and primary/metastasis progression in the intraperitoneal site, and dissemination/metastasis via intravenous inoculation. We have shown that particular chemokines and chemokine receptors favor metastasis of neuroblastoma [Zhang et al, Neoplasia, 2007]. In fact, the chemokine receptor CXCR4 figures prominently in the neuroblastoma stemness phenotype. A number of established targeted therapeutics eg, sunatinib, rapamycin, have been validated as potential anti-neuroblastoma therapeutics in our models [Zhang et al, Neoplasia,2008; Zhang et al, 2010, submitted]. Finally, another natural compound, squalene, and intrinsic metabolite of the mevalonate pathway, was shown to chemoprotect mouse bone marrow against cisplatin toxicity when cisplatin is used to treat neuroblastoma xenografts [Das et al, Neoplasia, 2008]. This compound has potential for clinical application and in combination with other anti-tumor agents.
    These cancer studies are supported with funding from the Canadian Cancer Society (NCIC) and the James Birrell Neuroblastoma Research Fund at HSC.
  • 2. Development and Physiological Role of the Pulmonary Neuroendocrine Cell System and Pulmonary Disease Pathophysiology
    This close collaboration with Dr E Cutz (Div.of Pathology) over a period of 25 years has elaborated on an important lung function. Our initial descriptive morphological studies have evolved into studies utilizing biochemical, molecular, electrophysiological and functional physiological methodologies in concert with development of unique in vitro and in vivo models. Here we have directed our efforts into three complementary directions and with collaborations with HSC and outside investigators.
    A] Development and Physiological Role of the Pulmonary Neuroendocrine Cell System: During the past 6 years we have expanded the knowledge base on the pulmonary neuroendocrine cell system. Further evidence has been obtained to support the role of these cells which we show are well innervated [Pan et al, 2006], are connected via the vagus nerve to the nodose ganglion and thereon towards the brain stem control of breathing. We have shown that they possess an pO2 sensitive membrane localized NADPH oxidase complexed specific K+ channels that mediate downstream release of the vasoactive serotonin from these cells, in addition to bioactive neuropeptides involved in lung development. We have identified sensitive markers that permit topographic mapping of the innervation interaction with the neuroendocrine cells by confocal microscopy. Electrophysiological studies confirmed the excitability of these cells making them true neurosensory mediators of lung hypoxia. At the molecular level we have defined specific protein oxidase component complexes that signal changes in pO2 [reviewed in Cutz et al]. We have also shown that serotonin release can occur from a separate cellular pool via mechanotransduction thus implicating breathing movements in fetal life as a means of delivering serotonin to surrounding lung tissue where it can function for fetal lung development and may be important in pathological conditions, eg, CF lung disease.
    We work with animal models and human lung tissue and have been seeking the progenitors of the pulmonary neuroendocrine cells. To this end we have recently shown that the neurogenic transcription factors, Mash-1 and Prox-1, govern development and maturation of neuroendocrine cell progenitors, and that the system is paced by pO2 during fetal [McGovern et al, Lab Invest, 2010]. Since branching morphogenesis of lung is also paced by pO2 we believe that pO2 plays a critical role in the pacing of lung growth and maturation during fetal life. We discovered a critical threshold gestation time when hypoxia sensitivity is lost suggesting an explanation for why premature infants may be able to maintain lung functions and a possible pathophysiological explanation for defects exhibited by certain pediatric defective lung syndromes.
    B] We have extended our studies to understanding lung pathophysiology in CF and other lung pathologies [Pan et al, 2006, Oliver et al, 2009]. Our studies in CF have been conducted in collaboration with Dr. Bear using CF mouse models and we identified major defects in innervation of the neuroendocrine cells and smooth muscle in neonatal Cftr-/- mice. We also have preliminary expression profiling evidence of significant deficiencies in neurogenesis in the Cftr-/- mice and predict that this might explain an ineffective neuroimmunnomodulatory control of innate immunity required for control of early infections of CF lungs. These studies are also being extended to the CF pig model as it more closely approximates human lung CF pathophysiology. If proven in humans [continuing studies] this could identify the means to target the problem in the critical neonatal period.
    The work has been supported by funding from the Canadian Institutes for Health Research (CIHR) and the Canadian Cystic Fibrosis Foundation (CCFF).
