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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 March 17, 2014

 


In recent years, a trend toward a single-cell analysis is showing researchers
that individual cells within a tumor are capable of amassing mutations which
make them more aggressive — and treatment resistant. David Langenau hopes
to to identify other cell mutations that lead to leukemia relapse.

Image Credit: Cancer Cell, 06 March 2014.






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A common mutation drives leukemia relapse

Harvard stem cell scientists have identified a mutation in human acute lymphoblastic leukemia that most likely drives relapse of the disease. The finding in zebrafish, may be clinically relevant for humans.

The research, published in Cancer Cell, could translate into improved patient care in this particular blood cancer, which typically affects children — but is more deadly in adults.


In recent years, a trend toward a single-cell analysis is showing researchers that individual cells within a tumor are capable of amassing mutations making them more aggressive — and treatment resistant.

So while 99% of a tumor may be destroyed by the initial cancer treatment, a particularly aggressive cell can survive and causing a cancer patient to relapse six months later.


Harvard Stem Cell Institute faculty member David Langenau, PhD, with his lab in the Department of Pathology at Massachusetts General Hospital, used zebrafish to search for the rare, relapse-driving leukemia cells and then designed therapies that could kill the cells.

They found that at least half of relapse-driving leukemic cells had a mutation activating the Akt pathway which rendered cells resistant to common chemotherapy, while increasing growth.

Langenau's lab then examined human acute lymphoblastic leukemia and discovered that inhibiting the Akt pathway restored leukemic cell response to chemotherapy.


"The Akt pathway appears to drive treatment resistance. We also found that this same pathway increases growth of leukemic cells and increases the fraction of cells capable of relapsing."

David Langenau, PhD, Harvard Stem Cell Institute Principal Faculty member, and member in the Department of Pathology at Massachusetts General Hospital

"Our work will likely help in identifying patients that are prone to relapse and would benefit from co-treatment with inhibitors of the Akt pathway and typical front-line cancer therapy."

Jessica Blackburn, PhD, study first author


In addition to determining how best to translate this finding into use in a clinic setting, Langenau hopes to to identify other mutations that lead to relapse. The work could identify a host of potential drug targets for patients with aggressive leukemias.

The research took five-and-a-half years to complete, and was the most labor-intensive project Langenau and his lab members took on, completeing over 6,000 zebrafish transplant experiments.

Highlights
Spontaneous and continued clonal evolution occurs within single T-ALL cells
Clonal evolution enhances LPC frequency, growth, and therapy resistance
Clonal evolution can activate the Akt/mTORC1 pathway to increase LPC frequency
Akt inhibitors sensitize LPCs to dexamethasone-induced killing

Summary
Clonal evolution and intratumoral heterogeneity drive cancer progression through unknown molecular mechanisms. To address this issue, functional differences between single T cell acute lymphoblastic leukemia (T-ALL) clones were assessed using a zebrafish transgenic model. Functional variation was observed within individual clones, with a minority of clones enhancing growth rate and leukemia-propagating potential with time. Akt pathway activation was acquired in a subset of these evolved clones, which increased the number of leukemia-propagating cells through activating mTORC1, elevated growth rate likely by stabilizing the Myc protein, and rendered cells resistant to dexamethasone, which was reversed by combined treatment with an Akt inhibitor. Thus, T-ALL clones spontaneously and continuously evolve to drive leukemia progression even in the absence of therapy-induced selection.

Authors
Jessica S. Blackburn, Sali Liu, Jayme L. Wilder, Kimberly P. Dobrinski, Riadh Lobbardi, Finola E. Moore, Sarah A. Martinez, Eleanor Y. Chen, Charles Lee, David M. Langena