Cecilia Williams

Cecilia Williams

Principal Researcher
Visiting address: Blickagången 16, 14152 Flemingsberg
Postal address: H7 Medicin, Huddinge, H7 GUT Williams, 171 77 Stockholm
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About me

  • How sex differences and hormone signalling influence cancer

    Cecilia Williams leads a group at KI that is shared with her lab at KTH and SciLifeLab. She received her PhD training in DNA sequencing technologies and the p53 tumor suppressor gene at KTH, postdoc training in gene expression profiling techniques and stem cells, and was later a researcher at Karolinska Institutet where she studied the role of estrogen receptor beta. She joined the Center of Nuclear Receptors and Cell Signaling at University of Houston as faculty 2009-2015. Her main activities at the GUT division at Med-H are focused on understanding how hormonal signalling and sex differences impact cancer, in particular colorectal cancer, and the supervision of doctoral students.


    Education
    1994 M.S. (Civ. Ing.) in Chemical Engineering with specialization in Biotechnology, KTH Royal Institute of Technology, Stockholm
    2002 Ph.D. Biotechnology, KTH Royal Institute of Technology. /Molecular Archaeology of Cancer - Analysis of the Human p53 Tumor Suppressor Gene.

Research

  • How sex differences and hormone signalling influence cancer

    The Williams’ group focuses on understanding key molecular mechanisms in cancer, applying a combination of large-scale genomic approaches, focused mechanistic experiments, and animal studies. The goal is to understand critical pathways so that we can define biomarkers of their activity and suggest better cancer treatments and preventive approaches. The hormone estrogen increases the risk of breast cancer, but can simultaneously protect against colorectal cancer. It is not understood exactly how, but if we can achieve a detailed knowledge of this mechanism, we could design approaches that can protect against colon cancer while not promoting breast cancer.

    Estrogenic signaling is mediated by the estrogen receptors, ERα, ERβ, and GPER1. ERα and ERβ are ligand-activated nuclear receptors and, as such, excellent therapeutic targets. Our research focuses on understanding estrogen-induced pathways in breast and colon cancer, and the impact that environmental or dietary estrogenic exposure may have. Our previous work includes the identification of the estrogen-regulated transcriptome, cistrome, and microbiome, with a focus on cancer.

Selected publications

Articles

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Selected grants

  • Swedish Research Council
    1 January 2023 - 31 December 2026
    Colorectal cancer is a leading cause of cancer mortality. The disease exhibits distinct sex differences in incidence, tumor location, tumor characteristics, and survival, and estrogen reduces the incidence and mortality. Emerging data support that estrogen receptor beta (ERβ) mediates this effect. We have demonstrated that intestinal ERβ is protective in both sexes. Our preliminary data show that ERβ in the tumor microenvironment reduces the number of tumor-infiltrating macrophages, stemness markers, and stabilizes circadian clock regulation, in part by modifying inflammatory NFkB signaling. We will test our specific hypotheses using intestinal-specific knockout mice, tumor models, engineered cell lines, organotypic patient-derived cultures, and advanced technologies. Technologies includes high-throughput hyperplex immunofluorescence COMET for spatial proteomics to characterize the immune cell landscape in situ, multiplex plasma cytokine analysis, and capture Hi-C and RIME to deduce and characterize the related molecular mechanisms. The overarching goal is to understand the critical mechanistic background needed to develop useful strategies for chemoprevention and precision medicine, for example, co-administration of receptor-selective ligands and immune checkpoint inhibitors. In addition, we will provide an in-depth understanding of colitis, colon carcinogenesis, peripheral circadian rhythmicity, stemness, and related sex differences.

Grants

  • Swedish Research Council
    1 January 2024 - 31 December 2026
    Pathologists routinely perform cancer identification and risk assessments on breast tissue section images and medical patient data. Spatial Transcriptomics (ST) is a novel technology developed in Sweden that allows measuring where in a tissue section a certain RNA was expressed. Our overall aims are to evaluate (a) how the additional consideration of ST gene expression data in addition to tissue section images improves the identification and classification of cancer sub-types in breast tissue sections, (b) if the additional consideration of normal breast tissue adjacent to tumor tissue allows finding cancer onset signatures in the images or in the ST expression data and (c) if considering genome sequence and/or clinical patient data further improves cancer classification.We will computationally analyze our own novel large ST dataset consisting of 48 breast tissue sections from eleven individuals with different cancer types together with non-cancer sections from the same individuals. Whole genome sequencing data is available from the tumor and matched peripheral blood as control from five individuals. Detailed clinical characteristics are available for all individuals.We might be able to give advice on how the novel ST technology can improve traditional cancer identification and classification as well as how the inclusion of additional non-cancer samples, genome sequence information and clinical patient data can improve the classification outcome.
  • Swedish Cancer Society
    1 January 2022
    Colon and rectal cancer is the third most common cause of cancer death for both men and women in Sweden. There is a great need to develop better prevention, treatments and prognostic biomarkers. The female sex hormone estrogen is protective, but estrogen has side effects that make it unsuitable as a contraceptive. We have shown that a special estrogen receptor, ERbeta, in the intestinal epithelial cells is the protein that mediates the protective effect of estrogen. Our hypothesis is that activation of the ERbeta receptor can be used for a safe preventive treatment with few or no side effects. Our new results show that the receptor has a cancer-protective effect in both sexes. In addition, we see a strong anti-inflammatory effect in the intestine and signs that the receptor also seems to be able to regulate the biological circadian rhythm of the intestine. Both inflammation and the intestinal circadian rhythm are associated with cancer development. A partial hypothesis is that the intestinal microflora is also affected by ERbeta activation. Our aim here is to explore exactly how this works and clarify how the receptor protects against the onset of cancer. Our goal is to be able to develop a new safe preventive treatment that protects both men and women. Such treatment may be suitable for people in risk groups who have hereditary syndromes that increase the risk of rectal and colon cancer, as well as for the elderly.
  • Swedish Research Council
    1 December 2018 - 30 November 2024
  • Swedish Research Council
    1 January 2018 - 31 December 2021
  • VINNOVA
    1 June 2014 - 28 February 2018
  • National Cancer Institute
    1 August 2013 - 31 May 2019
  • Epigenetic regulation in mammary stem/progenitor cells and its contribution to malignant transformation
    Fundação para a Ciência e Tecnologia
    15 March 2012 - 14 July 2015

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