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Rizwan Haq, MD, PhD


Medical Oncology

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Physician

  • Physician
  • Assistant Professor, Harvard Medical School

Centers/Programs

Clinical Interests

  • Developmental therapeutics
  • Melanoma
  • Targeted therapies

Diseases Treated

Contact Information

  • Appointments617-632-5055
  • Office Phone Number617-632-5055
  • Fax617-632-6727

Bio

Dr. Haq is a graduate of the University of Toronto, where he completed his B.Sc. (Hon), and MD/PhD. His PhD was at the Ontario Cancer Institute/Princess Margaret Hospital in the laboratory of Dr Brent Zanke. He completed his clinical training in internal medicine at The Johns Hopkins Hospital in Baltimore, followed by medical oncology training at Dana-Farber Cancer Institute and Massachusetts General Hospital. He joined the laboratory of Dr David E. Fisher, where he conducted translational work in the melanoma; and was an attending oncologist at Massachusetts General Hospital.

He was recruited back to Dana-Farber Cancer Institute in 2014. His research focuses on resistance to melanoma therapies, including targeted agents and immunotherapies. He has been a contributing author of numerous high profile publications, including those published in Cancer CellNatureProceedings of the National Academy of Sciences USA. At Dana-Farber Cancer Institute, Dr. Haq devotes part of his time to developing the next generation of melanoma therapeutics and translating them to innovative investigator-initiated clinical trials. His clinical practice is dedicated to patients with melanoma. 

Board Certification:

  • Internal Medicine
  • Medical Oncology

Fellowship:

  • Dana-Farber/Partners CancerCare, Medical Oncology

Residency:

  • Johns Hopkins Hospital, Osler Housestaff Training Program

Medical School:

