Associate Professor in Medicine-Hematology/Oncology, Northwestern University Medical School
Oncology
Dr. Hidayatullah G. Munshi, MD
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Hidayatullah Munshi works in the field of Oncology. He went to Harvard Medical School. Harvard Medical School is a one of the best medicals schools. Harvard Medical School has a rank of 1 in research and a 12 in primary care He received awards:"Elected Member". Hidayatullah Munshi is a published MD. He has 48 publications published. The most current publication "Ca2+ regulates calmodulin binding to IQ motifs in IRS-1." Hidayatullah G. Munshi accepts Medicare payments and is listed with Medicare.gov.
Publications
- Differential Regulation of ZEB1 and EMT by MAPK-Interacting Protein Kinases (MNK) and eIF4E in Pancreatic Cancer.
- Ablation of 5-lipoxygenase mitigates Pancreatic lesion development.
- Snail Cooperates with KrasG12D In Vivo to Increase Stem Cell Factor and Enhance Mast Cell Infiltration.
- BET Bromodomain Inhibitors Block Growth of Pancreatic Cancer Cells in Three-Dimensional Collagen.
- Snail Cooperates with KrasG12D to Promote Pancreatic Fibrosis.
- Concurrent PEDF deficiency and Kras mutation induce invasive pancreatic Cancer and adipose-rich stroma in mice.
- Interplay between ?1-integrin and Rho signaling regulates the differential scattering and motility of pancreatic Cancer cells by snail and slug.
- Contribution of Epithelial-to-Mesenchymal Transition and Cancer Stem Cells to Pancreatic Cancer Progression.
- MT1-MMP cooperates with KrasG12D to promote Pancreatic fibrosis through increased TGF-{beta} signaling.
- Ethanol differentially regulates Snail family of transcription factors and invasion of premalignant and malignant Pancreatic ductal cells.
- Pancreatic Cancer cells respond to type I collagen by inducing snail expression to promote membrane type 1 matrix metalloproteinase-dependent collagen invasion.
- Mast cell 5-lipoxygenase activity promotes intestinal polyposis in APCDelta468 mice.
- Three-dimensional collagen I promotes gemcitabine resistance in pancreatic Cancer through MT1-MMP-mediated expression of HMGA2.
- Role of interferon {alpha} (IFN{alpha})-inducible Schlafen-5 in regulation of anchorage-independent growth and invasion of malignant melanoma cells.
- Rho-ROCK-myosin signaling mediates membrane type 1 matrix metalloproteinase-induced cellular aggregation of keratinocytes.
- Metabolic Syndrome after hormone-modifying therapy: risks associated with antineoplastic therapy.
- Crosstalk between mast cells and pancreatic Cancer cells contributes to pancreatic tumor progression.
- Care of the cancer survivor: metabolic Syndrome after hormone-modifying therapy.
- Slug is a downstream mediator of transforming growth factor-beta1-induced matrix metalloproteinase-9 expression and invasion of oral Cancer cells.
- Ovarian Cancer cell detachment and multicellular aggregate formation are regulated by membrane type 1 matrix metalloproteinase: a potential role in I.p. metastatic dis...
- Epidermal growth factor receptor-mediated membrane type 1 matrix metalloproteinase endocytosis regulates the transition between invasive versus expansive growth of ova...
- Evaluating the supportive care costs of severe radiochemotherapy-induced mucositis and pharyngitis : results from a Northwestern University Costs of Cancer Program pil...
- Transforming growth factor-beta 1 promotes matrix metalloproteinase-9-mediated oral Cancer invasion through snail expression.
- Extracellular matrix-mediated membrane-type 1 matrix metalloproteinase expression in Pancreatic ductal cells is regulated by transforming growth factor-beta1.
- Enzastaurin (LY317615), a protein kinase Cbeta inhibitor, inhibits the AKT pathway and induces apoptosis in multiple Myeloma cell lines.
