Dr. Pan is a board-certified, fellowship-trained medical oncologist with the Stanford Medicine Cancer Center and a clinical associate professor in the Department of Medicine, Division of Oncology.

He diagnoses and treats various oncological conditions and specializes in the treatment of bone and soft sarcoma. He creates personalized and comprehensive care plans for each patient he serves.

Dr. Pan’s research focuses include understanding how genomic alterations impact the biological behavior and prognosis of sarcomas. In his work, he identifies new targets for developing innovative therapeutics for sarcoma treatment.

He has published more than fifty papers and many abstracts and presented in many cancer and immunology conferences. His papers have been published in the Journal of Clinical Oncology, JCO Precision Oncology, Nature Review Clinical Oncology, JCO Oncology Practice, Journal of Hematology and Oncology, and other peer-reviewed journals. He has also presented to his peers at international, national, and regional meetings, including the annual meetings of the American Society of Clinical Oncology, the Chinese Society Of Clinical Oncology, and the Connective Tissue Oncology Society.

Dr. Pan is a member of the American Society of Clinical Oncology, the American Association of Immunologists, and the American Association for Advancement of Science.

Clinical Focus

  • Medical Oncology

Academic Appointments

Professional Education

  • Board Certification: American Board of Internal Medicine, Medical Oncology (2022)
  • Fellowship: Stanford University Hematology and Oncology Fellowship (2002) CA
  • Residency: St Mary's Medical Center Internal Medicine Residency CA
  • Medical Education: Fujian Medical University (1984) China

All Publications

  • Rapid Response of a BRCA2/TP53/PTEN-Deleted Metastatic Uterine Leiomyosarcoma to Olaparib: A Case Report. The Permanente journal Pan, M., Ganjoo, K., Karam, A. 2021; 25


    None: Patients with metastatic uterine leiomyosarcoma (uLMS) have poor prognosis due to limited treatment options, especially when disease progresses on doxorubicin and gemcitabine-docetaxel regimens. Here we report a patient whose metastatic uLMS contains a BRCA2 deep deletion as well as TP53 and PTEN deep deletion. The patient responded rapidly to olaparib, a poly (ADP-ribose) polymerase inhibitor, after progressing on gemcitabine-docetaxel, doxorubicin, and temozolomide regimens. This case report shall be helpful to the treatment of other patients with metastatic uLMS that harbors a BRCA2 mutation or deletion.

    View details for DOI 10.7812/TPP/20.251

    View details for PubMedID 33970096

  • Fourteen-Day Gemcitabine-Docetaxel Chemotherapy Is Effective and Safer Compared to 21-Day Regimen in Patients with Advanced Soft Tissue and Bone Sarcoma CANCERS Pan, M., Trieu, M. K., Sidhu, M., Yu, J., Seto, T., Ganjoo, K. 2021; 13 (8)


    Gemcitabine-docetaxel (G-D) combination is an effective chemotherapy for patients with advanced soft tissue and bone sarcoma, first developed with G administered on days 1 and 8, and D on day 8 every 21 days and later modified to be administered every 14 days in 2012. The 14-day regimen has become increasingly adopted. However, its efficacy and toxicities have not been compared. We identified 161 patients with metastatic or locally advanced soft tissue and bone sarcoma treated with either a 14-day or 21-day regimen within Northern California Kaiser Permanente from 1 January 2017 to 30 July 2020 and compared the outcomes and toxicity profiles of patients treated with the either regimen. Seventy-nine (49%) and 82 (51%) patients received the 14-day and the 21-day regimen, respectively, with similar response rate (22.8% and 15.8%, p = 0.26), median progression-free survival (PFS, 4.0 and 3.2 months, p = 0.15), and median overall survival (OS, 12.6 and 14.7 months, p = 0.55). Subset analysis of the untreated patients (approximately 60% of the entire cohort) as well as the patients with leiomyosarcoma only (approximately 50% of the entire cohort) showed that OS was not significantly different between the two regimens. Febrile neutropenia requiring hospitalization occurred in 10 and one patients (p = 0.006) and intolerance leading to discontinuation of chemotherapy occurred in 12 and two patients (p = 0.006) treated with the 21-day and the 14-day regimens, respectively. CDKN2A deletion/mutation or CDK4 amplification was associated with worse median OS (p = 0.06), while a RB1 deletion/mutation was associated with better median PFS (p = 0.05), and these two genomic alterations were mutually exclusive. Our data demonstrate that, compared to the traditional 21-day G-D regimen, the 14-day G-D regimen is equally effective but safer. In addition, CDKN2A and RB1 pathways play significant role on the outcomes of the patients.

