Clinical Focus

  • Residency

Honors & Awards

  • Northern California Chapter Resident Research Award Finalist, American College of Surgeons (4/30/2016)
  • Resident Research Award, Department of Surgery, Division of General Surgery, Stanford University School of Medicine (2014)
  • Advanced Residency Training at Stanford (ARTS) Program, Stanford University (2013)
  • American College of Surgeons Resident Research Scholarship, American College of Surgeons (2013)
  • Resident Reviewer for JAMA Surgery, Journal of the American Medical Association (2013)
  • A. P. Giannini Foundation Postdoctoral Research Fellowship, A. P. Giannini Foundation for Medical Research (2012)
  • Resident’s Prize Finalist at the Pacific Coast Surgical Association’s 83rd Annual Meeting, Pacific Coast Surgical Association (2012)
  • Outstanding Poster/Abstract Presentation, Stanford Medical Student Research Symposium, Stanford University School of Medicine (2009)
  • International Academy of Achievement Student Delegate, International Academy of Achievement (2007)
  • Kaiser Permanente Latino Association Scholar Award, Kaiser Permanente (2007)
  • American Medical Association (AMA) Minority Scholar Award, American Medical Association (2006)
  • Howard Hughes Medical Institute (HHMI) Research Training Fellowship for Medical Students, Howard Hughes Medical Institute (2006)
  • The Paul & Daisy Soros Fellowships for New Americans, Paul & Daisy Soros Foundation (2006)
  • Stanford Medical Scholars Award, Stanford University School of Medicine (2005)

Boards, Advisory Committees, Professional Organizations

  • Ph.D. Candidate in the laboratory of Dr. Irving Weissman, Department of Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine (2013 - Present)
  • Resident in General Surgery, Stanford Hospital and Clinics (2009 - Present)

Membership Organizations

  • Society of Robotic Surgery, Member
  • Society of American Gastrointestinal and Endoscopic Surgeons, Member
  • Americas Hepato Pancreato Biliary Association, Member
  • North American NeuroEndocrine Tumor Society, Member
  • American College of Surgeons, Member
  • American Medical Association, Member

Professional Education

  • Doctor of Medicine, Stanford University, MED-MD (2009)
  • Bachelor of Science, Johns Hopkins University, UG Other not listed (1999)

Lab Affiliations

All Publications

  • Identification of tumorigenic cells and therapeutic targets in pancreatic neuroendocrine tumors PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA Krampitz, G. W., George, B. M., Willingham, S. B., Volkmer, J., Weiskopf, K., Jahchan, N., Newman, A. M., Sahoo, D., Zemek, A. J., Yanovsky, R. L., Nguyen, J. K., Schnorr, P. J., Mazur, P. K., Sage, J., Longacre, T. A., Visser, B. C., Poultsides, G. A., Norton, J. A., Weissman, I. L. 2016; 113 (16): 4464-4469


    Pancreatic neuroendocrine tumors (PanNETs) are a type of pancreatic cancer with limited therapeutic options. Consequently, most patients with advanced disease die from tumor progression. Current evidence indicates that a subset of cancer cells is responsible for tumor development, metastasis, and recurrence, and targeting these tumor-initiating cells is necessary to eradicate tumors. However, tumor-initiating cells and the biological processes that promote pathogenesis remain largely uncharacterized in PanNETs. Here we profile primary and metastatic tumors from an index patient and demonstrate that MET proto-oncogene activation is important for tumor growth in PanNET xenograft models. We identify a highly tumorigenic cell population within several independent surgically acquired PanNETs characterized by increased cell-surface protein CD90 expression and aldehyde dehydrogenase A1 (ALDHA1) activity, and provide in vitro and in vivo evidence for their stem-like properties. We performed proteomic profiling of 332 antigens in two cell lines and four primary tumors, and showed that CD47, a cell-surface protein that acts as a "don't eat me" signal co-opted by cancers to evade innate immune surveillance, is ubiquitously expressed. Moreover, CD47 coexpresses with MET and is enriched in CD90(hi)cells. Furthermore, blocking CD47 signaling promotes engulfment of tumor cells by macrophages in vitro and inhibits xenograft tumor growth, prevents metastases, and prolongs survival in vivo.

