Tissue Regeneration & Cancer

Regeneration is the ability to maintain a robust capacity to repair following injury. It is key to preserving tissue and organ integrity, as well as whole body fitness. However, uncontrolled regenerative power can lead to diseases like cancer, with far reaching impact to overall health.The Tissue Regeneration and Cancer MSc Research Programme, hosted by the School of Cancer Sciences, will deliver high quality research, training and mentorship to excellent and ambitious students interested in cancer research, including- but not limited to- its intersection with stem cell biology, immunity, metabolism, development, regenerative biology, and behavioural science.

• MSc (Research): 1 year full-time; 2 years part-time;

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Research projects
Research projects
An assessment of vulnerabilities in phosphoinositide signaling to attenuate metastatic colorectal cancer.

Supervisors: David Bryant , Emma Sandilands  and Archana Katoch

Project summary: Mutation in the lipid phosphatidylinositol-3-kinase (PI3K) or in PTEN, the phosphatase that reverses PI3K action is frequent in human cancers. We utilise organoids derived from poor outcome colorectal cancers which are genetically engineered ex vivo, transplanted in vivo, and the effect on tumourigenesis and metastasis examined. We identified that PTEN knockout rapidly accelerates metastasis. Our current work using CRISPR in vivo is identifying which additional PI3K pathway enzymes can, conversely to PTEN loss, attenuate metastasis.

This project aims to identify the mechanism of action of PI3K pathway enzymes that attenuate colorectal cancer tumourigenesis and metastasis. The candidate will join a team of researchers utilise a combination of cutting-edge mouse models of metastatic colorectal cancer and organoids to understand how inhibiting the PI3K pathway may be a potential treatment to perturb tumourigenesis and metastasis.

The candidate will receive training in CRISPR-mediated genetic editing, molecular analysis of cancer cells, 3-Dimensional culture techniques, advanced live imaging and image analysis.

References

Nikolatou K, Sandilands E, Román-Fernández A, Cumming EM, Freckmann E, Lilla S, Buetow L, McGarry L, Neilson M, Shaw R, Strachan D, Miller C, Huang DT, McNeish IA, Norman JC, Zanivan S, Bryant DM. PTEN deficiency exposes a requirement for an ARF GTPase module for integrin-dependent invasion in ovarian cancer. EMBO J. 2023 Sep 18;42(18):e113987. doi: 10.15252/embj.2023113987. Epub 2023 Aug 14. PMID: 37577760; PMCID: PMC10505920.

Jackstadt R, van Hooff SR, Leach JD, Cortes-Lavaud X, Lohuis JO, Ridgway RA, Wouters VM, Roper J, Kendall TJ, Roxburgh CS, Horgan PG, Nixon C, Nourse C, Gunzer M, Clark W, Hedley A, Yilmaz OH, Rashid M, Bailey P, Biankin AV, Campbell AD, Adams DJ, Barry ST, Steele CW, Medema JP, Sansom OJ. Epithelial NOTCH Signaling Rewires the Tumor Microenvironment of Colorectal Cancer to Drive Poor-Prognosis Subtypes and Metastasis. Cancer Cell. 2019 Sep 16;36(3):319-336.e7. doi: 10.1016/j.ccell.2019.08.003. PMID: 31526760; PMCID: PMC6853173.

Nacke M, Sandilands E, Nikolatou K, Román-Fernández Á, Mason S, Patel R, Lilla S, Yelland T, Galbraith LCA, Freckmann EC, McGarry L, Morton JP, Shanks E, Leung HY, Markert E, Ismail S, Zanivan S, Blyth K, Bryant DM. An ARF GTPase module promoting invasion and metastasis through regulating phosphoinositide metabolism. Nat Commun. 2021 Mar 12;12(1):1623. doi: 10.1038/s41467-021-21847-4. PubMed PMID: 33712589; PubMed Central PMCID: PMC7955138.

Román-Fernández Á, Roignot J, Sandilands E, Nacke M, Mansour MA, McGarry L, Shanks E, Mostov KE, Bryant DM. The phospholipid PI(3,4)P(2) is an apical identity determinant. Nat Commun. 2018 Nov 28;9(1):5041. doi: 10.1038/s41467-018-07464-8. PubMed PMID: 30487552; PubMed Central PMCID: PMC6262019

Assessing the activity of novel compounds in Human Derived Biliary Tract Cancer preclinical models.