    View details for DOI 10.3390/cancers13081983

    View details for Web of Science ID 000644016300001

    View details for PubMedID 33924080

  • Case series of MET exon 14 skipping mutation-positive non-small-cell lung cancers with response to crizotinib and cabozantinib ANTI-CANCER DRUGS Wang, S. Y., Zhang, B. M., Wakelee, H. A., Koontz, M. Z., Pan, M., Diehn, M., Kunder, C. A., Neal, J. W. 2019; 30 (5): 537–41
  • Oxaliplatin-Fluoropyrimidine Chemotherapy Plus Bevacizumab in Advanced Neuroendocrine Tumors: An Analysis of 2 Phase II Trials. Pancreas Kunz, P. L., Balise, R. R., Fehrenbacher, L., Pan, M., Venook, A. P., Fisher, G. A., Tempero, M. A., Ko, A. H., Korn, W. M., Hwang, J., Bergsland, E. K. 2016; 45 (10): 1394-1400


    This study aimed to determine the safety and effectiveness of bevacizumab (B) plus FOLFOX or CAPOX in advanced neuroendocrine tumors (NETs) by performing a combined analysis of 2 separate prospective phase II studies.In the FOLFOX/B study, patients received chemotherapy without scheduled breaks in 3 cohorts: carcinoid, pancreatic NET, and poorly differentiated neuroendocrine carcinomas. In the CAPOX/B study, NET subtypes were pooled, and patients were treated with 4 cycles of CAPOX/B followed by optional maintenance therapy. Primary end points were radiographic response rate (RR) after 12 cycles (FOLFOX/B), progression-free survival (PFS) (CAPOX/B), and toxicity (both).Seventy-six patients (FOLFOX/B, n = 36; CAPOX/B, n = 40) were included. In FOLFOX/B, RR for carcinoid at 12 cycles 3/22 (13.6%), median PFS 19.3 months; RR for pancreatic NET at 12 cycles 4/12 (41.7%), median PFS 21 months; RR 1/2 (50%) in poorly differentiated neuroendocrine carcinoma; pooled RR 25% and median PFS 21 months (1-year PFS 68%). In CAPOX/B (pooled NET), RR 18% and median PFS 16.7 months (1-year PFS 65%). Predictable toxicity was observed.Neither study met its primary end point, but radiographic responses and prolonged disease stability in previously progressing patients suggest that selected patients with NET may benefit from oxaliplatin-fluoropyrimidine chemotherapy plus bevacizumab and that the combination may warrant further study.

    View details for PubMedID 27171514

  • Brg1 governs a positive feedback circuit in the hair follicle for tissue regeneration and repair. Developmental cell Xiong, Y., Li, W., Shang, C., Chen, R. M., Han, P., Yang, J., Stankunas, K., Wu, B., Pan, M., Zhou, B., Longaker, M. T., Chang, C. 2013; 25 (2): 169-181


