Matthias J. Szabolcs, MD

Board Certifications: 
Anatomic Pathology
Accepting New Patients
Profile Headshot


Areas of Expertise / Conditions Treated

Surgical Pathology

Academic Appointments

  • Professor of at CUMC

Hospital Affiliations

  • NewYork-Presbyterian/Columbia


  • Spanish
  • German


  • Male

Insurance Accepted


  • EPO
  • HMO
  • Medicare Managed Care
  • NY Signature
  • POS
  • PPO
  • Signature Administrators
  • Student Health


  • EPO
  • Great West
  • HMO
  • POS
  • PPO


  • HMO
  • Medicare Managed Care
  • PPO


  • ConnectiCare
  • EPO
  • Essential Plan
  • HMO
  • Medicaid Managed Care
  • Medicare Managed Care
  • POS
  • PPO
  • Select Care (Exchange)
  • Vytra

Empire Blue Cross Blue Shield

  • Blue Priority
  • EPO
  • HMO
  • Medicare (Mediblue)
  • NYP Employee Plan
  • Pathway (Exchange)
  • POS
  • PPO

Local 1199

  • Local 1199


  • MagnaCare


  • Multiplan

Oxford Health Plans

  • Freedom
  • Liberty
  • Medicare Managed Care




  • Columbia University Employee Plan
  • Compass (Exchange)
  • EPO
  • Essential Plan
  • HMO
  • Medicaid (Community Plan)
  • Medicare Managed Care
  • POS
  • PPO

*Please contact the provider’s office directly to verify that your particular insurance is accepted.

Credentials & Experience

Education & Training

  • University of Vienna Faculty of Medicine (Austria)
  • Internship: 1990 General Hospital of Vienna
  • Residency: NewYork-Presbyterian Hospital/Columbia University Medical Center

Board Certifications

  • Anatomic Pathology


Among my scientific contributions relevant to this project is the analysis of various genetically engineered mouse models (GEMs), which generate cancerous and precancerous lesions and correlate such lesions with those occurring in humans. One publication in Carcinogenesis 2006 (ref. 1), describes an aggressive subtype of prostate cancer generated by conditional overexpression of the Erbb2/Neu oncogene in mouse prostatic apical cells with a comprehensive gene expression analysis which revealed concomitant overexpression of Egfr, Erbb3 and phosphorylated androgen receptor in such cancers. This was confirmed by tissue microarray analysis of both human and mouse tissues demonstrating that in human prostate cancer heterodimerization of either EGFR or NEU with ERBB3 rather than the EGFR/NEU heterodimer promote tumorigenesis and tumor progression with respect to the Erbb pathway. My task was to perform the histopathological and immunohistochemical analysis of all tissues including scoring of all tissue microarrays for EGRF, NEU and ERBB3. A similar project was the study of the relation of the NOTCH1 receptor with downstream expression of c-MYC in mouse and human breast cancer (ref 2, 3), which was done on a molecular and protein level establishing MYC as a molecular target of NOTCH signaling. High protein levels of MYC in human tumors correlated significantly with increased Notch signaling using immunohistochemistry on tissue microarrays. I performed the immunohistochemical analysis of all tumors for this project. With respect to breast cancers in GEMs lacking the BRCA1/BARD1 heterodimer I could establish that their morphology resembles those of basal-like breast cancers in humans. Consequently such GEM models were used to dissect, which binding sites, binding partners and enzymatic functions of BRCA1 are important for its tumor suppression function (ref 4,5,6). A further study established IRS2 as potential pharmacological target for cancers with inactivation of the PTEN tumor suppressor demonstrating lack of progression to invasive carcinoma in GEMs deficient for this protein and high levels of IRS2 in human cancer with PTEN inactivation (ref 7) based on histological and immunohistochemical analysis. With respect to pharmacological targets and agents for cancer therapy, I conducted the analysis for several projects validating 1) IGF1R as a potential target for KRAS induced basal cell-like breast cancer in mice (ref 8), 2) a direct c-MYC inhibitor reducing pancreas cancer of mice (ref. 9), 3) the combination of metformin and elrotinib and metformin have a synergistic effect on human basal cell cancer (ref. 10) and 4) the role of Ctip in Brca1 deleted breast cancer models (ref 11).