    View details for DOI 10.1073/pnas.1600007113

    View details for Web of Science ID 000374393800063

    View details for PubMedID 27035983

  • Multiple Endocrine Neoplasia Genetics and Clinical Management SURGICAL ONCOLOGY CLINICS OF NORTH AMERICA Norton, J. A., Krampitz, G., Jensen, R. T. 2015; 24 (4): 795-?
  • Better Survival But Changing Causes of Death in Patients With Multiple Endocrine Neoplasia Type 1. Annals of surgery Norton, J. A., Krampitz, G., Zemek, A., Longacre, T., Jensen, R. T. 2015; 261 (6): e147-8

    View details for DOI 10.1097/SLA.0000000000001211

    View details for PubMedID 26291955

  • Skin fibrosis. Identification and isolation of a dermal lineage with intrinsic fibrogenic potential. Science Rinkevich, Y., Walmsley, G. G., Hu, M. S., Maan, Z. N., Newman, A. M., Drukker, M., Januszyk, M., Krampitz, G. W., Gurtner, G. C., Lorenz, H. P., Weissman, I. L., Longaker, M. T. 2015; 348 (6232)


    Dermal fibroblasts represent a heterogeneous population of cells with diverse features that remain largely undefined. We reveal the presence of at least two fibroblast lineages in murine dorsal skin. Lineage tracing and transplantation assays demonstrate that a single fibroblast lineage is responsible for the bulk of connective tissue deposition during embryonic development, cutaneous wound healing, radiation fibrosis, and cancer stroma formation. Lineage-specific cell ablation leads to diminished connective tissue deposition in wounds and reduces melanoma growth. Using flow cytometry, we identify CD26/DPP4 as a surface marker that allows isolation of this lineage. Small molecule-based inhibition of CD26/DPP4 enzymatic activity during wound healing results in diminished cutaneous scarring. Identification and isolation of these lineages hold promise for translational medicine aimed at in vivo modulation of fibrogenic behavior.

    View details for DOI 10.1126/science.aaa2151

    View details for PubMedID 25883361

  • RET gene mutations (genotype and phenotype) of multiple endocrine neoplasia type 2 and familial medullary thyroid carcinoma. Cancer Krampitz, G. W., Norton, J. A. 2014; 120 (13): 1920-1931


    The rapid technical advances in molecular biology and accelerating improvements in genomic and proteomic diagnostics have led to increasingly personalized strategies for cancer therapy. Such an approach integrates the genomic, proteomic, and molecular information unique to the individual to provide an accurate genetic diagnosis, molecular risk assessment, informed family counseling, therapeutic profiling, and early preventative management that best fits the particular needs of each patient. The discovery of mutations in the RET proto-oncogene resulting in variable onset and severity of multiple endocrine neoplasia type 2 (MEN2) was the first step in developing direct genetic testing for at-risk individuals. Patients with germline RET mutations may undergo risk assessment and appropriate intervention based on specific mutations. Moreover, family members of affected individuals receive counseling based on understanding of the genetic transmission of the disease. Increasingly, clinicians are able to make therapeutic choices guided by an informative biomarker code. Improvements in detection and management of patients with MEN2 resulting from understanding of the RET proto-oncogene are evidence of the benefits of personalized cancer medicine. This review describes the discovery of the RET proto-oncogene, the association between genotype and phenotype, and the role of mutation analysis on diagnosis and treatment of MEN2. Cancer 2014. © 2014 American Cancer Society.

