Explore This Lab


Our lab’s research focuses on identifying the molecular changes that lead to formation and progression of tumor in patients with hereditary brain tumor syndromes (neurofibromatosis 1, neurofibromatosis 2, schwannomatosis, tuberous sclerosis and von Hipple Lindau). In collaboration with both clinical groups and basic science/mouse modelling groups, our research focuses on translating novel findings to clinical pathology; identifying biomarkers that aid in diagnosis and classification of NF associated tumors; analyzing human tumors to validate novel findings in animal models; and identifying activated pathways that may be targetable by therapy and may help in the development of new treatment modalities by analyzing the effects on treated tumors (in animals and humans). For example, Schwannomas are benign nerve sheath tumors that may arise in people with no underlying genetic syndrome (solitary, sporadic schwannomas) or in the context of two hereditary tumor syndromes: neurofibromatosis 2 and schwannomatosis. Although all schwannomas share the loss of function of the NF2 gene, our hypothesis is that additional microenvironmental factors or epigenetic events are responsible for the clinical manifestations associated with these tumors, such as pain, hearing loss or rapid tumor growth. The identification of these events and of the pathways involved may aid in the diagnosis of the different subclinical types of schwannomas as well as in the development of targeted therapies. Our recent work in collaboration with researchers and clinicians at MGH has unraveled molecular pathways of angiogenesis in schwannomas, leading to targeted antiangiogenesis therapy with clinical improvement in a small series of patients with NF2-associated schwannomas.

Group Members

Meet our research team:

  • Anat Stemmer-Rachamimov, MD
    Associate Professor of Pathology, Harvard Medical School
    Associate Neuropathologist, Massachusetts General Hospital
  • James Kim, Lab Manager
  • Frances Chaves, Research Technician II
  • Anna Levitz, Research Technician I
  • Maia Livneh, Research Technician I


Zhao Y, Liu P, Zhang N, Chen J, Landegger LD, Wu L, Zhao F, Zhao Y, Zhang Y, Zhang J, Fujita T, Stemmer- Rachamimov A, Ferraro GB, Liu H, Muzikansky A, Plotkin SR, Stankovic KM, Jain RK, Xu L.Targeting the cMET pathway augments radiation response without adverse effect on hearing in NF2 schwannoma models. Proc Natl Acad Sci USA. 2018; 27:115(9).

Miettinen MM, Antonescu CR, Fletcher CDM, Kim A, Lazar AJ, Quezado MM, Reilly KM, Stemmer-Rachamimov A, Stewart DR, Viskochil D, Widemann B, Perry A. Histopathologic evaluation of atypical neurofibromatous tumors and their transformation into malignant peripheral nerve sheath tumor in patients with neurofibromatosis 1-a consensus overview. Hum Pathol. 2017; 67:1-10.

Multiple synchronous sites of origin of vestibular schwannomas in neurofibromatosis Type 2.Stivaros SM, Stemmer-Rachamimov AO, Alston R, Plotkin SR, Nadol JB, Quesnel A, O'Malley J, Whitfield GA, McCabe MG, Freeman SR, Lloyd SK, Wright NB, Kilday JP, Kamaly-Asl ID, Mills SJ, Rutherford SA, King AT, Evans DG. J Med Genet. 2015 Aug;52(8):557-62.

Anti-VEGF treatment improves neurological function and augments radiation response in NF2 schwannoma model. Gao X, Zhao Y, Stemmer-Rachamimov AO, Liu H, Huang P, Chin S, Selig MK, Plotkin SR, Jain RK, Xu L. Proc Natl Acad Sci U S A. 2015 Nov 24;112(47):14676-81.

Identification of a progenitor cell of origin capable of generating diverse meningioma histological subtypes. Kalamarides M, Stemmer-Rachamimov AO, Niwa-Kawakita M, Chareyre F, Taranchon E, Han ZY, Martinelli C, Lusis EA, Hegedus B, Gutmann DH, Giovannini M. Oncogene. 2011 May 19;30(20):2333-44.

Hearing improvement after bevacizumab in patients with neurofibromatosis type 2. Plotkin SR, Stemmer-Rachamimov AO, Barker FG 2nd, Halpin C, Padera TP, Tyrrell A, Sorensen AG, Jain RK, di Tomaso E. N Engl J Med. 2009 Jul 23;361(4):358-67.