    Hair follicle stem cells (bulge cells) are essential for hair regeneration and early epidermal repair after wounding. Here we show that Brg1, a key enzyme in the chromatin-remodeling machinery, is dynamically expressed in bulge cells to control tissue regeneration and repair. In mice, sonic hedgehog (Shh) signals Gli to activate Brg1 in bulge cells to begin hair regeneration, whereas Brg1 recruits NF-κB to activate Shh in matrix cells to sustain hair growth. Such reciprocal Brg1-Shh interaction is essential for hair regeneration. Moreover, Brg1 is indispensable for maintaining the bulge cell reservoir. Without Brg1, bulge cells are depleted over time, partly through the ectopic expression of the cell-cycle inhibitor p27(Kip1). Also, bulge Brg1 is activated by skin injury to facilitate early epidermal repair. Our studies demonstrate a molecular circuit that integrates chromatin remodeling (Brg1), transcriptional regulation (NF-κB, Gli), and intercellular signaling (Shh) to control bulge stem cells during tissue regeneration.

    View details for DOI 10.1016/j.devcel.2013.03.015

    View details for PubMedID 23602386

  • Brg1 governs distinct pathways to direct multiple aspects of mammalian neural crest cell development PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA Li, W., Xiong, Y., Shang, C., Twu, K. Y., Hang, C. T., Yang, J., Han, P., Lin, C., Lin, C., Tsai, F., Stankunas, K., Meyer, T., Bernstein, D., Pan, M., Chang, C. 2013; 110 (5): 1738-1743


    Development of the cerebral vessels, pharyngeal arch arteries (PAAs). and cardiac outflow tract (OFT) requires multipotent neural crest cells (NCCs) that migrate from the neural tube to target tissue destinations. Little is known about how mammalian NCC development is orchestrated by gene programming at the chromatin level, however. Here we show that Brahma-related gene 1 (Brg1), an ATPase subunit of the Brg1/Brahma-associated factor (BAF) chromatin-remodeling complex, is required in NCCs to direct cardiovascular development. Mouse embryos lacking Brg1 in NCCs display immature cerebral vessels, aberrant PAA patterning, and shortened OFT. Brg1 suppresses an apoptosis factor, Apoptosis signal-regulating kinase 1 (Ask1), and a cell cycle inhibitor, p21(cip1), to inhibit apoptosis and promote proliferation of NCCs, thereby maintaining a multipotent cell reservoir at the neural crest. Brg1 also supports Myosin heavy chain 11 (Myh11) expression to allow NCCs to develop into mature vascular smooth muscle cells of cerebral vessels. Within NCCs, Brg1 partners with chromatin remodeler Chromodomain-helicase-DNA-binding protein 7 (Chd7) on the PlexinA2 promoter to activate PlexinA2, which encodes a receptor for semaphorin to guide NCCs into the OFT. Our findings reveal an important role for Brg1 and its downstream pathways in the survival, differentiation, and migration of the multipotent NCCs critical for mammalian cardiovascular development.

    View details for DOI 10.1073/pnas.1218072110

    View details for Web of Science ID 000314558100038

    View details for PubMedID 23319608

    View details for PubMedCentralID PMC3562770

  • Activation of NFAT Signaling in Podocytes Causes Glomerulosclerosis JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY Wang, Y., Jarad, G., Tripathi, P., Pan, M., Cunningham, J., Martin, D. R., Liapis, H., Miner, J. H., Chen, F. 2010; 21 (10): 1657-1666


    Mutant forms of TRPC6 can activate NFAT-dependent transcription in vitro via calcium influx and activation of calcineurin. The same TRPC6 mutants can cause FSGS, but whether this involves an NFAT-dependent mechanism is unknown. Here, we generated mice that allow conditional induction of NFATc1. Mice with NFAT activation in nascent podocytes in utero developed proteinuria and glomerulosclerosis postnatally, resembling FSGS. NFAT activation in adult mice also caused progressive proteinuria and FSGS. Ultrastructural studies revealed podocyte foot process effacement and deposition of extracellular matrix. NFAT activation did not initially affect expression of podocin, synaptopodin, and nephrin but reduced their expression as glomerular injury progressed. In contrast, we observed upregulation of Wnt6 and Fzd9 in the mutant glomeruli before the onset of significant proteinuria, suggesting a potential role for Wnt signaling in the pathogenesis of NFAT-induced podocyte injury and FSGS. These results provide in vivo evidence for the involvement of NFAT signaling in podocytes, proteinuria, and glomerulosclerosis. Furthermore, this study suggests that NFAT activation may be a key intermediate step in the pathogenesis of mutant TRPC6-mediated FSGS and that suppression of NFAT activity may contribute to the antiproteinuric effects of calcineurin inhibitors.