Supervisors: Chiara Braconi and Sergi Marco

Project summary: Biliary Tract Cancers (BTC) are tumours arising from the bile duct within and outside the liver. There is an unmet need to develop novel therapeutic strategies that can impact on survival of BTC patients. Here we will test novel compounds in multicellular, patients’ derived, preclinical models to identify the clinical potential of these compounds and define the best strategies for designing their clinical implementation. The candidate will develop skills in cell culturing, with particular reference to 3D models, and molecular biology with the development of stably transfected clones. She/he will also have an opportunity to develop troubleshooting skills and critical thinking. There will be particular attention to the training of the presentations skills with need to present regularly at the lab meeting and possibility to present at international meetings should the candidate be considered appropriately skilled and trained.

Developing CRISPR tools for targeting tumour suppressors in Mesothelioma.

Supervisors: Daniel Murphy and Jennifer Doig

Project summary: Join the world-leading Mesothelioma research laboratory of Prof Daniel J. Murphy to develop new CRISPR tools to investigate the functional role of under-investigated tumour suppressor genes in Mesothelioma. We are the UK’s only laboratory routinely using state of the art in vivo models to investigate this lethal cancer and your contribution could have a meaningful impact on our work. We will help you develop the skills you need to advance your career in an exciting area of cancer research, along with the transferable skill to give you flexibility in your future direction.

The primary aim of this project is to develop and validate CRISPR vectors targeting additional clinically relevant TSGs. Vectors will be designed and subcloned, then tested in cell culture for their ability to accurately disrupt TSG expression. Validated vectors will subsequently be used by Murphy lab personnel in vivo to understand the contribution of each TSG to Mesothelioma development. You will develop arrange of contemporary skills that will strengthen your potential to progress into a PhD programme or professional research laboratory. This will include CRISPR guide RNA design and subcloning, cell culture, recombinant vector production and validation, QPCR and protein immunoblotting. You will also advance your transferable skills including critical thinking, data evaluation & presentation and scientific writing of reports.

References

Farahmand P, Gyuraszova K, Rooney C, Raffo-Iraolagoitia XL, Jayasekera G, Hedley A, Johnson E, Chernova T, Malviya G, Hall H, Monteverde T, Blyth K, Duffin R, Carlin LM, Lewis D, Le Quesne J, MacFarlane M, Murphy DJ. Asbestos accelerates disease onset in a genetic model of malignant pleural mesothelioma. Front Toxicol. 2023 Jun 27;5:1200650. doi: 10.3389/ftox.2023.1200650. PMID: 37441092; PMCID: PMC10333928.

Exploiting mitochondrial inflammatory signals to engage anti-tumour immunity.

Supervisors: Stephen Tait  and Danny Huang  

Project summary: Cell death prevents and treats cancer. Typically, therapies cause apoptotic cell death of cancer cells. In brief, apoptosis requires mitochondria to activate proteases call caspases. Apoptosis is a silent form of cell death that fails to evoke an immune response. We have found that killing cells under caspase inhibition elicits powerful anti-tumour immunity that can eradicate cancer in experimental models. Underlying this are inflammatory signals sent out by the mitochondria. This project aims to understand the fundamental mechanisms of inflammation triggered by permeabilized mitochondria. It will entail a variety of cutting-edge methods including genome-engineering, high-resolution microscopy and in vivo tumour biology. Using this knowledge our goal is to enhance our ability to effectively kill cancer by engaging anti-tumour immunity.

References

Mitochondrial permeabilization engages NF-κB-dependent anti-tumour activity under caspase deficiency. Giampazolias et al, Nat Cell Biol. 2017 Sep;19(9):1116-1129.doi: 10.1038/ncb3596.

Mitochondrial inner membrane permeabilization enables mtDNA release during apoptosis. Riley et al, EMBO J (2018)37:e99238 https://doi.org/10.15252/embj.201899238

Mitochondrial outer membrane integrity regulates a ubiquitin-dependent NF-κB inflammatory response. Vringer et al, doi: https://doi.org/10.1101/2023.09.21.558776

Apoptotic stress causes mtDNA release during senescence and drives the SASP. Victorelli et al, Nature volume 622, pages 627–636 (2023) https://www.nature.com/articles/s41586-023-06621-4

Investigating Metabolic changes in PPARG Driven Prostate Cancer

Supervisors: Imran Ahmad and Tom MacVicar

Project summary: There exists a huge degree of prostate cancer cell metabolic remodelling to enable tumours to grow and combat androgen deprivation therapy. The mitochondria are essential organelles that support tumour adaptation, by dynamically reprogramming during tumorigenesis. Previous work in our group has identified the key role of the metabolic regulator PPARG in driving metastatic prostate cancer.

