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Welcome to The Visible Embryo, a comprehensive educational resource on human development from conception to birth.

The Visible Embryo provides visual references for changes in fetal development throughout pregnancy and can be navigated via fetal development or maternal changes.

The National Institutes of Child Health and Human Development awarded Phase I and Phase II Small Business Innovative Research Grants to develop The Visible Embryo. Initally designed to evaluate the internet as a teaching tool for first year medical students, The Visible Embryo is linked to over 600 educational institutions and is viewed by more than one million visitors each month.

Today, The Visible Embryo is linked to over 600 educational institutions and is viewed by more than 1 million visitors each month. The field of early embryology has grown to include the identification of the stem cell as not only critical to organogenesis in the embryo, but equally critical to organ function and repair in the adult human. The identification and understanding of genetic malfunction, inflammatory responses, and the progression in chronic disease, begins with a grounding in primary cellular and systemic functions manifested in the study of the early embryo.

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Pregnancy Timeline by SemestersFetal liver is producing blood cellsHead may position into pelvisBrain convolutions beginFull TermWhite fat begins to be madeWhite fat begins to be madeHead may position into pelvisImmune system beginningImmune system beginningPeriod of rapid brain growthBrain convolutions beginLungs begin to produce surfactantSensory brain waves begin to activateSensory brain waves begin to activateInner Ear Bones HardenBone marrow starts making blood cellsBone marrow starts making blood cellsBrown fat surrounds lymphatic systemFetal sexual organs visibleFinger and toe prints appearFinger and toe prints appearHeartbeat can be detectedHeartbeat can be detectedBasic Brain Structure in PlaceThe Appearance of SomitesFirst Detectable Brain WavesA Four Chambered HeartBeginning Cerebral HemispheresFemale Reproductive SystemEnd of Embryonic PeriodEnd of Embryonic PeriodFirst Thin Layer of Skin AppearsThird TrimesterSecond TrimesterFirst TrimesterFertilizationDevelopmental Timeline
CLICK ON weeks 0 - 40 and follow along every 2 weeks of fetal development
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Home | Pregnancy Timeline | News Alerts |News Archive Dec 10, 2013

 

Cancer cells dividing in culture.

https://www.youtube.com/watch?v=fTBZ6hV3pEg







WHO Child Growth Charts

 

 

 

Gene promotes 1 in 100 of tumors

Researchers have identified a gene that drives the development of tumours in over one per cent of all cancer patients. This is the first time that the gene CUX1 has been broadly linked to cancer development.

The team discovered that, when CUX1 is deactivated, a biological pathway is activated that increases tumour growth. Drugs that inhibit the biological pathway are currently being used in the clinic and are in development thus highlighting a potential new targeted therapy for patients with this type of cancer-causing mutation.

Around 300,000 people in the UK each year are diagnosed with cancer, and for more than 3,000 of these patients, an inactive CUX1 gene may be an underlying factor for their disease.

"Our research is a prime example of how understanding the genetic code of cancers can drive the search for targeted cancer therapies that work more effectively and efficiently," says Dr David Adams, lead author from the Wellcome Trust Sanger Institute. "This could improve the lives of thousands of people suffering from cancer."


The team used genetic data from over 7,600 cancer patients, collected and sequenced by the International Cancer Genome Constortium (ICGC) and other groups.

They found that in around one per cent of the cancer genomes studied, mutations deactivated CUX1, an event associated with tumour growth. CUX1 is mutated at a relatively low frequency, but across many different types of cancer.

Because previous studies focused on genes that are mutated at a high rate in one cancer type to find cancer drivers, CUX1 was missed as a driver of cancer.


"Our work harnesses the power of combining large-scale cancer genomics with experimental genetics," says Dr Chi Wong, first author from the Wellcome Trust Sanger Institute and practising Haematologist at Addenbrooke's Hospital. "CUX1 defects are particularly common in myeloid blood cancers, either through mutation or acquired loss of chromosome 7q. As these patients have a dismal prognosis currently, novel targeted therapies are urgently needed."

"Data collected from large consortia such the ICGC, provides us with a new and broader way to identify genes that can underlie the development of cancers," says Professor David Tuveson from Cold Spring Harbor Laboratory. "We can now look at cancers as groups of diseases according to their tissues of origin and collectively examine and compare their genomes."


The team silenced CUX1 in cultured cells to understand how inactivating it might lead to the development of tumours.