  • 3. Tissue Engineering/Regenerative Medicine
    My interest in regenerative medicine approaches for pediatric disease first began in the 1980’s with a collaborative effort with Dr. G Wilson where I developed a protocol for decellularization of tissues to produce an extracellular matrix (ACM) capable of being repopulated with host cells for tissue engineering. This initial focus was on vascular structures and in the past 6 years the focus has turned to tissue engineering of bladder as the first step to broader expansion into developing a focus in pediatric regenerative medicine with Dr W Farhat. With Dr Farhat we applied the ACM idea to bladder which led to modifications that improved recellularization and tissue engraftment in animal models [Cartwright et al, 2006]. We also developed the means to incorporate biologicals, eg, VEGF to stimulate earlier angiogenesis necessary for graft survival. An important initiative around this focus was the development of an ex-vivo tissue bioreactor to serve several key purposes [Wallis et al, Tissue Eng, 2008]. With the tissue bioreactor we are able to simulate mechanical movements that play a key role in the growth and functional development of the different cell types in dynamic organs like bladder [Farhat & Yeger, World J Urol, 2008; Farhat et al, Biomed Mater, 2008]. A further development [collaboration with Dr.H. Cheng] is the application of MRI to monitor the process of tissue re-implantation and dynamic growth [Cartwright et al, Biomed Mater Res, 2008].
    The tissue bioreactor and mechanical simulation also has implications for other dynamic organs like heart. The tissue bioreactor is being refined to give it much greater versatility and broader applicability as well as marketability. Since we have considered how stem cell technology could be incorporated into the ex-vivo development of tissues we have carried out initial studies exploring the ability of bone marrow derived mesenchymal stem cells to develop into bladder smooth muscle and have encouraging results. We are entertaining the possibility of incorporating iPS cells into our system and it is obvious that an ex-vivo tissue bioreactor would be of great advantage for functional validation of biografts prior to implantation into patients. This idea is a leading edge concept for the field of pediatric regenerative medicine and one we are pursuing actively.
    The research here has been supported by funding to Dr. Farhat and from industry contributions.
  • 4. CCN Research:
    I have been involved in the investigation of the CCN (Cyr61, CTGF, Nov) family of proteins in various pathological processes in normal development since 1994 having developed a close working arrangement with Prof Bernard Perbal previously with Universite Paris VII [see *publications below]. During this association the International CCN Society was formed and biennial international meetings have been held since then. The last meeting was in Toronto, Oct 2008, which I organized, and was quite successful in helping to bring greater visibility to the ICCNS and the organ journal, Journal of Cell Communication and Signaling, under Springer [Irvine et al, 2009;Yeger & Perbal, 2007]. The workshops have expanded to bring in investigators working in the field of the extracellular matrix since the CCN proteins are matricellular proteins [Kyurkchiev et al, 2004]. In collaboration with Dr Riser at Baxter Research we have reported an important role for CCN3(Nov) in diabetic nephropathy [Riser et al, Am J Pathol, 2009,2010]. We have explored CCN3 expression with novel in vitro models of neurogenesis (ICCNS meeting, 2008). CCN proteins may figure prominently into different aspects of regenerative medicine. We envision that CCN proteins are centrally involved in the cell-matrix interactions required for proper ex-vivo tissue reconstruction. A major concern here is avoidance of fibrotic reactions that could compromise functions of tissue constructs and their successful translation to patients. Our pediatric regenerative medicine group at SickKids is gearing up to design models and protocols pertinent to pediatric regenerative medicine; here CCN proteins would be considered as they are likely involved in active tissue formation and organ development.
    Work on CCN proteins has been supported by funding to B. Perbal and in part to H. Yeger from various agencies.

Selected Recent Publications -* CCN relevant

  • Ambekar C, Das B, Yeger H, Dror Y. .
    SBDS-deficiency results in deregulation of reactive oxygen species leading to increased cell death and decreased cell growth.
    Pediatr Blood Cancer 55: 1138-44, 2010.
  • Smith KM, Datti A, Fujitani M, Grinsgtein N, Zhang L, Mrorozova O, Blakely KM, Rotenberg SA, Hansford LM, Miller FD, Yeger H, Irwin MS, Moffat J, Marra MA, Baruchel S, Wrana JL, Kaplan DR. .
    Selective targeting of neuroblastoma tumour-initiating cells by compounds identified in stem cell-based small molecule screens.
    EMBO Mol Med 2:371-84, 2010.