In this project, the candidate will use tumour models including genetically engineered mice to investigate how mitochondria contribute to tumorigenesis and treatment resistance. The candidate will study mitochondrial dynamics in these models with metabolomic and proteomic techniques. These studies will improve our basic understanding of metabolic changes in tumours and may identify novel therapeutic targets for prostate cancer.
References

Galbraith LCA, Mui E, Nixon C, Hedley A, Strachan D, MacKay G, Sumpton D, Sansom OJ, Leung HY, Ahmad I. “PPAR-gamma induced AKT3 expression increases levels of mitochondrial biogenesis driving prostate cancer”. Oncogene 2021; doi: 10.1038/s41388-021-01707-7

Live imaging cell death and its clearance during tissue remodelling and cancer.

Supervisors: Andrew J. Davidson and Stephen Tait

Project summary: Multi-cellular organisms are not created through cell proliferation alone. During development and tissue remodelling, healthy cells are deliberately removed through cell death in order to sculpt the tissue into its final form. However, if dead cells are not removed quickly through engulfment by other cells (such as macrophages), chronic inflammation is triggered. Therefore, the efficient clearance of cellular debris is vital for our health and wellbeing. Furthermore, in pathologies where cell death is elevated, overwhelmed clearance may exacerbate diseases such as cancer. In this project, we will use live-microscopy and the fruit fly, Drosophila melanogaster, to visualise the clearance of dead cells inside a living organism. Furthermore, we will combine advanced biosensors of cell death, the microinjection of dyes and Drosophila’s unrivalled genetics to investigate the importance of this clearance to development, tissue remodelling and tumourigenesis.

As part of this project, the student will gain extensive experience in live-imaging, including training on a variety of different confocal microscopes. Furthermore, the student will learn genetics, Drosophila husbandry and cell culture, as well as specialist techniques such as microinjection. The student will also receive mentoring on scientific critical thinking and writing. By the end of the project, the student will be well placed for a future career in biomedical sciences.

References

Heron, R., Amato, C., Wood, W. & Davidson, A. J. Understanding the diversity and dynamics of in vivo efferocytosis: Insights from the fly embryo. Immunol Rev, doi:10.1111/imr.13266 (2023).

Botto, M. et al. Homozygous C1q deficiency causes glomerulonephritis associated with multiple apoptotic bodies. Nat Genet 19, 56-59, doi:10.1038/ng0598-56 (1998).

Raymond, M. H. et al. Live cell tracking of macrophage efferocytosis during Drosophila embryo development in vivo. Science 375, 1182-1187, doi:10.1126/science.abl4430 (2022).

Kurant, E., Axelrod, S., Leaman, D. & Gaul, U. Six-microns-under acts upstream of Draper in the glial phagocytosis of apoptotic neurons. Cell 133, 498-509, doi:10.1016/j.cell.2008.02.052 (2008).

Metabolic adaptations of intestinal stem cells in health and disease.

Supervisors: Julia Cordero and Vignir Helgason

Project summary: Metabolism is a key determinant of cellular phenotype, amenable to nutritional and/or pharmacological therapeutic interventions. Although the impact of diet and metabolism in homeostatic intestinal stem cell (ISC) renewal and differentiation is well documented, the metabolic adaptations of ISCs to tissue injury and their influence on regeneration and cancer are largely unknown. While recent studies on mammalian systems have provided significant insight into ISC metabolism, these rely largely on in vitro cultures. The use of in vivo models is important to account for the influence of the natural microenvironment on ISC metabolism. Research on the adult Drosophila midgut — an organ with remarkable homology to the mammalian small intestine—has provided invaluable knowledge on ISC biology in health and disease. We use the adult Drosophila midgut as a high throughput in vivo paradigm for characterization of metabolic changes in ISCs following tissue damage and their functional role in intestinal regeneration and tumourigenesis. During this project, the student will receive theoretical and practical training in genetics, imaging, metabolism, intestinal biology, tissue regeneration and cancer.

