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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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The World Health Organization (WHO) has created a new Web site to help researchers, doctors and
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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 Jan 8, 2015

Telomeres, stained RED, cap the ends of shromosomes. A small molecule called 6-thiodG
takes advantage of the cell's 'biological clock' and could be manipulated to stop
the growth of cancer cells in culture and decrease the growth of tumors.

 






 

 

'Biological clock' may be able to kill cancer cells

Cell biologists have targeted telomeres in mice with a small molecule called 6-thiodG. This molecule can take advantage of a cell's 'biological clock' and kill cancer cells — and shrink tumors.

Dr. Jerry W. Shay, Professor and Vice Chairman of Cell Biology at the University of Tennesee Southwestern, along with Dr. Woodring E. Wright, Professor of Cell Biology and Internal Medicine, found that 6-thio-2'-deoxyguanosine could stop the growth of cancer cells in culture and decrease the growth of tumors in mice.

"We observed broad efficacy against a range of cancer cell lines with very low concentrations of 6-thiodG, as well as tumor burden shrinkage in mice," said Dr. Shay, Associate Director of the Harold C. Simmons Comprehensive Cancer Center.

Dr. Shay and Dr. Wright hold The Southland Financial Corporation Distinguished Chair in Geriatrics, and are co-senior authors of the paper appearing in the journal Cancer Discovery.


6-thiodG targets a unique mechanism thought to regulate how long cells stay alive, a type of aging clock.

This biological clock is defined by DNA structures known as telomeres that cap the ends of chromosomes to protect them from accumulated damage which accrues with each cell division. Once telomeres shorten to a critical length, the cell no longer divides and dies — apoptosis.

Cancer cells are protected from apoptosis by an RNA protein complex called telomerase. Telomerase ensures that telomeres do not shorten with every division.


Telomerase is therefore the subject of intense research as a target for cancer therapy. Drugs that successfully block its action have been developed, but these drugs have to be administered for long periods of time to successfully trigger cell death and shrink tumors, leading to considerable toxicities. This outcome is partially because cells in any one tumor have chromosomes with different telomere lengths and any one cell's telomeres must be critically shortened to induce death.


6-thiodG is used as a substrate by telomerase and disrupts the normal way cells maintain telomere length.

Because 6-thiodG is not normally used in telomeres, its presence acts as an 'alarm' signal recognized by the cell as damage. As a result, the cell stops dividing and dies.


Telomerase is an almost universal oncology target, yet there are few telomerase-directed therapies in human clinical trials, researchers noted.

"Using telomerase to incorporate toxic products into telomeres is remarkably encouraging at this point," said Dr. Wright.

Importantly, unlike many other telomerase-inhibiting compounds, the researchers did not observe serious side effects in the blood, liver and kidneys of the mice that were treated with 6-thiodG.

"Since telomerase is expressed in almost all human cancers, this work represents a potentially innovative approach to targeting telomerase-expressing cancer cells with minimal side effects on normal cells," said Dr. Shay. "We believe this small molecule will address an unmet cancer need in an underexplored area that will be rapidly applicable to the clinic."

Abstract
The relationships between telomerase and telomeres represent attractive targets for new anticancer agents. Here, we report that the nucleoside analogue 6-thio-2′-deoxyguanosine (6-thio-dG) is recognized by telomerase and is incorporated into de novo–synthesized telomeres. This results in modified telomeres, leading to telomere dysfunction, but only in cells expressing telomerase. 6-Thio-dG, but not 6-thioguanine, induced telomere dysfunction in telomerase-positive human cancer cells and hTERT-expressing human fibroblasts, but not in telomerase-negative cells. Treatment with 6-thio-dG resulted in rapid cell death for the vast majority of the cancer cell lines tested, whereas normal human fibroblasts and human colonic epithelial cells were largely unaffected. In A549 lung cancer cell–based mouse xenograft studies, 6-thio-dG caused a decrease in the tumor growth rate superior to that observed with 6-thioguanine treatment. In addition, 6-thio-dG increased telomere dysfunction in tumor cells in vivo. These results indicate that 6-thio-dG may provide a new telomere-addressed telomerase-dependent anticancer approach.

SIGNIFICANCE: Telomerase is an almost universal oncology target, yet there are few telomerase-directed therapies in human clinical trials. In the present study, we demonstrate a small-molecule telomerase substrate approach that induces telomerase-mediated targeted “telomere uncapping,” but only in telomerase-positive cancer cells, with minimal effects in normal telomerase-negative cells. Cancer Discov; 5(1); 1–14. ©2015 AACR.

UT Southwestern researchers collaborated with researchers in the Department of Biochemistry at Hacettepe University in Ankara, Turkey, including Ilgen Mender, Visiting Junior Researcher at UT Southwestern, and Zeliha Dikmen; and Dr. Sergei Gryaznov, Chief Technology Officer with AuraSense Therapeutics.

The work is supported by a SPORE (Specialized Program of Research Excellence) grant from the National Cancer Institute, the Harold C. Simmons Comprehensive Cancer Center, and the Southland Financial Corporation Distinguished Chair in Geriatric Research.

UT Southwestern's Harold C. Simmons Comprehensive Cancer Center is the only National Cancer Institute-designated cancer center in North Texas and one of just 66 NCI-designated cancer centers in the nation. The Harold C. Simmons Cancer Center includes 13 major cancer care programs with a focus on treating the whole patient with innovative treatments, while fostering groundbreaking basic research that has the potential to improve patient care and prevention of cancer worldwide. In addition, the Center's education and training programs support and develop the next generation of cancer researchers and clinicians.

In addition, the Simmons Cancer Center is among only 30 U.S. cancer research centers to be named a National Clinical Trials Network Lead Academic Site, a prestigious new designation by the NCI, and the only Cancer Center in North Texas to be so designated. The designation and associated funding is designed to bolster the cancer center's clinical cancer research for adults and to provide patients access to cancer research trials sponsored by the NCI, where promising new drugs often are tested.

About UT Southwestern Medical Center
UT Southwestern, one of the premier academic medical centers in the nation, integrates pioneering biomedical research with exceptional clinical care and education. The institution's faculty includes many distinguished members, including six who have been awarded Nobel Prizes since 1985. Numbering approximately 2,800, the faculty is responsible for groundbreaking medical advances and is committed to translating science-driven research quickly to new clinical treatments. UT Southwestern physicians provide medical care in 40 specialties to about 92,000 hospitalized patients and oversee approximately 2.1 million outpatient visits a year.

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