    View details for DOI 10.1681/ASN.2009121253

    View details for Web of Science ID 000282999000013

    View details for PubMedID 20651158

    View details for PubMedCentralID PMC3013542

  • Enhanced NFATc1 nuclear occupancy causes T cell activation independent of CD28 costimulation JOURNAL OF IMMUNOLOGY Pan, M., Winslow, M. M., Chen, L., Kuo, A., Felsher, D., Crabtree, G. R. 2007; 178 (7): 4315-4321


    TCR signals induce the nuclear localization of NFATc proteins, which are removed from the nucleus after rephosphorylation by glycogen synthase kinase 3 and other kinases. Rapid nuclear export might allow continuous monitoring of receptor occupancy, making the transcriptional response proportional to the duration of TCR/CD28 signaling. To investigate this possibility, we analyzed mice in which T cells express a NFATc1 variant (NFATc1(nuc)) with serine-to-alanine changes at the glycogen synthase kinase 3 phosphorylation sites. NFATc1(nuc) T cells have constitutively nuclear NFATc1, enhanced T cell activation in vivo, and calcineurin-independent proliferation in vitro. NFATc1(nuc) T cells are hypersensitive to TCR/CD3 stimulation, resulting in enhanced proliferation and cytokine production that is independent of CD28 costimulation. These results support the notion that CD28 inhibits nuclear export of NFATc transcription factors. In addition, NFATc1(nuc) destabilizes a positive feedback loop in which NFATc1 activates its own transcription as well as its targets, such as CD40 ligand and Th1/Th2 cytokines.

    View details for Web of Science ID 000245197300038

    View details for PubMedID 17371988

  • Stringent control of NFATc1 nuclear occupancy is critical for maintaining balanced immune response GENE THERAPY AND MOLECULAR BIOLOGY Pan, M., Winslow, M. M., Keum, J. S., Crabtree, G. R. 2007; 11B: 171-176
  • Calcineurin/NFAT signaling in osteoblasts regulates bone mass DEVELOPMENTAL CELL Winslow, M. M., Pan, M., Starbuck, M., Gallo, E. M., Deng, L., Karsenty, G., Crabtree, G. R. 2006; 10 (6): 771-782


    Development and repair of the vertebrate skeleton requires the precise coordination of bone-forming osteoblasts and bone-resorbing osteoclasts. In diseases such as osteoporosis, bone resorption dominates over bone formation, suggesting a failure to harmonize osteoclast and osteoblast function. Here, we show that mice expressing a constitutively nuclear NFATc1 variant (NFATc1(nuc)) in osteoblasts develop high bone mass. NFATc1(nuc) mice have massive osteoblast overgrowth, enhanced osteoblast proliferation, and coordinated changes in the expression of Wnt signaling components. In contrast, viable NFATc1-deficient mice have defects in skull bone formation in addition to impaired osteoclast development. NFATc1(nuc) mice have increased osteoclastogenesis despite normal levels of RANKL and OPG, indicating that an additional NFAT-regulated mechanism influences osteoclastogenesis in vivo. Calcineurin/NFATc signaling in osteoblasts controls the expression of chemoattractants that attract monocytic osteoclast precursors, thereby coupling bone formation and bone resorption. Our results indicate that NFATc1 regulates bone mass by functioning in both osteoblasts and osteoclasts.

    View details for DOI 10.1016/j.devcel.2006.04.006

    View details for Web of Science ID 000238244700011

    View details for PubMedID 16740479