- Differential regulation of membrane type 1-matrix metalloproteinase activity by ERK 1/2- and p38 MAPK-modulated tissue inhibitor of metalloproteinases 2 expression con...
- Calcium-induced matrix metalloproteinase 9 gene expression is differentially regulated by ERK1/2 and p38 MAPK in oral keratinocytes and oral squamous cell carcinoma.
- Glycosylation broadens the substrate profile of membrane type 1 matrix metalloproteinase.
- Loss of adhesion-regulated proteinase production is correlated with invasive activity in oral squamous cell carcinoma.
- Calcium regulation of matrix metalloproteinase-mediated migration in oral squamous cell carcinoma cells.
- Proteinase suppression by E-cadherin-mediated cell-cell attachment in premalignant oral keratinocytes.
- Metastatic dedifferentiated chordoma with elevated beta-hCG: a case report.
- Zileuton, 5-lipoxygenase inhibitor, acts as a chemopreventive agent in intestinal polyposis, by modulating polyp and systemic inflammation.
- GLI2-dependent c-MYC upregulation mediates resistance of pancreatic Cancer cells to the BET bromodomain inhibitor JQ1.
- Three-Dimensional Collagen I Promotes Gemcitabine Resistance In Vitro in Pancreatic Cancer Cells through HMGA2-Dependent Histone Acetyltransferase Expression.
- Chemotherapy in patients with prostate specific antigen-only Disease after primary therapy for prostate carcinoma: a phase II trial of oral estramustine and oral etopo...
- Severe Neutropenia: a diagnostic approach.
- Ca2+ regulates calmodulin binding to IQ motifs in IRS-1.
- Mouse hepatitis virus infection suppresses modulation of mouse spleen T-cell activation.
- Reciprocal interactions between adhesion receptor signaling and MMP regulation.
- Analysis of matrix degradation.
- Activation-coupled membrane-type 1 matrix metalloproteinase membrane trafficking.
- Differential growth factor regulation of N-cadherin expression and motility in normal and malignant oral epithelium.
- Modulation of the membrane type 1 matrix metalloproteinase cytoplasmic tail enhances tumor cell invasion and proliferation in three-dimensional collagen matrices.
- Collagen regulation of let-7 in pancreatic Cancer involves TGF-β1-mediated membrane type 1-matrix metalloproteinase expression.
- Therapy of locally advanced Pancreatic adenocarcinoma: unresectable and borderline patients.
- Biochemical role of the collagen-rich tumour microenvironment in pancreatic Cancer progression.
Schools
Harvard Medical School
University Wash Hosps
University Mich Hospital
Procedures Preformed
- Thoracentesis
Conditions Treated
- Acute Leukemia
- Anemia
- Antiphospholipid Syndrome (APS)
- Breast Cancer
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Doctors Specialties
- Hematology
- Medical Oncology
- Oncology
Accepted Insurances
- Aetna HMO
- Choice Plus POS II
- Blue Card PPO
- Blue Cross Blue Shield of Illinois PPO
- Great West Healthcare-Cigna PPO
- Commercial Insurance Company
- Health and Life PPO
- Platinum PPO
- First Health (Coventry Health Care) PPO
- GEHA
- Group Health Cooperative
- HealthLink PPO
- Choice Care PPO
- Medicare MCR
- MultiPlan PPO
- PHCS Network PPO
- State Farm
- Choice Plus POS
- Options PPO
- United Healthcare
Awards
- Elected Member
Education
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McGaw Medical Center of Northwestern University -
University of Washington -
Harvard Medical School
Hospital
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Northwestern Memorial Hospital -
Jesse Brown Veterans Affairs Medical Center
Helpful Reviews
Medicare Facts
| National Provider Identifier [NPI] | 1437258340 |
| Last Name Of The Provider | MUNSHI |
| First Name Of The Provider | HIDAYATULLAH |
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