Within the Department of Pathology, my unique expertise lies in combining both clinical and mouse pathology, which expands my knowledge and experience in analyzing both human and mouse models of breast cancer. Transgenic mouse models are an important part of cancer research in general and breast cancer research, which is one of the neoplasms for which a large number of transgenic mouse model have been created, in particular. It is paramount to have accurate pathohistological assessment of any lesion occurring in such genetically engineered mice (GEMs) in order to exploit the full potential of this experimental approach. For the last eleven years I have been involved in the histopathological and immunohistochemical analysis of GEMs particularly as they relate to breast and pancreatic cancer. Each year my laboratory analyzes ~1,000 GEMs generating more than 8,000 blocks for histology and more than 15,000 immunohistochemical stains using a fully automated staining system. I consider myself qualified to perform the histopathological analysis for this proposal, because I have board experience in mouse models such as Brca1 and Brca2 related defects and the MMTV-PyMT and 4T1 model system. I am familiar with the histopathological changes occurring in all organ systems of respective GEMs, which will guarantee rapid processing of the pathohistological data. There is access to a computer-aided image analysis system, which will be used to assess tumor progression and metastases quantitatively. Our laboratory routinely performs the immunohistochemical analysis, e.g. cellular amount of pAKT, proliferation and apoptosis index and immune cell analysis requisite to the proposed project. In summary, I have demonstrated in the past that I have the expertise and ability to generate prompt, accurate and reproducible histopathological data relevant to the research groups.


CORE B (Federal Gov)

Apr 1 2014 - Mar 31 2019


Jan 13 2014 - Nov 30 2018


Jul 1 2002 - Aug 31 2015


Jan 1 2009 - Dec 31 2013

Selected Publications

1. Li Z, Szabolcs M, Terwilliger JD, Efstratiadis A. Prostatic intraepithelial neoplasia and adenocarcinoma in mice expressing a probasin-Neu oncogenic transgene. Carcinogenesis. 2006 May;27(5):1054-67. PMID: 16401639

2.   Klinakis A, Szabolcs M, Politi K, Kiaris H, Artavanis-tsakonas S, Efstratitdis A. Myc is a Notch1 transcriptional target and a requisite for Notch1-induced mammary tumorigenesis in mice. Proc Natl Acad Sci U S A. 2006; 103(24):9262-7. PMID: 16751266

3.  Efstratiadis A, Szabolcs M, Klinakis A. Notch, Myc and Breast Cancer. Cell Cycle. 2007 Feb 9;6(4). PMID: 17329972

4.  Shakya R, Szabolcs M, Mc Carthy E, Ospina E, Basso K, Nandula S, Murty V, Baer R, Ludwig T. The basal-like mammary carcinomas induced by Brca1 or Bard1 inactivation implicate the BRCA1/BARD1 heterodimer in tumor suppression. Proc Natl Acad Sci U S A. 2008;105(19):7040-5. PMID: 18443292

5.   Shakya R, Reid LJ, Reczek CR, Cole F, Egli D, Lin CS, deRooij DG, Hirsch S, Ravi K, Hicks JB, Szabolcs M, Jasin M, Baer R, Ludwig T. BRCA1 tumor suppression depends on BRCT phosphoprotein binding, but not on its E3 ligase activity. Science 2011; 334(6055):525-528 PMID:22034435

6.   Reczek CR, Szabolcs M, Stark JM, Ludwig T, Baer R. The interaction between CTIP and BRCA1 is not essential for resection mediated DNA repair of tumor suppression. J Cell Biol. 2013 May 27; 201(5):693-707. PMID: 23712259

7. Szabolcs M, Keniry M, Simpson L, Reid LJ, Koujak S, Schiff SC, Davidian G, Licata S, Gruvberger-Saal S, Murty VV, Nandula S, Efstratiadis A, Kushner JA, White MF, Parsons R. Irs2 inactivation suppresses tumor progression in Pten+/- mice. Am J Pathol. 2009; 174:276-86. PMID: 19095950

8. Klinakis A, Szabolcs M, Chen G, Xuan S, Hibshoosh H, Efstratiadis A. Ifgr1 is a therapeutic target in a mouse model of basal-like breast cancer. Proc Natl Acad Sci U S A. 2009;106:2359-64. PMID: 19174523 

9.   Stellas D, Szabolcs M, Koul S, Li Z, Polyzos A, Anagnostopoulos C, Cournia Z, Tamvakopoulos C, Klinakis A, Efstratiadis A. Therapeutic effect of an anti-myc drug on mouse pancreatic cancer. J Natl Cancer Inst. 2014 Oct 11; 106(12). pii: dju320. doi: 10.1093/jnci/dju320. PMID:25306215

10. Lau YK, Du X, Rayannavar V, Hopkins B, Shaw J, Bessler E, Thomas T, Pires MM, Keniry M, Parsons RE, Cremers S, Szabolcs M, Maurer MA. Metformin and erlotinib synergize to inhibit basal breast cancer. Oncotarget. 2014 Nov 15; 5(21):10503-17. PMID: 25361177

11. Reczek CR, Shakya R, Miteva Y, Szabolcs M, Ludwig T, Baer R. The DNA resection protein CtIP promotes mammary tumorigenesis. Oncotarget. 2016 Apr 6. [Epub ahead of print] PMID:27058754