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• HSC_population_dynamics___TG001_2_samples

  My research project aims to use the clonal dynamics of spontaneously occurring somatic mutations to answer fundamental questions about human haematopoietic stem cell (HSC) biology. The four major questions I will address are: 1. How do age and aging affect normal human HSC dynamics in vivo? 2. How do in vivo perturbations, particularly chemotherapy and increased levels of reactive oxygen species, affect HSC population dynamics? 3. Is response to in vitro perturbation heritable and/or correlated with other features such as age of individual and contribution of the lineage to peripheral blood? 4. How are HSC dynamics altered in people with early driver mutations (clonal haematopoiesis)?

  Study EGAS00001003688

• HSC_population_dynamics___PX001_samples

  My research project aims to use the clonal dynamics of spontaneously occurring somatic mutations to answer fundamental questions about human haematopoietic stem cell (HSC) biology. The four major questions I will address are: 1. How do age and aging affect normal human HSC dynamics in vivo? 2. How do in vivo perturbations, particularly chemotherapy and increased levels of reactive oxygen species, affect HSC population dynamics? 3. Is response to in vitro perturbation heritable and/or correlated with other features such as age of individual and contribution of the lineage to peripheral blood? 4. How are HSC dynamics altered in people with early driver mutations (clonal haematopoiesis)?

  Study EGAS00001004146

• HSC_population_dynamics___KX009_samples

  My research project aims to use the clonal dynamics of spontaneously occurring somatic mutations to answer fundamental questions about human haematopoietic stem cell (HSC) biology. The four major questions I will address are: 1. How do age and aging affect normal human HSC dynamics in vivo? 2. How do in vivo perturbations, particularly chemotherapy and increased levels of reactive oxygen species, affect HSC population dynamics? 3. Is response to in vitro perturbation heritable and/or correlated with other features such as age of individual and contribution of the lineage to peripheral blood? 4. How are HSC dynamics altered in people with early driver mutations (clonal haematopoiesis)?

  Study EGAS00001004580

• HSC_population_dynamics___KX010_samples

  My research project aims to use the clonal dynamics of spontaneously occurring somatic mutations to answer fundamental questions about human haematopoietic stem cell (HSC) biology. The four major questions I will address are: 1. How do age and aging affect normal human HSC dynamics in vivo? 2. How do in vivo perturbations, particularly chemotherapy and increased levels of reactive oxygen species, affect HSC population dynamics? 3. Is response to in vitro perturbation heritable and/or correlated with other features such as age of individual and contribution of the lineage to peripheral blood? 4. How are HSC dynamics altered in people with early driver mutations (clonal haematopoiesis)?

  Study EGAS00001004581

• HSC_population_dynamics___LEUK4_samples

  My research project aims to use the clonal dynamics of spontaneously occurring somatic mutations to answer fundamental questions about human haematopoietic stem cell (HSC) biology. The four major questions I will address are: 1. How do age and aging affect normal human HSC dynamics in vivo? 2. How do in vivo perturbations, particularly chemotherapy and increased levels of reactive oxygen species, affect HSC population dynamics? 3. Is response to in vitro perturbation heritable and/or correlated with other features such as age of individual and contribution of the lineage to peripheral blood? 4. How are HSC dynamics altered in people with early driver mutations (clonal haematopoiesis)?

  Study EGAS00001004247

• HSC_population_dynamics___CB001_samples

  My research project aims to use the clonal dynamics of spontaneously occurring somatic mutations to answer fundamental questions about human haematopoietic stem cell (HSC) biology. The four major questions I will address are: 1. How do age and aging affect normal human HSC dynamics in vivo? 2. How do in vivo perturbations, particularly chemotherapy and increased levels of reactive oxygen species, affect HSC population dynamics? 3. Is response to in vitro perturbation heritable and/or correlated with other features such as age of individual and contribution of the lineage to peripheral blood? 4. How are HSC dynamics altered in people with early driver mutations (clonal haematopoiesis)?

  Study EGAS00001003397

• Exome sequence of probands in Barrett's oesophagus families

  Barrett?s oesophagus is common in the UK affecting 2 % of the population. Family history has been recorded among the 4000 Barrett's cases collected so far and have 241 families. Among them we have assessed 6 multiplex families with proven Barrett?s and defined as having 1 pro band and at least 3 affected first degree members. We propose to exome sequence the probands of these six families to assess the presence of pathogenic rare coding variants.