    View details for DOI 10.1002/cncr.28661

    View details for PubMedID 24699901

  • Pancreatic neuroendocrine tumours: hypoenhancement on arterial phase computed tomography predicts biological aggressiveness HPB Worhunsky, D. J., Krampitz, G. W., Poullos, P. D., Visser, B. C., Kunz, P. L., Fisher, G. A., Norton, J. A., Poultsides, G. A. 2014; 16 (4): 304-311


    Contrary to pancreatic adenocarcinoma, pancreatic neuroendocrine tumours (PNET) are commonly hyperenhancing on arterial phase computed tomography (APCT). However, a subset of these tumours can be hypoenhancing. The prognostic significance of the CT appearance of these tumors remains unclear.From 2001 to 2012, 146 patients with well-differentiated PNET underwent surgical resection. The degree of tumour enhancement on APCT was recorded and correlated with clinicopathological variables and overall survival.APCT images were available for re-review in 118 patients (81%). The majority had hyperenhancing tumours (n = 80, 68%), 12 (10%) were isoenhancing (including cases where no mass was visualized) and 26 (22%) were hypoenhancing. Hypoenhancing PNET were larger, more commonly intermediate grade, and had higher rates of lymph node and synchronous liver metastases. Hypoenhancing PNET were also associated with significantly worse overall survival after a resection as opposed to isoenhancing and hyperenhancing tumours (5-year, 54% versus 89% versus 93%). On multivariate analysis of factors available pre-operatively, only hypoenhancement (HR 2.32, P = 0.02) was independently associated with survival.Hypoenhancement on APCT was noted in 22% of well-differentiated PNET and was an independent predictor of poor outcome. This information can inform pre-operative decisions in the multidisciplinary treatment of these neoplasms.

    View details for DOI 10.1111/hpb.12139

    View details for Web of Science ID 000332989700002

    View details for PubMedID 23991643

  • Man with hypoechoic lesion abutting the pancreas. JAMA surgery Krampitz, G. W., Mills, A. M., Visser, B. C. 2014; 149 (4): 393-394

    View details for DOI 10.1001/jamasurg.2013.778

    View details for PubMedID 24522561

  • Pancreatic neuroendocrine tumors CURRENT PROBLEMS IN SURGERY Krampitz, G. W., NORTON, J. A. 2013; 50 (11): 509-545

    View details for DOI 10.1067/j.cpsurg.2013.08.001

    View details for Web of Science ID 000327104300002

    View details for PubMedID 24206780

  • Current management of the Zollinger-Ellison syndrome. Advances in surgery Krampitz, G. W., Norton, J. A. 2013; 47: 59-79


    In summary, ZES is a syndrome caused by gastrinoma, usually located within the gastrinoma triangle and associated with symptoms of peptic ulcer disease, GERD, and diarrhea. The diagnosis of ZES is made by measuring fasting levels of serum gastrin, BAO, and the secretin stimulation test. Because of the high association of ZES and MEN1, HPT must be excluded by obtaining a serum calcium and parathyroid hormone level. Treatment of ZES consists of medical control of symptoms with PPIs and evaluation for potentially curative surgical intervention. Noninvasive imaging studies including SRS, CT, and MRI should be performed initially to evaluate for metastases and identify resectable disease. Invasive imaging modalities such as EUS may be performed to further evaluate primary tumors. IOUS, palpation, and duodenotomy are used for intraoperative localization of gastrinomas. In patients with MEN1, surgical resection should be pursued only if there is an identifiable tumor larger than 2 cm and after surgery for the primary hyperparathyroidism (3 1/2-gland parathyroidectomy). All patients with resectable localized sporadic gastrinoma should undergo surgical exploration, even those with biochemical evidence but negative imaging studies. Tumor is most commonly found in the duodenum, and the cure rate is high. In patients with liver metastases, surgery should be considered if all identifiable tumor can be safely removed. A multidisciplinary approach including surgical and nonsurgical therapies should be taken in patients with advanced disease.