They found that when CUX1 is deactivated, it reduced a biological inhibitor, PIK3IP1, in its inhibitory effects.

This mobilized an enzyme responsible for cell growth, phosphoinositide 3-kinase (PI3K), increasing the rate of tumour progression.


The team has already identified several dozen other genes that when mutated at a low frequency could promote cancer development. They plan to silence these genes in mice to fully understand how their inactivation may lead to cancer development and the mechanisms by which this occurs.

"Drugs that inhibit PI3K signalling are currently undergoing clinical trial," says Professor Paul Workman, Deputy Chief Executive and Head of Cancer Therapeutics at The Institute of Cancer Research, London. "This discovery will help us to target these drugs to a new group of patients who will benefit from them and could have a dramatic effect on the lives of many cancer sufferers."

Published in Nature Genetics 08 Dec 2013.

Abstract
A major challenge in cancer genetics is to determine which low-frequency somatic mutations are drivers of tumorigenesis. Here we interrogate the genomes of 7,651 diverse human cancers and find inactivating mutations in the homeodomain transcription factor gene CUX1 (cut-like homeobox 1) in ~1–5% of various tumors. Meta-analysis of CUX1 mutational status in 2,519 cases of myeloid malignancies reveals disruptive mutations associated with poor survival, highlighting the clinical significance of CUX1 loss. In parallel, we validate CUX1 as a bona fide tumor suppressor using mouse transposon-mediated insertional mutagenesis and Drosophila cancer models. We demonstrate that CUX1 deficiency activates phosphoinositide 3-kinase (PI3K) signaling through direct transcriptional downregulation of the PI3K inhibitor PIK3IP1 (phosphoinositide-3-kinase interacting protein 1), leading to increased tumor growth and susceptibility to PI3K-AKT inhibition. Thus, our complementary approaches identify CUX1 as a pan-driver of tumorigenesis and uncover a potential strategy for treating CUX1-mutant tumors.

Nature Genetics (2013) doi:10.1038/ng.2846
Received 16 June 2013 Accepted 08 November 2013 Published online 08 December 2013

https://www.youtube.com/watch?v=fTBZ6hV3pEg

Authors
Chi C. Wong, Inigo Martincorena3, Alistair G. Rust, Mamunur Rashid, Constantine Alifrangis, Ludmil B. Alexandrov, Jessamy C. Tiffen, Christina Kober, Chronic Myeloid

Disorders Working Group of the International Cancer Genome Consortium5, Anthony R. Green, Charles E. Massie, Jyoti Nangalia, Stella Lempidaki, Hartmut Döhner, Konstanze Döhner, Sarah J. Bray, Ultan McDermott, Elli Papaemmanuil, Peter J. Campbell & David J. Adams. (2013) 'Inactivating CUX1 mutations promote tumorigenesis'

 

Funding

A full list of funding can be found on the paper

Participating Centres

1. Experimental Cancer Genetics, Wellcome Trust Sanger Institute, Hinxton, Cambridge, CB10 1SA, UK.

2. Department of Haematology, University of Cambridge, Hills Road, Cambridge, CB2 0SP, UK.

3. The Cancer Genome Project, Wellcome Trust Sanger Institute, Hinxton, Cambridge, CB10 1SA, UK.

4. Department of Biochemistry, Biocenter University of Würzberg, D-97074 Würzberg, Germany.

5. See Supplementary Note for members and affiliations,

6. Cambridge Institute for Medical Research, University of Cambridge, Hills Road, Cambridge, CB2 0SP, UK.

7. Wellcome Trust/MRC Stem Cell Institute, University of Cambridge, Cambridge, UK. Department of Physiology, Development and Neuroscience, University of Cambridge, CB2 3DY, UK.

10. Department of Internal Medicine III, University of Ulm, Albert-Einstein-Allee 23 89081, Ulm, Germany.

The Wellcome Trust Sanger Institute is one of the world's leading genome centres. Through its ability to conduct research at scale, it is able to engage in bold and long-term exploratory projects that are designed to influence and empower medical science globally. Institute research findings, generated through its own research programmes and through its leading role in international consortia, are being used to develop new diagnostics and treatments for human disease.

http://www.sanger.ac.uk

The Wellcome Trust is a global charitable foundation dedicated to achieving extraordinary improvements in human and animal health. We support the brightest minds in biomedical research and the medical humanities. Our breadth of support includes public engagement, education and the application of research to improve health. We are independent of both political and commercial interests.

http://www.wellcome.ac.uk