Bio


Arian Lundberg, Ph.D. MSc. is a Post-Doctoral scholar at the Department of Radiation Oncology of Stanford University.

Dr. Lundberg awarded his Ph.D. in Medical Bioinformatics, focusing on the transcriptional gene expression signatures in breast cancer from Karolinska Institute - Sweden. He mainly worked with data derived from clinically annotated cancer specimens of Swedish and International breast cancer cohorts. During his Ph.D. Dr. Lundberg acquired knowledge about molecular biomarkers for prognostication and prediction of treatment response in breast cancer.

He holds two Master's of Science degrees in Bioinformatics from Lund University - Sweden and Computational Biophysics/Biochemistry from Stockholm University - Sweden, respectively.

Dr. Lundberg is currently working in Prof. Li Lab, involving in the development and clinical validation of prognostic and diagnostic biomarkers for early detection of cancer, as well as prediction of treatment response in precision cancer medicine.

Professional Education


  • Doctor of Philosophy, Karolinska Institutet (2019)
  • Master of Science, Stockholms Universitet (2014)
  • Master of Science, Lunds Universitet (2013)
  • Bachelor of Science, Unlisted School (2008)

Stanford Advisors


All Publications


  • The long-term prognostic and predictive capacity of cyclin D1 gene amplification in 2305 breast tumours. Breast cancer research : BCR Lundberg, A., Lindström, L. S., Li, J., Harrell, J. C., Darai-Ramqvist, E., Sifakis, E. G., Foukakis, T., Perou, C. M., Czene, K., Bergh, J., Tobin, N. P. 2019; 21 (1): 34

    Abstract

    Use of cyclin D1 (CCND1) gene amplification as a breast cancer biomarker has been hampered by conflicting assessments of the relationship between cyclin D1 protein levels and patient survival. Here, we aimed to clarify its prognostic and treatment predictive potential through comprehensive long-term survival analyses.CCND1 amplification was assessed using SNP arrays from two cohorts of 1965 and 340 patients with matching gene expression array and clinical follow-up data of over 15 years. Kaplan-Meier and multivariable Cox regression analyses were used to determine survival differences between CCND1 amplified vs. non-amplified tumours in clinically relevant patient sets, within PAM50 subtypes and within treatment-specific subgroups. Boxplots and differential gene expression analyses were performed to assess differences between amplified vs. non-amplified tumours within PAM50 subtypes.When combining both cohorts, worse survival was found for patients with CCND1-amplified tumours in luminal A (HR = 1.68; 95% CI, 1.15-2.46), luminal B (1.37; 1.01-1.86) and ER+/LN-/HER2- (1.66; 1.14-2.41) subgroups. In gene expression analysis, CCND1-amplified luminal A tumours showed increased proliferation (P < 0.001) and decreased progesterone (P = 0.002) levels along with a large overlap in differentially expressed genes when comparing luminal A and B-amplified vs. non-amplified tumours.Our results indicate that CCND1 amplification is associated with worse 15-year survival in ER+/LN-/HER2-, luminal A and luminal B patients. Moreover, luminal A CCND1-amplified tumours display gene expression changes consistent with a more aggressive phenotype. These novel findings highlight the potential of CCND1 to identify patients that could benefit from long-term treatment strategies.

    View details for DOI 10.1186/s13058-019-1121-4

    View details for PubMedID 30819233

    View details for PubMedCentralID PMC6394106

  • PAM50 Provides Prognostic Information When Applied to the Lymph Node Metastases of Advanced Breast Cancer Patients. Clinical cancer research : an official journal of the American Association for Cancer Research Tobin, N. P., Lundberg, A., Lindström, L. S., Harrell, J. C., Foukakis, T., Carlsson, L., Einbeigi, Z., Linderholm, B. K., Loman, N., Malmberg, M., Fernö, M., Czene, K., Perou, C. M., Bergh, J., Hatschek, T. 2017; 23 (23): 7225–31

    Abstract

    Purpose: Transcriptional pathway activity and the molecular subtypes of breast cancer metastases have been shown to significantly influence patient postrelapse survival. Here, we further determine the relevance of clinically employed gene signatures in the advanced breast cancer (ABC) setting.Experimental Design: Sufficient RNA for expression profiling was obtained from distant metastatic or inoperable loco-regional relapse tissue by fine-needle aspiration from 109 patients of the Swedish TEX clinical trial. Gene signatures (GGI, 70 gene, recurrence score, cell-cycle score, risk of recurrence score, and PAM50) were applied to all metastases, and their relationship to long- (5-year) and short-term (1.5-year) postrelapse survival at all and locoregional lymph nodes (n = 40) versus other metastatic sites (n = 69) combined was assessed using Kaplan-Meier and/or multivariate Cox regression analyses.Results: The majority of metastases were classified into intermediate or high-risk groups by all signatures, and a significant association was found between metastatic signature subgroups and primary tumor estrogen receptor status and histologic grade (P < 0.05). When considering all sites of metastasis, only PAM50 was statistically significant in Kaplan-Meier analysis (Log-rank P = 0.008 and 0.008 for long- and short-term postrelapse breast cancer-specific survival, respectively). This significance remained in both uni- and multivariate models when restricting analyses to lymph node metastases only, and a similar trend was observed in other metastatic sites combined, but did not reach formal significance.Conclusions: Our findings are the first to demonstrate that the PAM50 signature can provide prognostic information from the lymph node metastases of ABC patients. Clin Cancer Res; 23(23); 7225-31. ©2017 AACR.