  • Loai Y, Yeger H, Coz C, Antoon R, Islam SS, Moore K, Farhat WA. .
    Bladder tissue engineering: tissue regeneration and neovascularization of HA-VEGF-incorporated bladder acellular constructs in mouse and porcine animal models.
    J Biomed Mater Res A 94:1205-15,2010.
  • Gisselsson D, Lindgren D, Mengelbier LH, Ora I, Yeger H. .
    Genetic bottlenecks and the hazardous game of population reduction in cell line based research.
    Exp Cell Res. 2010 Jul 16. [Epub ahead of print]
  • Evren S, Loai Y, Antoon R, Islam S, Yeger H, Moore K, Wong K, Gorczynski R, Farhat WA. .
    Urinary Bladder Tissue Engineering Using Natural Scaffolds in a Porcine Model: Role of Toll-Like Receptors and Impact of Biomimetic Molecules.
    Cells Tissues Organs. 2010 Jun 30. [Epub ahead of print]
  • * Riser BL, Najmabadi F, Perbal B, Rambow JA, Riser ML, Sukowski E, Yeger H, Riser SC, Peterson DR. .
    CCN3/CCN2 regulation and the fibrosis of diabetic renal disease.
    J Cell Commun Signal. 4 :39-50, 2010.
  • McGovern S, Pan J, Oliver G, Cutz E,Yeger H. .
    The role of hypoxia and neurogenic genes (Mash-1 and Prox-1) in the developmental programming and maturation of pulmonary neuroendocrine cells in fetal mouse lung.
    Lab Invest 90:180-95,2010.
  • Oliver J, Kushwah R, Wu J, Cutz E, Yeger H, Waddell TK, Hu J. .
    Gender differences in pulmonary regenerative response to naphthalene-induced bronchiolar epithelial cell injury.
    Cell Prolif 42:672-87, 2009.
  • Cutz E, Pan J, Yeger H. .
    The role of NOX2 and “novel oxidases” in airway chemoreceptor O(2) signaling.
    Adv Exp Med Biol 648:427-38, 2009.
  • Rigat B, Yeger H, Shehnaz D, Mahuran D.
    GM2 activator protein inhibits platelet activating factor signaling in rats.
    Biochem Biophys Res Commun 385:576-80, 2009.
  • Zhang L, Smith KM, Chong AL, Stempak D, Yeger H, Marrano P, Thorner PS, Irwin MS, Kaplan DR, Baruchel S.
    In vivo antitumor and antimetastatic activity of sunitinib in preclinical neuroblastoma mouse model.
    Neoplasia 11:426-35, 2009. C
  • Riser BL, Najmabadi F, Perbal B, Peterson DR, Rambow JA, Riser ML, Sukowski E, Yeger H, Riser SC. .
    CCN3 (NOV) Is a Negative Regulator of CCN2 (CTGF) and a Novel Endogenous Inhibitor of the Fibrotic Pathway in an in Vitro Model of Renal Disease.
    Am J Pathol 174:1725-35, 2009.
  • * Irvine AE, Perbal B,Yeger H.
    Report on the fifth international workshop on the CCN family of genes.
    J Cell Commun Signal 2:95-100,2009.
  • Cutz E, Fu XW, Yeger H, Nurse CA.
    Functional live imaging of the pulmonary neuroepithelial body microenvironment.
    Am J Respir Cell Mol Biol 40:119-20, 2009.
  • Farhat WA, Yeger H.
    Does mechanical stimulation have any role in urinary bladder tissue engineering? World
    J Urol 26:301-5, 2008.
  • Das B, Antoon R, Tsuchida R, Lotfi S, Morozova O, Farhat W, Malkin D, Koren G, Yeger H, Baruchel S.
    Squalene selectively protects mouse bone marrow progenitors against cisplatin and carboplatin-induced cytotoxicity in vivo without protecting tumor growth.
    Neoplasia 10:1105-19, 2008.
  • Das B, Tsuchida R, Malkin D, Koren G, Baruchel S, Yeger H. .
    Hypoxia enhances tumor stemness by increasing the invasive and tumorigenic side-population fraction.
    Stem Cells 26:1818-30, 2008.
  • Farhat WA, Chen J, Haig J, Antoon R, Litman J, Sherman C, Darwin K, Yeger.
    H. Porcine bladder acellular matrix (ACM): protein expression, mechanical properties.
    Biomed Mater 3:25015, 2008. Epub June 3.
