Tissue Microarray and Imaging Core

The HCC Tissue Microarray and Imaging Core is dedicated to the construction and evaluation of high-quality tissue microarrays for cancer research. Tissue microarrays enable large-scale, high-throughput in situ analysis of gene and protein expression. By providing access to this resource, as well as enabling computer-based image analysis, the Core facilitates translational research and the discovery and validation of novel potential drug targets.

The Tissue Microarray & Imaging Core is a CLIA and CAP certified core laboratory offering variety of construction and imaging services. 

Core services include construction of standard and custom tissue microarrays; as well as web-based digital pathology services using the Leica systems. These services include slide scanning, image viewing and storage, and access to quantitative image analysis algorithms to facilitate tissue-based research.  

Publication Acknowledgement

If research supported by this core facility results in publication, please acknowledge this support by including the following in your publication(s):

We thank Harvard Cancer Consortium in Boston, MA, for the use of the Tissue Microarray Imaging Core, which provided ______________________________ service. Harvard Cancer Consortium is supported in part by a NCI Cancer Center Support Grant # NIH 5 P30 CA06516.

• Construction of high-quality tissue microarrays
• Coring of FFPE for RNA or DNA extraction
• Digitizing whole slide and TMA's [bright field and immunofluorescent] using the Leica imaging platforms
• Access to Leica's Image Analysis Toolbox

Go to MGB-RCMS to place an order or to set up a new user account:

T-cell Subset Features and Distributions Evolve Across the Colorectal Precancer-Cancer Spectrum.  

Principal Investigator: Shuji Ogino (DFCI) Jonathan Nowak (BWH)

• To study the immune microenvironment of colorectal cancer (CRC) precursors the authors used TMAs containing tissues from precancerous lesions from 3 prospective cohorts  (HPFS, NHS, NHS2).
• Multispectral immunofluorescence assays and digital image analysis were utilized to identify and quantify T cell subsets (CD4+ vs CD8+) and their state/function (naïve, memory, regulatory).
• The findings revealed that T-cell infiltration patterns vary across different histopathological types of the colorectal neoplastic spectrum from precursors to invasive carcinomas.
• Compared to invasive CRC, precursors showed higher densities of CD3+CD4+ cells and CD3+CD8+ (naive, memory, and regulatory), suggesting that immune exclusion contributes to the development of invasive cancer.

Core Contribution: The TMI core constructed the high-density TMAs containing tissue cores from normal mucosa (n=907) precancerous lesions (n=790) and CRCs (n=1,035) used for IF studies. 

Publication

Takashima Y, Dias Costa A, Akimoto N, Ugai T, Bell P, Väyrynen JP, Hornick JL, Mino-Kenudson M, Zhong Y, Ugai S, Haruki K, Yao Q, Matsuda K, Higashioka M, Buchanan DD, Phipps AI, Peters U, Giannakis M, Song M, Chan AT, Fuchs CS, Nowak JA, Ogino S. Cancer Immunol Res. 2025 Nov. Online ahead of print. PMID: 41222477.

The SLC1A1/EAAT3 dicarboxylic amino acid transporter is an epigenetically dysregulated nutrient carrier that sustains oncogenic metabolic programs. 

Principal Investigator: Toni Choueiri (DFCI), Sabina Signoretti (BWH)

• By performing functional in vivo screens, the authors identified the aspartate and glutamate transporter SLC1A1 as a putative oncogenic driver in VHL-deficient clear cell Renal Cell Carcinoma (ccRCC).
• VHL inactivation was shown to promote SLC1A1 expression via H3K27ac dysregulation.
• SLC1A1 inactivation, genetically or pharmacologically, depleted Asp/Glu-derived metabolites and inhibited ccRCC growth in vitro and in vivo.
• Analysis of RNA-seq data showed that SLC1A1 expression was negatively correlated with immune cell signatures.
• Immunohistochemistry (IHC) analysis of ccRCC patient tissues revealed that elevated SLC1A1 expression was associated with advanced stage and development of metastases.

Core Contribution: The TMI core constructed the high-density RCC TMAs containing tissue cores from 188 patients used for SLC1A1 IHC. 

Publication

Grubb T, Koochaki P, Matar S, Ghandour F, Machaalani M, Saad E, Tang C, Reznik E, Khatun J, Salem C, Dubasik N, Orlando DA, Guenther MG, Parajuli G, Srivastava RM, Martinez SR, Coker JA, Kotecha RR, Hakimi AA, Asara JM, Chan TA, Vanharanta S, Stauffer SR, Kaelin WG Jr, Signoretti S, Choueiri TK, Chakraborty AA. Nat Commun. 2025 Nov 14;16(1):10012. PMID: 41238532

The SLC1A1/EAAT3 dicarboxylic amino acid transporter is an epigenetically dysregulated nutrient carrier that sustains oncogenic metabolic programs. 

Principal Investigator: Alan D'Andrea (DFCI), Geoffrey Shapiro (DFCI)

• The authors examined the impact of cyclin D1 on replication stress (RS) and  DNA double-strand breaks (DSBs) using a mantle cell lymphoma (MCL) as a naturally occurring model of cyclin D1 overexpression.
• Cyclin D1 overexpression elevated RS, increased DNA damage, and upregulated polymerase theta (POLΘ)-mediated microhomology-mediated end- joining (MMEJ) DNA repair, which was essential to withstand cyclin D1-induced RS. 
• Inhibition of POLΘ in cyclin D1-overexpressed settings further exacerbated RS, ultimately leading to apoptosis. This effect was amplified in ATM-deficient cells.
• POLΘ inhibition is therefore an effective strategy in the context of cyclin D1 overexpression and ATM deficiency and may provide a unique therapeutic approach for treating MCL and potentially other malignancies.

Core Contribution: The TMI core scanned whole tissue slides (from MCL mouse model) immunostained for pRPAS4/S8 and g-H2AX (in the SHP Core) that were subsequently evaluated by image analysis. 

Publication

Abeykoon JP, Asada S, Zhu G, Hirohashi Y, Moreau L, Iyer D, Mukkavalli S, Parmar K, Zambrano G, Jiang L, Yi D, Manske M, Gwin K, King RL, Cerhan JR, Wu X, Lou Z, Shapiro GI, Witzig T, D'Andrea A. J Clin Invest. 2025 Jul 3;135(17). PMID: 40608419.

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