ALISON RAE MOLITERNO, M.D.
Osteopathic Medicine at Wolfe St, Baltimore, MD
License number
Maryland D43432
Category
Osteopathic Medicine
Type
Internal Medicine
License number
Maryland D43432
Category
Osteopathic Medicine
Type
Hematology
Address
Address
600 N Wolfe St, Baltimore, MD 21287
Phone
(410) 955-3142
Personal information
See more information about ALISON RAE MOLITERNO at radaris.comName
Address
Phone
Baltimore, MD
3910 Clover Hill Rd, Baltimore, MD 21218
Professional information
Physician At Johns Hopkins School Of Medicine
Position:
Physician at Johns Hopkins School of Medicine
Location:
Baltimore, Maryland Area
Industry:
Research
Work:
Johns Hopkins School of Medicine
-
Physician
Alison Rae Moliterno, Baltimore MD
Specialties:
Hematologist
Address:
720 Rutland Ave, Baltimore, MD 21205
600 N Wolfe St, Baltimore, MD 21287
600 N Wolfe, Baltimore, MD 21287
600 N Wolfe St, Baltimore, MD 21287
600 N Wolfe, Baltimore, MD 21287
Education:
Doctor of Medicine
Board certifications:
American Board of Internal Medicine Certification in Internal Medicine, American Board of Internal Medicine Sub-certificate in Hematology (Internal Medicine)
Dr. Alison R Moliterno, Baltimore MD - MD (Doctor of Medicine)
Specialties:
Hematology
Address:
Johns Hopkins Outpatient Center
1800 Orleans St SUITE 7, Baltimore 21287
(410) 614-0167 (Phone)
1800 Orleans St SUITE 7, Baltimore 21287
(410) 614-0167 (Phone)
Certifications:
Hematology, 1996, Internal Medicine, 2006
Awards:
Healthgrades Honor Roll
Languages:
English
Hospitals:
Johns Hopkins Outpatient Center
1800 Orleans St SUITE 7, Baltimore 21287
The Johns Hopkins Hospital
1800 Orleans St, Baltimore 21287
1800 Orleans St SUITE 7, Baltimore 21287
The Johns Hopkins Hospital
1800 Orleans St, Baltimore 21287
Education:
Medical School
State University of New York At Buffalo
Graduated: 1989
Johns Hopkins Bayview M C
Johns Hopkins University School Med
State University of New York At Buffalo
Graduated: 1989
Johns Hopkins Bayview M C
Johns Hopkins University School Med
Antibodies To The Cytoplasmic Domain Of The Thrombopoietin Receptor
US Patent:
6696549, Feb 24, 2004
Filed:
Aug 31, 2000
Appl. No.:
09/652037
Inventors:
Jerry Spivak - Baltimore MD
Alison Moliterno - Baltimore MD
Alison Moliterno - Baltimore MD
Assignee:
The Johns Hopkins University - Baltimore MD
International Classification:
C07K 1628
US Classification:
53038822, 5303879, 5303881, 530351
Abstract:
Impaired TPO-mediated platelet protein tyrosine phosphorylation was consistently observed in patients with polycythemia vera (PV) as well as those with idiopathic myelofibrosis (IMF), in contrast to patients with essential thrombocytosis, chronic myelogenous leukemia, secondary erythrocytosis, iron deficiency anemia, hemochromatosis or normal volunteers. Moreover, the platelet TPO receptor, Mpl, was not detectable by immunoblotting with an antibody to the extracellular domain, by chemical crosslinking of TPO to the surface of platelets, or by flow cytometry using an antibody to the extracellular domain, in 34 of 34 PV patients and also in 13 of 14 IMF patients. Impaired TPO-induced protein tyrosine phosphorylation in PV and IMF platelets was uniformly associated with markedly reduced or absent expression of the extracellular domain of Mpl. Thus the reduced detectablility of Mpl by these methods can be used a marker of PV and IMF. The abnormality appears to distinguish PV from other forms of erythrocytosis and may be involved in the platelet function defect associated with PV.
Thrombopoietin Signaling Defect In Polycythemia Vera Platelets
US Patent:
6027902, Feb 22, 2000
Filed:
May 20, 1998
Appl. No.:
9/081619
Inventors:
Jerry Spivak - Baltimore MD
Alison Moliterno - Baltimore MD
Alison Moliterno - Baltimore MD
Assignee:
Johns Hopkins University - Baltimore MD
International Classification:
G01N 3353, G01N 33567
US Classification:
435 71
Abstract:
Impaired TPO-mediated platelet protein tyrosine phosphorylation was consistently observed in patients with polycythemia vera (PV) as well as those with idiopathic myelofibrosis (IMF), in contrast to patients with essential thrombocytosis, chronic myelogenous leukemia, secondary erythrocytosis, iron deficiency anemia, hemochromatosis or normal volunteers. Moreover, the platelet TPO receptor, Mpl, was not detectable by immunoblotting with an antibody to the extracellular domain, by chemical crosslinking of TPO to the surface of platelets, or by flow cytometry using an antibody to the extracellular domain, in 34 of 34 PV patients and also in 13 of 14 IMF patients. Impaired TPO-induced protein tyrosine phosphorylation in PV and IMF platelets was uniformly associated with markedly reduced or absent expression of the extracellular domain of Mpl. Thus the reduced detectablility of Mpl by these methods can be used a marker of PV and IMF. The abnormality appears to distinguish PV from other forms of erythrocytosis and may be involved in the platelet function defect associated with PV.
Methods To Assay A Thrombopoietin Signaling Defect In Polycythemia Vera Platelets
US Patent:
6150120, Nov 21, 2000
Filed:
May 20, 1998
Appl. No.:
9/081618
Inventors:
Jerry L Spivak - Baltimore MD
Alison Moliterno - Baltimore MD
Alison Moliterno - Baltimore MD
Assignee:
The Johns Hopkins University - Baltimore MD
International Classification:
G01N 3353
US Classification:
435 724
Abstract:
Impaired TPO-mediated platelet protein tyrosine phosphorylation was consistently observed in patients with polycythemia vera (PV) as well as those with idiopathic myelofibrosis (IMF), in contrast to patients with essential thrombocytosis, chronic myelogenous leukemia, secondary erythrocytosis, iron deficiency anemia, hemochromatosis or normal volunteers. Moreover, the platelet TPO receptor, Mpl, was not detectable by immunoblotting with an antibody to the extracellular domain, by chemical crosslinking of TPO to the surface of platelets, or by flow cytometry using an antibody to the extracellular domain, in 34 of 34 PV patients and also in 13 of 14 IMF patients. Impaired TPO-induced protein tyrosine phosphorylation in PV and IMF platelets was uniformly associated with markedly reduced or absent expression of the extracellular domain of Mpl. Thus the reduced detectablility of Mpl by these methods can be used a marker of PV and IMF. The abnormality appears to distinguish PV from other forms of erythrocytosis and may be involved in the platelet function defect associated with PV.