    View details for PubMedID 24298844

  • Lymph Nodes and Survival in Pancreatic Neuroendocrine Tumors ARCHIVES OF SURGERY Krampitz, G. W., Norton, J. A., Poultsides, G. A., Visser, B. C., Sun, L., Jensen, R. T. 2012; 147 (9): 820-827


    Lymph node metastases decrease survival in patients with pancreatic neuroendocrine tumors (pNETs).Prospective database searches.National Institutes of Health (NIH) and Stanford University Hospital (SUH).A total of 326 patients underwent surgical exploration for pNETs at the NIH (n = 216) and SUH (n = 110).Overall survival, disease-related survival, and time to development of liver metastases.Forty patients (12.3%) underwent enucleation and 305 (93.6%) underwent resection. Of the patients who underwent resection, 117 (35.9%) had partial pancreatectomy and 30 (9.2%) had a Whipple procedure. Forty-one patients also had liver resections, 21 had wedge resections, and 20 had lobectomies. Mean follow-up was 8.1 years (range, 0.3-28.6 years). The 10-year overall survival for patients with no metastases or lymph node metastases only was similar at 80%. As expected, patients with liver metastases had a significantly decreased 10-year survival of 30% (P < .001). The time to development of liver metastases was significantly reduced for patients with lymph node metastases alone compared with those with none (P < .001). For the NIH cohort with longer follow-up, disease-related survival was significantly different for those patients with no metastases, lymph node metastases alone, and liver metastases (P < .001). Extent of lymph node involvement in this subgroup showed that disease-related survival decreased as a function of the number of lymph nodes involved (P = .004).As expected, liver metastases decrease survival of patients with pNETs. Patients with lymph node metastases alone have a shorter time to the development of liver metastases that is dependent on the number of lymph nodes involved. With sufficient long-term follow-up, lymph node metastases decrease disease-related survival. Careful evaluation of number and extent of lymph node involvement is warranted in all surgical procedures for pNETs.

    View details for Web of Science ID 000308883700011

    View details for PubMedID 22987171

  • Hypoxia-inducible factor-dependent histone deacetylase activity determines stem cell fate in the placenta DEVELOPMENT Maltepe, E., Krampitz, G. W., Okazaki, K. M., Red-Horse, K., Mak, W., Simon, M. C., Fisher, S. J. 2005; 132 (15): 3393-3403


    Hypoxia-inducible factor (HIF) is a heterodimeric transcription factor composed of HIFalpha and the arylhydrocarbon receptor nuclear translocator (ARNT/HIF1beta). Previously, we have reported that ARNT function is required for murine placental development. Here, we used cultured trophoblast stem (TS) cells to investigate the molecular basis of this requirement. In vitro, wild-type TS cell differentiation is largely restricted to spongiotrophoblasts and giant cells. Interestingly, Arnt-null TS cells differentiated into chorionic trophoblasts and syncytiotrophoblasts, as demonstrated by their expression of Tfeb, glial cells missing 1 (Gcm1) and the HIV receptor CXCR4. During this process, a region of the differentiating Arnt-null TS cells underwent granzyme B-mediated apoptosis, suggesting a role for this pathway in murine syncytiotrophoblast turnover. Surprisingly, HIF1alpha and HIF2alpha were induced during TS cell differentiation in 20% O2; additionally, pVHL levels were modulated during the same time period. These results suggest that oxygen-independent HIF functions are crucial to this differentiation process. As histone deacetylase (HDAC) activity has been linked to HIF-dependent gene expression, we investigated whether ARNT deficiency affects this epigenetic regulator. Interestingly, Arnt-null TS cells had reduced HDAC activity, increased global histone acetylation, and altered class II HDAC subcellular localization. In wild-type TS cells, inhibition of HDAC activity recapitulated the Arnt-null phenotype, suggesting that crosstalk between the HIFs and the HDACs is required for normal trophoblast differentiation. Thus, the HIFs play important roles in modulating the developmental plasticity of stem cells by integrating physiological, transcriptional and epigenetic inputs.

    View details for DOI 10.1242/dev.01923

    View details for Web of Science ID 000231627800007

    View details for PubMedID 15987772