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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
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Home | Pregnancy Timeline | News Alerts |News Archive Sep 9, 2013

 

ALL Child

ALL is the most common cancer occurring in children today
and can occur in some adult cases. Children are at the highest
risk between 2 and 4 years of age. This risk decreases from age 4
to mid-20s, increasing again after age 50. The average person
has a 1 in 1,000 chance of getting ALL.

The American Cancer Society estimated the following statistics for 2010:
Approximately 43,050 new cases of all types of leukemia.
Approximately 5,330 new cases of acute lymphoblastic leukemia
(1 out of 3 were adult cases). Approximately 1,420 deaths from ALL
(3 out of 4 were adult cases).






WHO Child Growth Charts

 

 

 

Pax5 gene mutations seen in childhood leukemia

For the first time, a genetic link specific to risk of childhood leukemia has been identified, according to a team of researchers from Memorial Sloan-Kettering Cancer Center, St. Jude Children's Research Hospital, University of Washington, and other institutions.

The discovery was reported online today in the journal Nature Genetics.

"We're in unchartered territory," said study author Kenneth Offit, MD, MPH, Chief of the Clinical Genetics Service at Memorial Sloan-Kettering. "At the very least this discovery gives us a new window into inherited causes of childhood leukemia. More immediately, testing for this mutation may allow affected families to prevent leukemia in future generations."

The mutation was first observed in a family treated at Memorial Sloan-Kettering of which several family members of different generations had been diagnosed with childhood acute lymphoblastic leukemia (ALL). A second, non-related, leukemia-prone family cared for at a different hospital was later found to have the same mutation. A series of experiments were conducted confirming that the observed mutation compromised the normal function of the gene, which may increase the risk of developing ALL.


ALL, or childhood acute lymphoblastic leukemia, is the most common form of cancer in children, with 3,000 children and young adults being diagnosed each year in the United States.

The inherited genetic mutation is located in a gene called PAX5, which is known to play a role in the development of some B cell cancers, including ALL

PAX5, a transcription factor or "master gene," regulates the activity of several other genes and is essential for maintaining the identity and function of B cells. In all study participants, one of the two copies of the PAX5 gene was missing, leaving only the mutated version.

The research continues as researchers believe additional genetic factors play a role in the development of ALL in these patients.


Dr. Offit hopes that ongoing research will also determine what percentage of childhood ALL patients have the PAX5 mutation. Current estimates suggest that it is rare. Additionally, the newly discovered gene mutation may someday help scientists determine how to target transcription factors to treat other non-inherited forms of leukemia where the PAX5 mutation is present.

"With a better understanding of the genetic elements that induce cancer susceptibility, or drive cancer to grow, we can more precisely target therapy as well as potentially prevent cancer from occurring in the first place," added Dr. Offit.

In 1996, a similar study of cancer-prone families allowed Dr. Offit and his team to identify the most common mutation of BRCA2, associated with an increased risk of breast and ovarian cancer, and particularly common among individuals of Ashkenazi Jewish ancestry.

Abstract
Somatic alterations of the lymphoid transcription factor gene PAX5 (also known as BSAP) are a hallmark of B cell precursor acute lymphoblastic leukemia (B-ALL)1, 2, 3, but inherited mutations of PAX5 have not previously been described. Here we report a new heterozygous germline variant, c.547G>A (p.Gly183Ser), affecting the octapeptide domain of PAX5 that was found to segregate with disease in two unrelated kindreds with autosomal dominant B-ALL. Leukemic cells from all affected individuals in both families exhibited 9p deletion, with loss of heterozygosity and retention of the mutant PAX5 allele at 9p13. Two additional sporadic ALL cases with 9p loss harbored somatic PAX5 substitutions affecting Gly183. Functional and gene expression analysis of the PAX5 mutation demonstrated that it had significantly reduced transcriptional activity. These data extend the role of PAX5 alterations in the pathogenesis of pre-B cell ALL and implicate PAX5 in a new syndrome of susceptibility to pre-B cell neoplasia.

This research was supported by the Starr Cancer Research Initiative and by the National Institutes of Health under grant CA21765.

About Memorial Sloan-Kettering Cancer Center

Memorial Sloan-Kettering Cancer Center is the world's oldest and largest private cancer center with more than 125 years devoted to exceptional patient care, innovative research, and outstanding educational programs. We are one of 41 National Cancer Institute–designated Comprehensive Cancer Centers, with state-of-the-art science flourishing side by side with clinical studies and treatment.

The close collaboration between our physicians and scientists enables us to provide patients with the best care available as we work to discover more-effective strategies to prevent, control, and ultimately cure cancer in the future. Our education programs train future physicians and scientists, and the knowledge and experience they gain at Memorial Sloan-Kettering has an impact on cancer treatment and biomedical research around the world. For more information, go to http://www.mskcc.org.

Original press release:http://www.eurekalert.org/pub_releases/2013-09/mscc-rug090613.php