  • Wallis MC, Yeger H, Cartwright L, Shou Z, Radisic M, Haig J, Suoub M, Antoon R, Farhat W. .
    Feasibility study of a novel urinary bioreactor.
    Tissue Eng Part A 14: 339-48, 2008.
  • Tsuchida R, Das B, Yeger H, Koren G, Shibuya M, Thorner PS , Baruchel S, Malkin D.
    Cisplatin treatment increases survival and expansion of a highly tumorigenic side-population fraction by upregulating VEGF/Flt1 autocrine signaling: implications in solid tumor chemotherapy.
    Oncogene 27: 3923-34, 2008.
  • Cutz E, Yeger H, Pan J, Ito T. .
    Pulmonary neuroendocrine cell system in health and disease.
    Curr Respir Med Rev 4:174-86, 2008.
  • * Yeger H, Perbal B.
    The CCN family of genes: a perspective on CCN biology and therapeutic potential.
    J Cell Commun Signal 1: 159-64, 2007.
  • Cutz E, Yeger H, Pan J.
    Pulmonary neuroendocrine cell system in pediatric lung disease-recent advances.
    Pediatr Dev Pathol 10: 419-35, 2007.
  • Hansford LM, McKee AE, Zhang L, George RE, Gerstle JT, Thorner PS, Smith KM, Look TA, Yeger H, Miller FD, Irwin MS, Thiele CJ, and Kaplan DR.
    Neuroblastoma cells isolated from bone marrow metastases contain a naturally enriched tumor-initiating cell.
    Cancer Res 67:11234-43,2007.
  • Zhang L, Yeger H, Das B, Irwin MS, Baruchel S. .
    Tissue microenvironment modulates CXCR4 expression and tumor metastasis in neuroblastoma.
    Neoplasia 9: 36-46,2007.
  • Farhat WA, Chen J, Sherman C, Cartwright L, Bahoric A, Yeger H. .
    Impact of fibrin glue and urinary bladder cell spraying on the in-vivo acellular matrix cellularization: a porcine pilot study.
    Can J Urol.13:3000-8, 2006.
  • Pan J, Luk C, Kent G, Cutz E, Yeger H. .
    Pulmonary neuroendocrine cells, airway innervation and smooth muscle are altered in Cftr null mice.
    Am J Respir Cell Mol Biol. 35(3):320-6,2006.
  • Cartwright LM, Shou Z, Yeger H, Farhat WA. .
    Porcine bladder acellular matrix porosity: Impact of hyaluronic acid and lyophilization.
    J Biomed Mater Res A 77: 180-4, 2006.
  • Cartwright L, Farhat WA, Sherman C, Chen J, Babyn P, Yeger H, Cheng HL. .
    Dynamic contrast-enhanced MRI to quantify VEGF-enhanced tissue-engineered bladder graft neovascularization: Pilot study.
    J Biomed Mater Res A 77: 390-5, 2006.
  • Pan J, Copland I, Post M, Yeger H, Cutz E. .
    Mechanical stretch induced serotonin release from Pulmonary Neuroendocrine Cells: Implications for lung development.
    Am J Physiol Lung Cell Mol Physiol. 290:L185-93, 2006.
  • Das B, Yeger H, Tsuchida R, Torkin R, Gee MF, Thorner PS, Shibuya M, Malkin D, Baruchel S. .
    A hypoxia-driven vascular endothelial growth factor/Flt1 autocrine loop interacts with hypoxia-inducible factor-1alpha through mitogen-activated protein kinase/extracellular signal-regulated kinase 1/2 pathway in neuroblastoma.
    Cancer Res. 2005 Aug 15;65(16):7267-75.
  • Li W, Kessler P, Yeger H, Alami J, Reeve AE, Heathcott R, Skeen J, Williams BR. .
    A gene expression signature for relapse of primary wilms tumors.
    Cancer Res 65:2592-601, 2005.
  • Torkin R, Lavoie J-F, Kaplan D-R, Yeger H. .
    Induction of caspase-dependent, p53 mediated apoptosis by apigenin in human neuroblastoma.
    Mol Cancer Ther 4:1-11, 2005.
  • * Kyurkchiev S, Yeger H, Bleau AM, Perbal B. .
    Potential cellular conformations of the CCN3(NOV) protein.
    Cell Commun Signal 2: 9-15, 2004.