References

Nászai M., Bellec K., Yu Y, Román-Fernández A., Sandilands E., Johansson J., Campbell A.D., Norman J.C., Sansom O.J., Bryant D.M., Cordero J.B1. RAL GTPases mediate EGFR-driven intestinal stem cell proliferation and tumourigenesis. Elife. 2021 Jun 7;10:e63807.

Perochon, J., Aughey, G.N., Southall, T.D., and Cordero, J.B1. Dynamic adult tracheal plasticity drives stem cell adaptation to changes in intestinal homeostasis. Nature Cell Biology, 23(5), pp. 485-496. (doi: 10.1038/s41556-021-00676-z). News and Views. Nature Cell Biology, 23, 580–582 (2021). doi.org/10.1038/s41556-021-00695-w

Parvy JP1, Yu Y, Dostalova A, Kondo S, Kurjan A, Bulet P, Lemaitre B, Vidal M, Cordero JB1. The antimicrobial peptide Defensin cooperates with Tumour Necrosis Factor to drive tumour cell death in Drosophila. Elife. 2019 Jul 30;8. pii: e45061. doi: 10.7554/eLife.45061. Recommended by the Faculty of 1000.

Scopelliti A1*, Bauer C*, Yu Y, Zhang T, Krüspig B, Murphy DJ, Vidal M, Maddocks OK, Cordero JB1. A neuronal relay mediates a nutrient responsive gut/fat body axis regulating energy homeostasis in adult Drosophila. Cell Metab. Oct 15. pii: S1550-4131(18)30629-6. doi: 10.1016/j.cmet.2018.09.021. Recommended by the Faculty of 1000.

Role of INPP4b in PTEN-driven Prostate Cancer

Supervisors: Imran Ahmad and David Bryant

Project summary: The tumour suppressor gene PTEN is one of the most often deleted genes in human prostate cancer. Previous work from our groups have elucidated how PTEN loss, often with co-operating mutations, can drive metastatic prostate cancer. Our recent work, using a forward transposon-based screen, has identified loss of INPP4b co-operating with PTEN loss to drive treatment resistant prostate cancer. In this innovative project, the candidate will use 3D tumour models combined with orthotopic mouse models to investigate how INPP4B loss contributes to prostate tumourigenesis in a PTEN loss background. The candidate will study enzymes involved in phosphatidylinositol signaling pathways, to improve our basic understanding of this pathway in tumours and may identify novel therapeutic targets for prostate cancer.

References

Galbraith LCA, Mui E, Nixon C, Hedley A, Strachan D, MacKay G, Sumpton D, Sansom OJ, Leung HY, Ahmad I. “PPAR-gamma induced AKT3 expression increases levels of mitochondrial biogenesis driving prostate cancer”. Oncogene 2021; doi: 10.1038/s41388-021-01707-7

Roman-Fernandez A, Roignot J, Sandilands E, Nacke M, Mansour MA, McGarry L, Shanks E, Mostov KE, Bryant DM. The phospholipid PI(3,4)P2 is an apical identity determinant. Nat Commun. 2018; 9: 5041.

Ahmad I, Mui E, Galbraith L, Patel R, Tan EH, Salji M, Rust AG, Repiscak P, Hedley A, Markert E, Loveridge C, van der Weyden L, Edwards J, Sansom OJ, Adams DJ, Leung HY. Sleeping Beauty screen reveals Pparg activation in metastatic prostate cancer. Proc Natl Acad Sci USA. 2016; 113: 8290-5. 

Overview
Overview
Programme description

Students will undergo 1-year of full-time research in a laboratory chosen from our supervisory pool of world-renowned principal investigators. A further year is allowed for thesis writing.

In addition to their research time, students will have the opportunity to participate in research seminars [Glasgow Cancer Seminar Series ], tutorials, science retreats and interactive discussion groups. Bioinformatic, research integrity and data management training courses are also offered to PGR students. Our skills pathway  sets out recommended courses at different stages of PGR research study.

