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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 Oct 11, 2013

 

Luika Timmerman showed that growth of about one-third of triple-negative
breast cancers overproduce a cell-surface protein called xCT (green)—
which she targeted with an FDA-approved drug to slow tumor growth.

 








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Triple-negative breast cancer slowed with FDA approved drug

FDA-Approved drug curbs tumor growth in mouse model for deadly form of breast cancer.


Roughly one in six women with breast cancer have triple-negative breast cancer, and only about three out of four with this type survive five years or more. These tumors sometimes grow aggressively, advancing from being undetectable to difficult-to-treat between regular screening mammography exams.


Drugs now are available that effectively target the estrogen and HER2 receptor proteins, which are found in many breast tumors, and these drugs spare most normal cells in the body.

However, triple-negative breast cancers do not make either of these receptors. To treat patients with triple-negative breast cancer, physicians use older chemotherapies that produce side effects in normal tissues, limiting the number of doses patients can receive.


UCSF researcher Luika Timmerman, PhD, an investigator in the UCSF Helen Diller Family Comprehensive Cancer Center, found that many cell lines obtained from triple-negative breast cancer are especially dependent on cystine, one of the 20 amino acid building blocks all cells need.

Timmerman used an FDA-approved drug to inhibit activity of a transporter protein that ferries cystine into triple-negative breast cancer cells, and found it significantly inhibited their growth in culture and when cells were transplanted into mice.

Timmerman described her discovery in a study published online on Oct. 3 in the journal Cancer Cell.


Timmerman found that she could significantly slow growth of triple-negative tumors using an FDA-approved anti-inflammatory drug called sulfasalazine.

Sulfasalazine blocks a specific cystine transporter called xCT.

While sulfasalazine itself would not be appropriate for treating cancer, Timmerman said, it could serve as a “lead compound” in the development of drugs that specifically target xCT on tumor cells.


“This study of human tumors in mice and of breast cancer cell lines demonstrates the potential of targeting not only this cystine transporter, but also other metabolic abnormalities in cancer,” Timmerman adds.

Timmerman has spent several years studying the abnormal metabolic behavior of cancer cells.“Different cancers seem to acquire different metabolic abnormalities that might in some cases give them a growth or survival advantage,” she has determined. “One of the strengths of this study was the large number of different cell lines I was able to test. When I saw similar results in many samples, I felt I was looking at a fundamental metabolic behavior that we could exploit to specifically target triple-negative tumors that overexpress the xCT cystine transporter, a significant group of previously untargettable tumors.”

Timmerman initially focused on investigating the amino acid glutamine among different breast cancer-derived cell lines, because glutamine metabolism was long known to be perturbed in cancer. She tracked gene activity through “microarray” data to functional differences among tumors and tumor cell lines in culture.

But she also measured amino acids and other molecules in cell culture to detect metabolic changes. When she did, she noticed that cystine and glutamate levels are frequently correlated in triple-negative cancers.


A series of experiments led to the discovery that the cystine transporter xCT was abundant and active in many triple-negative tumors and tumor cell lines. Timmerman then tested sulfasalazine on tumors grown in mice, and in tumor cell lines, and found that blocking xCT activity strongly retarded the growth of triple-negative tumors.


“We have identified a compelling therapeutic target commonly expressed by breast tumors of poorest prognosis, and a lead compound for rapid, effective drug development,” Timmerman said.

Timmerman conducted many of her experiments using breast cancer cell lines obtained from a large collection developed by one of the senior authors, Joe Gray, PhD, formerly head of the breast oncology program at UCSF and currently associate director for translational research for the Knight Cancer Institute at Oregon Health & Science University in Portland.

Abstract Highlights
Most breast tumors survive glutamine restriction, limiting its therapeutic use
A subset of triple-negative breast tumors are true glutamine auxotrophs
Conventional biomarkers of glutamine reliance do not identify true auxotrophs
Triple-negative tumors require cystine import via the xCT transporter
Summary

A handful of tumor-derived cell lines form the mainstay of cancer therapeutic development, yielding drugs with an impact typically measured as months to disease progression. To develop more effective breast cancer therapeutics and more readily understand their clinical impact, we constructed a functional metabolic portrait of 46 independently derived breast cell lines. Our analysis of glutamine uptake and dependence identified a subset of triple-negative samples that are glutamine auxotrophs. Ambient glutamine indirectly supports environmental cystine acquisition via the xCT antiporter, which is expressed on one-third of triple-negative tumors in vivo. xCT inhibition with the clinically approved anti-inflammatory sulfasalazine decreases tumor growth, revealing a therapeutic target in breast tumors of poorest prognosis and a lead compound for rapid, effective drug development.

Before leading her own lab, Timmerman began her cancer metabolism studies working as a postdoctoral fellow in the lab of another senior author, Frank McCormick, PhD, FRS, director of the UCSF Helen Diller Family Comprehensive Cancer Center.

Additional study authors include UCSF researchers Raymond Louie, PhD, Merce Padro, Anneleen Daemen, Denise Chan, PhD, and Laura van’t Veer, PhD; Mariia Yuneva of the MRC National Institute of Medical Research in London; Thomas Holton from San Francisco State University; Min Hu from the Novartis Institutes for BioMedical Research in Shanghai; Stephen Ethier from the University of South Carolina; and Kornelia Polyak from the Dana-Farber Cancer Institute. The research was funded by the National Institutes of Health, the Bay Area Breast Cancer SPORE, the Durra Family Fund, the Mount Zion Health Fund, and the Prospect Creek Foundation.

UCSF is a leading university dedicated to promoting health worldwide through advanced biomedical research, graduate-level education in the life sciences and health professions, and excellence in patient care. It includes top-ranked graduate schools of dentistry, medicine, nursing and pharmacy, a graduate division with nationally renowned programs in basic biomedical, translational and population sciences, as well as a preeminent biomedical research enterprise and two top-ranked hospitals, UCSF Medical Center and UCSF Benioff Children’s Hospital.

Original press releas: http://www.ucsf.edu/news/2013/10/109376/scientists-identify-triple-negative-breast-cancer-target-drug-development