    View details for DOI 10.1158/1078-0432.CCR-17-2301

    View details for PubMedID 28972041

    View details for PubMedCentralID PMC5822712

  • Gene Expression Signatures and Immunohistochemical Subtypes Add Prognostic Value to Each Other in Breast Cancer Cohorts. Clinical cancer research : an official journal of the American Association for Cancer Research Lundberg, A., Lindström, L. S., Harrell, J. C., Falato, C., Carlson, J. W., Wright, P. K., Foukakis, T., Perou, C. M., Czene, K., Bergh, J., Tobin, N. P. 2017; 23 (24): 7512–20

    Abstract

    Purpose: Gene signatures and Ki67 stratify the same breast tumor into opposing good/poor prognosis groups in approximately 20% of patients. Given this discrepancy, we hypothesized that the combination of a clinically relevant signature and IHC markers may provide more prognostic information than either classifier alone.Experimental Design: We assessed Ki67 alone or combined with ER, PR and HER2 (forming IHC subtypes), and the research versions of the Genomic Grade Index, 70-gene, cell-cycle score, recurrence score (RS), and PAM50 signatures on matching TMA/whole tumor sections and microarray data in two Swedish breast cancer cohorts of 379 and 209 patients, with median follow-up of 12.4 and 12.5 years, respectively. First, we fit Cox proportional hazards models and used the change in likelihood ratio (Δ LR) to determine the additional prognostic information provided by signatures beyond that of (i) Ki67 and (ii) IHC subtypes. Second and uniquely, we then assessed whether signatures could compete well with pathology-based IHC classifiers by calculating the additional prognostic information of Ki67/IHC subtypes beyond signatures.Results: In cohort 1, only RS and PAM50 provided additional prognostic information beyond Ki67 and IHC subtypes (Δ LR-χ2 Ki67: RS = 12.8, PAM50 = 20.7, IHC subtypes: RS = 12.9, PAM50 = 11.7). Conversely, IHC subtypes added prognostic information beyond all signatures except PAM50. Similar results were observed in cohort 2.Conclusions: RS and PAM50 provided more prognostic information than the IHC subtypes in all breast cancer patients; however, the IHC subtypes did not add any prognostic information to PAM50. Clin Cancer Res; 23(24); 7512-20. ©2017 AACR.

    View details for DOI 10.1158/1078-0432.CCR-17-1535

    View details for PubMedID 28972043

    View details for PubMedCentralID PMC5822691

  • Sequence Variants of BRCA1 and BRCA2 Genes in Four Iranian Families with Breast and Ovarian Cancer. Iranian journal of public health Keshavarzi, F., Noughani, A. E., Ayoubian, M., Zeinali, S. 2011; 40 (2): 57–66

    Abstract

    BRCA1 and BRCA2 genes have been recognized to be responsible for 20-30% of hereditary breast cancers and approximately 50% of familial breast and ovarian cancers. Therefore, the demand for BRCA1 and BRCA2 mutation screening is rapidly increasing as their identification will affect medical management of people at increased risk. Because of high costs involved in analysis of BRCA1 and 2 genes, contribution of different mutation types in BRCA1 and 2 and not knowing who should be tested has hampered wide spread use of molecular testing of high -risk families. There is a need to identify the genes and types of mutations involved in breast or ovarian cancers at different age of onsets and polymorphism and polymorphic variations in our population.Twenty-seven patients with either early onset breast cancer (at age≤ 35 years) or a personal and/or family history of breast or ovarian cancer and 50 control subjects participated in this study. After collecting blood samples and extracting DNA, BRCA1 and BRCA2 genes were fully sequenced.Thirteen missense substitutions in BRCA1 and BRCA2 (9 and 4, respectively) were revealed. Two nucleotide substitutions were novel (Gly1140Ser in BRCA1 and Glu1391Gly in BRCA2). The Glu1038Pro and Gly1140Ser were found in large series of breast and ovarian cancer and matched controls.Some nucleotide substitutions were seen only in single families and other in several. In other cases, mutations were seen in both BRCA1 and BRCA2 genes. Clinical significance of these mutations was evaluated comparing with normal controls.

    View details for PubMedID 23113073

    View details for PubMedCentralID PMC3481774