Students will have a primary and secondary research supervisor and 2 reviewers, who will oversee annual research progress. Students will give an introductory talk after the initial review panel meeting and within 4 months of starting their research year. At the end of their research year, students will write a MSc by Research thesis report (max 50,000 words) to be assessed by an internal and external examiner. The examiner may require a viva voce. Students will have up to 12 months after their year of laboratory research to fulfil these requirements for degree award.

Application deadline

31 July 2024

School of Cancer Science

You will study in state-of-the-art laboratory space at our School of Cancer Sciences . The school provides multiple centralised facilities operated by expert managers.  These include tissue culture, flow cytometry, imaging, metabolomic, proteomics, genomics, high content screening, histology facilities and biological service unit.

We bring together world-leading fundamental stem cell, inflammation, cancer and tissue regeneration research with established clinical and discovery research excellence.

The School of Cancer Sciences includes:

• Beatson CRUK Scotland Institute ,
• Wolfson Wohl Cancer Research Centre
• Paul O’Gorman Leukaemia Research Centre . 

Learning outcomes

Towards the end of the programme, students will have been exposed to and acquire a wealth of laboratory research techniques and conceptual learning knowledge.  These will include but not be limited to the following:

Technique learning

• 3D organoid technology
• Advanced imaging
• Biochemistry
• Bioinformatics
• Cell and primary tissue culture
• Cell biology
• Cell Sorting
• Genomic engineering (CRISPR, RNA interference)
• Mass spectrometry
• Molecular biology
• Molecular genetics
• Statistics
• Tissue culture
• Use of genetically engineered mouse models for research
• Use of non-mammalian model organisms for research, such as the fruit fly Drosophila melanogaster.
• Various Omics (proteomics, metabolomics, transcriptomics)

Conceptual learning

• Cancer biology
• Cell death and mitochondrial biology
• Cell metabolism
• Drug screening and development
• Immunology
• Regenerative biology
• Stem cell biology
• Whole body physiology

Programme management team

Programme Director: Prof. Julia Cordero , Professor of Systemic Signalling Biology.

The programme is supported by:

• Professor Joanne Edwards , Professor of Translational Cancer Pathology and Director of Education
• Professor Helen Wheadon , Professor of Stem Cell Regulation and Deputy Director of Education
• Dr Heather Jorgensen , Senior Research Scientist and Post-Graduate Research Convenor
• Mrs Anne Best , Senior Administrator

Study options
Study options
MSc (Research)

• Duration: 1 year full-time; 2 years part-time

Entry requirements
Entry requirements

A 2.1 Honours degree or equivalent.

To be eligible for the MSc by Research in Tissue Regeneration and Cancer programme you should have a UK 2:1 honour degree, or its international equivalent, in a relevant biological or medical discipline. Candidates will have to meet the standard English language entry requirements of The University of Glasgow. All applicants will be asked to demonstrate a level of English language competency, regardless of their nationality or country of residence. 

You must demonstrate a level of English language competency that will enable you to succeed in your studies, regardless of your nationality or country of residence. The University accepts a wide range of international English qualifications and English language tests.

Find out more about English language requirements for the University of Glasgow.

English language requirements

For applicants whose first language is not English, the University sets a minimum English Language proficiency level.

International English Language Testing System (IELTS) Academic module (not General Training)

• 6.5 with no subtests under 6.0
• Tests must have been taken within 2 years 5 months of start date. Applicants must meet the overall and subtest requirements using a single test.

Common equivalent English language qualifications accepted for entry to this programme:
TOEFL (ibt, my best or athome)

• 79; with Reading 13; Listening 12; Speaking 18;Writing 21
• Tests must have been taken within 2 years 5 months of start date. Applicants must meet the overall and subtest requirements , this includes TOEFL mybest.

Pearsons PTE Academic

• 59 with minimum 59 in all subtests
• Tests must have been taken within 2 years 5 months of start date. Applicants must meet the overall and subtest requirements using a single test.

Cambridge Proficiency in English (CPE) and Cambridge Advanced English (CAE)

• 176 overall, no subtest less than 169
• Tests must have been taken within 2 years 5 months of start date. Applicants must meet the overall and subtest requirements using a single test.

Oxford English Test

• Oxford ELLT 7
• R&L: OIDI level no less than 6 with Reading: 21-24 Listening: 15-17
• W&S: OIDI level no less than 6

Trinity College Tests

Integrated Skills in English II & III & IV: ISEII Distinction with Distinction in all sub-tests.