  Dataset EGAD00001002181

• A developmental cell atlas of the human thyroid gland - WGS

  The thyroid gland produces hormones essential for health from embryogenesis to adulthood. Thyroid disorders, including congenital hypothyroidism and thyroid carcinoma, are prevalent and pose significant health challenges. Congenital hypothyroidism often results from thyroid dysgenesis or impaired hormone synthesis, is particularly prevalent in trisomy 21 (T21), while thyroid carcinoma is the most frequent endocrine malignancy, affecting both paediatric and adult populations. Understanding the molecular basis of these conditions requires deeper insights into fetal thyroid development. We generated a spatiotemporal atlas of the human thyroid during early pregnancy, revealing key cell types, including hormone-producing thyrocytes. Thyroid follicular cells are heterogeneous, with two functional cell states (fTFC1, fTFC2) that persist into adulthood, with fTFC2 characterised by elevated PAX8 expression. We demonstrated that T21 thyroids displayed dysgenesis with disrupted follicular morphology, and altered extracellular matrix interactions, and that the fTFC2 signature was enriched in paediatric papillary thyroid cancer compared to adults. These findings uncover thyrocyte heterogeneity across the lifespan, advancing understanding of thyroid development and disease.

  Dataset EGAD00001015447

• A developmental cell atlas of the human thyroid gland - RNA

  The thyroid gland produces hormones essential for health from embryogenesis to adulthood. Thyroid disorders, including congenital hypothyroidism and thyroid carcinoma, are prevalent and pose significant health challenges. Congenital hypothyroidism often results from thyroid dysgenesis or impaired hormone synthesis, is particularly prevalent in trisomy 21 (T21), while thyroid carcinoma is the most frequent endocrine malignancy, affecting both paediatric and adult populations. Understanding the molecular basis of these conditions requires deeper insights into fetal thyroid development. We generated a spatiotemporal atlas of the human thyroid during early pregnancy, revealing key cell types, including hormone-producing thyrocytes. Thyroid follicular cells are heterogeneous, with two functional cell states (fTFC1, fTFC2) that persist into adulthood, with fTFC2 characterised by elevated PAX8 expression. We demonstrated that T21 thyroids displayed dysgenesis with disrupted follicular morphology, and altered extracellular matrix interactions, and that the fTFC2 signature was enriched in paediatric papillary thyroid cancer compared to adults. These findings uncover thyrocyte heterogeneity across the lifespan, advancing understanding of thyroid development and disease.

  Dataset EGAD00001015448

• Integration of genomics and histology reveals diagnosis and effective therapy of refractory cancer of unknown primary with PDL1 amplification (H021)

  Identification of the tissue of origin in cancer of unknown primary (CUP) poses a diagnostic challenge and is critical for directing site-specific therapy. Currently, clinical decision making in patients with CUP primarily relies on histopathology and clinical features. Comprehensive molecular profiling has the potential to contribute to diagnostic categorization and, most importantly, guide CUP therapy through identification of actionable lesions. We here report the case of an advanced-stage malignancy initially mimicking poorly differentiated soft-tissue sarcoma that did not respond to multi-agent chemotherapy. Molecular profiling within a clinical whole-exome and transcriptome sequencing program revealed a heterozygous, highly amplified KRAS G12S mutation, compound-heterozygous TP53 mutation/deletion, high mutational load, and focal amplification of chromosomes 9p (including PDL1 [CD274] and JAK2) and 10p (including GATA3). Integrated analysis of molecular data and conventional histopathology suggested a diagnosis of triple-negative breast cancer (TNBC) and provided a rationale for immune checkpoint inhibitor therapy with pembrolizumab, which resulted in rapid clinical improvement and a lasting partial remission. Analysis of 157 TNBC samples from The Cancer Genome Atlas revealed focal, high-level PDL1 amplification coinciding with excessive PDL1 mRNA expression in 24% of cases. Collectively, these results illustrate the diagnostic utility of multidimensional tumor profiling in cases with non-descript histology and immune phenotype, demonstrate the predictive power of genomic PDL1 amplification for immune checkpoint inhibition, and suggest a targeted therapeutic strategy in chromosome 9p24.1/PDL1-amplified cancers.H021

  Study EGAS00001001846