  • University of Toronto

Research

Melanoma Translational Research

Characterization of genetics in patients with mucosal melanoma treated with immune checkpoint blockade. Cancer Med. 2021 04; 10(8):2627-2635.
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Tumor and immune reprogramming during immunotherapy in advanced renal cell carcinoma. Cancer Cell. 2021 May 10; 39(5):649-661.e5.
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Cytokine changes during immune-related adverse events and corticosteroid treatment in melanoma patients receiving immune checkpoint inhibitors. Cancer Immunol Immunother. 2021 Jan 22.
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Integrated molecular drivers coordinate biological and clinical states in melanoma. Nat Genet. 2020 12; 52(12):1373-1383.
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Clinical landscape of oncolytic virus research in 2020. J Immunother Cancer. 2020 10; 8(2).
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Author Correction: A single-cell and single-nucleus RNA-Seq toolbox for fresh and frozen human tumors. Nat Med. 2020 Aug; 26(8):1307.
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Vitamin D intake is associated with decreased risk of immune checkpoint inhibitor-induced colitis. Cancer. 2020 08 15; 126(16):3758-3767.
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A single-cell and single-nucleus RNA-Seq toolbox for fresh and frozen human tumors. Nat Med. 2020 05; 26(5):792-802.
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Inactivation of Fbxw7 Impairs dsRNA Sensing and Confers Resistance to PD-1 Blockade. Cancer Discov. 2020 09; 10(9):1296-1311.
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Treatment-Induced Tumor Dormancy through YAP-Mediated Transcriptional Reprogramming of the Apoptotic Pathway. Cancer Cell. 2020 01 13; 37(1):104-122.e12.
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Defining the landscape of ATP-competitive inhibitor resistance residues in protein kinases. Nat Struct Mol Biol. 2020 01; 27(1):92-104.
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Destabilization of NOXA mRNA as a common resistance mechanism to targeted therapies. Nat Commun. 2019 11 14; 10(1):5157.
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Complex inter-relationship of body mass index, gender and serum creatinine on survival: exploring the obesity paradox in melanoma patients treated with checkpoint inhibition. J Immunother Cancer. 2019 03 29; 7(1):89.
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A Cancer Cell Program Promotes T Cell Exclusion and Resistance to Checkpoint Blockade. Cell. 2018 11 01; 175(4):984-997.e24.
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Genomic correlates of response to immune checkpoint blockade in microsatellite-stable solid tumors. Nat Genet. 2018 09; 50(9):1271-1281.
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Trapping Cancers as They Adapt to Survive. Cancer Discov. 2017 11; 7(11):1216-1217.
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Characterization of Thyroid Disorders in Patients Receiving Immune Checkpoint Inhibition Therapy. Cancer Immunol Res. 2017 12; 5(12):1133-1140.
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Point of care assessment of melanoma tumor signaling and metastatic burden from µNMR analysis of tumor fine needle aspirates and peripheral blood. Nanomedicine. 2017 04; 13(3):821-828.
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Clinical profiling of BCL-2 family members in the setting of BRAF inhibition offers a rationale for targeting de novo resistance using BH3 mimetics. PLoS One. 2014; 9(7):e101286.
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A melanoma cell state distinction influences sensitivity to MAPK pathway inhibitors. Cancer Discov. 2014 Jul; 4(7):816-27.
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Metabolic dysregulation in melanoma: cause or consequence? Cancer Discov. 2014 Apr; 4(4):390-1.
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Molecular pathways: BRAF induces bioenergetic adaptation by attenuating oxidative phosphorylation. Clin Cancer Res. 2014 May 01; 20(9):2257-63.
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Improving apoptotic responses to targeted therapy. Oncotarget. 2013 Sep; 4(9):1331.
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Targeting melanoma by small molecules: challenges ahead. Pigment Cell Melanoma Res. 2013 Jul; 26(4):464-9.
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Oncogenic BRAF regulates oxidative metabolism via PGC1a and MITF. Cancer Cell. 2013 Mar 18; 23(3):302-15.
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BCL2A1 is a lineage-specific antiapoptotic melanoma oncogene that confers resistance to BRAF inhibition. Proc Natl Acad Sci U S A. 2013 Mar 12; 110(11):4321-6.
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PGC-1 coactivators regulate MITF and the tanning response. Mol Cell. 2013 Jan 10; 49(1):145-57.
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YY1 regulates melanocyte development and function by cooperating with MITF. PLoS Genet. 2012; 8(5):e1002688.
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A novel recurrent mutation in MITF predisposes to familial and sporadic melanoma. Nature. 2011 Nov 13; 480(7375):99-103.
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Antitussive and toxicological evaluation of Vitex negundo. Nat Prod Res. 2012; 26(5):484-8.
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Biology and clinical relevance of the micropthalmia family of transcription factors in human cancer. J Clin Oncol. 2011 Sep 01; 29(25):3474-82.
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Investigation of antitussive and toxicological activity of Ballota limbata in mice. Pharm Biol. 2011 Jun; 49(6):627-32.
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Monoamines block kainate- and carbachol-induced gamma-oscillations but augment stimulus-induced gamma-oscillations in rat hippocampus in vitro. Hippocampus. 2009 Mar; 19(3):273-88.
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A dish best served hot. Am J Med. 2006 Apr; 119(4):307-9.
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c-Met expression is regulated by Mitf in the melanocyte lineage. J Biol Chem. 2006 Apr 14; 281(15):10365-73.
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Age-old theories die hard. Clin Invest Med. 2003 Jun; 26(3):116-20.
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Chronic inflammatory demyelinating polyradiculoneuropathy in diabetic patients. Muscle Nerve. 2003 Apr; 27(4):465-70.
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Constitutive p38HOG mitogen-activated protein kinase activation induces permanent cell cycle arrest and senescence. Cancer Res. 2002 Sep 01; 62(17):5076-82.
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TEL-JAK2 constitutively activates the extracellular signal-regulated kinase (ERK), stress-activated protein/Jun kinase (SAPK/JNK), and p38 signaling pathways. Blood. 2002 Aug 15; 100(4):1438-48.
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Regulation of erythropoietin-induced STAT serine phosphorylation by distinct mitogen-activated protein kinases. J Biol Chem. 2002 May 10; 277(19):17359-66.
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NKIATRE is a novel conserved cdc2-related kinase. Genomics. 2001 Jan 15; 71(2):131-41.
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Chronic inflammatory demyelinating polyradiculoneuropathy: a study of proposed electrodiagnostic and histologic criteria. Arch Neurol. 2000 Dec; 57(12):1745-50.
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Escherichia coli Shiga toxins induce apoptosis in epithelial cells that is regulated by the Bcl-2 family. Am J Physiol Gastrointest Liver Physiol. 2000 May; 278(5):G811-9.
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Mitoxantrone-DHAP with GM-CSF: an active but myelosuppressive salvage therapy for relapsed/refractory aggressive non-Hodgkin's lymphoma. Leuk Lymphoma. 1999 Nov; 35(5-6):527-36.
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Identification of NKIAMRE, the human homologue to the mitogen-activated protein kinase-/cyclin-dependent kinase-related protein kinase NKIATRE, and its loss in leukemic blasts with chromosome arm 5q deletion. Cancer Res. 1999 Aug 15; 59(16):4069-74.
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Respiratory muscle involvement in Bethlem myopathy. Neurology. 1999 Jan 01; 52(1):174-6.
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Inhibition of apoptotic signaling pathways in cancer cells as a mechanism of chemotherapy resistance. Cancer Metastasis Rev. 1998 Jun; 17(2):233-9.
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Boston, MA 02215
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