University of Glasgow Pre-sessional courses

Tests are accepted for 2 years following date of successful completion.

Alternatives to English Language qualification

• Degree from majority-English speaking country (as defined by the UKVI including Canada if taught in English)
  • students must have studied for a minimum of 2 years at Undergraduate level, or 9 months at Master's level, and must have complete their degree in that majority-English speaking country and within the last 6 years
• Undergraduate 2+2 degree from majority-English speaking country (as defined by the UKVI including Canada if taught in English)
  • students must have completed their final two years study in that majority-English speaking country and within the last 6 years

For international students, the Home Office has confirmed that the University can choose to use these tests to make its own assessment of English language ability for visa applications to degree level programmes. The University is also able to accept UKVI approved Secure English Language Tests (SELT) but we do not require a specific UKVI SELT for degree level programmes. We therefore still accept any of the English tests listed for admission to this programme.

Pre-sessional courses

The University of Glasgow accepts evidence of the required language level from the English for Academic Study Unit Pre-sessional courses. We also consider other BALEAP accredited pre-sessional courses:

• School of Modern Languages and Cultures: English for Academic Study
• BALEAP guide to accredited courses

Fees and funding
Fees and funding
Tuition fees
2024/25

• UK: £4,786
• International & EU: £30,240

Prices are based on the annual fee for full-time study. Fees for part-time study are half the full-time fee.

Irish nationals who are living in the Common Travel Area of the UK, EU nationals with settled or pre-settled status, and Internationals with Indefinite Leave to remain status can also qualify for home fee status.

• Fee status and policies

Alumni discount

We offer a 20% discount to our alumni on all Postgraduate Research and full Postgraduate Taught Masters programmes. This includes University of Glasgow graduates and those who have completed Junior Year Abroad, Exchange programme or International Summer School with us. The discount is applied at registration for students who are not in receipt of another discount or scholarship funded by the University. No additional application is required.

Possible additional fees

• Re-submission by a research student £540
• Submission for a higher degree by published work £1,355
• Submission of thesis after deadline lapsed £350
• Submission by staff in receipt of staff scholarship £790

Students will be expected to pay a contribution to research running costs.  This is in addition to your tuition fees. The value of the contribution is negotiable and will be supplemented by the host laboratory and/or supported by the School of Cancer Sciences eg. for competitive candidates with part (tuition fees only) scholarships or fully self-funded students.

Support
Support

The College of Medical, Veterinary and Life Sciences  provides a vibrant, supportive and stimulating environment for all our postgraduate students. We aim to provide excellent support for our postgraduates through dedicated postgraduate convenors, highly trained supervisors and pastoral support for each student.
 
Our overarching aim is to provide a research training environment that includes:

• provision of excellent facilities and cutting edge techniques
• training in essential research and generic skills
• excellence in supervision and mentoring
• interactive discussion groups and seminars
• an atmosphere that fosters critical cultural policy and research analysis
• synergy between research groups and areas
• extensive multidisciplinary and collaborative research
• extensive external collaborations both within and beyond the UK 
• a robust generic skills programme including opportunities in social and commercial training

How to apply
How to apply
Identify potential supervisors

All Postgraduate Research Students are allocated a supervisor who will act as the main source of academic support and research mentoring. You need to identify a project from our programme projects list.  And then contact the potential supervisor to discuss your application before you apply. Please note, even if you have spoken to an academic staff member about your application, you still need to submit an online application form.

Gather your documents

Before applying to the MSc by Research Program in Tissue Regeneration and Cancer, gather the following supporting documentation:

Final or current degree transcripts including grades (and an official translation, if needed) – scanned copy in colour of the original document.

Degree certificates (and an official translation, if needed): scanned copy in colour of the original document

One academic or professional reference on headed paper and signed by the referee. References may be uploaded as part of the application form or you may enter your referees contact details on the application form. We will then email your referee and notify you when we receive the reference.  We can also accept confidential references direct to [email protected] , from the referee’s university or business email account.

Complete Curriculum Vitae, including any other prior positions and/or employments.

Completed cover letter: MSc (Research) Tissue Regeneration & Cancer

Apply now
Contact us
Before you apply

MSc (Research): email [email protected]

After you have submitted your application

MSc (Research): contact our Admissions team

Any references may be submitted by email to: [email protected]