Philadelphia University + Thomas Jefferson University


Highlighted Publications

Neupane M, Clark AP, Landini S, Birkbak NJ, Eklund AC, Schumacher SE, Beroukhim R, Szallasi Z, Vidal M, Hill DE, Silver DPMECP2 Is a Frequently Amplified Oncogene with a Novel Epigenetic Mechanism that Mimics the Role of Activated RAS in Malignancy. Cancer Discovery 2016 Jan; 6(1): 45-58.

We describe the first generation screen for new oncogenes and the initial characterization of a novel commonly amplified oncogene, MECP2.

Birkbak NJ, Wang ZC, Kim JY, Ecklund AC, Li Q, Tian R, Bowman-Colin C, Li Y, Greene-Colozzi A, Iglehart JD, Tung N, Ryan PD, Garber JE, *Silver DP, *Szallasi Z, *Richardson AL. Telomeric Allelic Imbalance Indicates Defective DNA Repair and Sensitivity to DNA-Damaging Agents. Cancer Discovery 2012; Apr; 2(4):366-75. (*co-senior authors)

This paper describes the first biomarker of chemotherapy response derived from counting the number of a specific kind of chromosomal abnormality.

Telli ML,  Timms  K,  Reid J  , Hennessy B, Mills G,  Jensen KC, Szallasi Z, Barry WT, Winer EP, Tung NM, Isakoff SJ, Greene-Colozzi A, Gutin A, Sangale Z, Iliev  D, Neff C, Abkevich V, Jones J, Lanchbury JS, Hartman A, Garber JE, Ford JM, Silver DP*, Richardson AL. Homologous Recombination Deficiency (HRD) Score Predicts Response to Platinum-Containing Neoadjuvant Chemotherapy in Patients with Triple Negative Breast Cancer. Clinical Cancer 2016 Aug; 22(15), 3764–3773. *Corresponding author*

Here we demonstrate the utility of a biomarker of chemotherapy response based upon telomeric allelic imbalance.

Recent Publications

Overexpression of BLM promotes DNA damage and increased sensitivity to platinum salts in triple-negative breast and serous ovarian cancers

Zoledronic acid alters hematopoiesis and generates breast tumor-suppressive bone marrow cells

MECP2 is a frequently amplified oncogene with a novel epigenetic mechanism that mimics the role of activated RAS in malignancy

BRCA1 pathway function in basal-like breast cancer cells

Mechanisms of BRCA1 tumor suppression

Mutational processes molding the genomes of 21 breast cancers

Telomeric allelic imbalance indicates defective DNA repair and sensitivity to DNA-damaging agents

Chek2 DNA damage response pathway and inherited breast cancer risk

Poly ADP-ribose polymerase inhibitors: Science and current clinical development

Prevalence and predictors of loss of wild type BRCA1 in estrogen receptor positive and negative BRCA1-associated breast cancers

Poly(ADP-ribose) polymerase inhibition: "Targeted" therapy for triple-negative breast cancer

Efficacy of neoadjuvant cisplatin in triple-negative breast cancer

Complex landscapes of somatic rearrangement in human breast cancer genomes

Estrogen receptor-negative breast cancer: New insights into subclassification and targeting

Cyclin A Is Redundant in Fibroblasts but Essential in Hematopoietic and Embryonic Stem Cells

Synthetic lethality - A new direction in cancer-drug development

Cancer: Crossing over to drug resistance

Further Evidence for BRCA1 Communication with the Inactive X Chromosome

Abnormalities of the inactive X chromosome are a common feature of brca1 mutant and sporadic basal-like breast cancer

Isosteric ramatroban analogs: Selective and potent CRTH-2 antagonists