  • * Yu C, Le A-T, Yeger H, Perbal B, Alman BA. .
    Nov (CCN3) regulation in the growth plate and CCN family member expression in cartilage neoplasia.
    J Pathol 201: 609-15, 2003.
  • * Yeger H. .
    Building a Solid Foundation: CCS in Developing Skeleton and the CCN Family Role.
    Cell Commun Signal. 2003 Oct 2;1(1):2. Epub 2003 Oct 02.
  • * Brigstock DR, Goldschmeding R, Katsube K-I, Lam SC-T, Lau LF, Lyons K, Naus C, Perbal B, Riser B, Takigawa M, Yeger H. .
    Proposal for a unified CCN nomenclature.
    J Clin Pathol:Mol Pathol 56:127-8, 2003.
  • * Manara MC, Perbal B, Benini S, Strammiello R, Cerisano V, Perdichizzi S, Serra M, Astolfi A, Bertoni F, Alami J, Yeger H, Picci P, Scotlandi K. .
    The expression of ccn3(nov) gene in musculoskeletal tumors.
    Am J Pathol 160:849-59, 2002.
  • * Ayer-Lelievre C, Brigstock D, Lau L, Pennica D, Perbal B, Yeger H. .
    Report on the first international workshop on the CCN family of genes.
    J Clin Pathol: Mol Pathol 54:105-107,2001.
  • * Kocialkowski S, Yeger H, Kingdom J, Perbal B, Schofield PN. .
    Expression of the human NOV gene in first trimester human fetal tissues.
    Anat Embryol 203: 417-427, 2001.
  • * Chevalier G, Yeger H, Martinerie C, Laurent M, Alami J, Schofield PN, Perbal B. .
    novH: differential expression in developing kidney and Wilms’ tumor.
    Am J Pathol 152:1563-1575, 1998. Books and Book Chapters:
  • Yeger H, Pan J, Cutz E. .
    Precursors and stem cells of the pulmonary neuroendocrine cell system in developing mammalian lung. Ch13 pp 287-306;
    In: Airway Chemoreceptors in the Vertebrates, Ed,
    Zaccone, G et al, Publishers Oxford and IBH, New Dehli. 2009.
  • Das B, Tsuchida R, Malkin D, Baruchel S, Yeger H. .
    Idea and evidence of tumor stemness switch.
    In: Regulatory Networks in Stem Cells; V.K. Rajasekhar, and Mohan Vemuri (eds),
    Humana Press, Totowa, NJ, 2009.
  • Cutz E, Fu XW, and Yeger H. .
    Methods to study neuroepithelial bodies as airway oxygen sensors.
    Methods in Enzymology 381: 26-42, 2004.
  • Cutz E, Fu XW, Yeger H, Peers C, Kemp PJ.
    Oxygen sensing in Pulmonary neuroepithelial bodies and related tumour cell model. In: Lahiri S, Prabhakar H. Semenza G. Oxygen sensing: Responses and adaptation to hypoxia,
    Lung Biology in Health and Disease, Marcel Dekker, NY, pp.567-602, 2003.
  • Yeger H, Youngson C, Cutz E. .
    In vitro models for isolation, culture and characterization of pulmonary neuroendocrine cells and neuroepithelial bodies.
    In: Cellular and Molecular Biologyof Airway Chemoreceptors. Cutz, E (ed).
    Landes Bioscience, Chapman & Hall, NY 1997 pp. 47-70.
  • Cutz E, Yeger H, Newman C, Wong V, Bienkowski E, Perrin DG.
    Effects of hypoxia on isolated pulmonary neuroepithelial body cells in vitro.
    In “Arterial chemoreception.” Eyraguirre C, Fidone SJ, Fitzgerald RS, Lahiri McDonald D (Eds).
    Springer Verlag, New York, pp 432-37, 1990.
  • Sarkar B, Mas A, Yeger H. .
    Placental metabolism of nickel.
    In: Nickel and Human Health. Nieboer E, Nriagu JO (Eds)
    John Wiley & Sons, New York, 1992, pp 573-586.
  • Youngson C, Nurse C, Yeger H, Cutz E. .
    Characterization of membrane currents in pulmonary neuroepithelial bodies: hypoxia-sensitive airway chemoreceptors.
    In Arterial Chemoreceptors: Cell to system. O'Regan R et al (Eds).
    Plenum press, New York, 1994, pp. 179-182.