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Cancer is the subject of intense research around the world, but many questions about how the disease works remain unanswered. Benign tumour in mouse skin; green and red mark proteins in the tumour that are normally found in 2 different skin cell types Invasive cancer in mouse skin; green marks a protein made by hair follicle cells, red marks basal tumour cells Possible cancer stem cells?
This factsheet was created by Cedric Blanpain.Images by Cedric Blanpain, Benjamin Beck, Khalil Kass Youssef and Gaelle Lapouge. We've worked with scientists and doctors to answer some of your most frequently asked questions about stem cell science and potential therapies. Smokers who've received a clean bill of health from their doctor may believe cigarettes haven't harmed their lungs. The study, published today in the journal Stem Cell, compared cells that line the airway from healthy nonsmokers with those from smokers with no detectable lung disease. The researchers found that in the cells lining the airways of the smokers's lungs, human embryonic stem cell genes had been turned on. This loss of control allows cancerous cells to multiply without restraint and enables them to migrate to other organs because the genetic programming that keeps them on task is in disarray. In the study, 21 healthy nonsmokers were compared to 31 smokers who had no lung disease symptoms and had normal X-rays as well as normal chest examinations.
Cells from basal cancers are able to switch relatively easily into cancer stem cell (CSC) state, unlike luminal breast cancer cells, which tend to remain in the non-CSC state.
The researchers, whose findings are published this week in the journal Cell, report that the ZEB1 gene is held in a poised state in basal non-CSCs, such that it can readily respond to environmental cues that consequently drive those non-CSCs into the dangerous CSC state. Transcription factors are genes that control the expression of other genes, and therefore have a significant impact on cell activities. Other earlier work led by Christine Chaffer, a postdoctoral researcher in the Weinberg lab, demonstrated that cancer cells are able to spontaneously become CSCs. Breast cancers are categorized into at least five different subgroups based on their molecular profiles. Chaffer and Marjanovic, a former research assistant in the Weinberg lab, studied non-CSCs from luminal- and basal-type cancers and determined that cells from basal cancers are able to switch relatively easily into CSC state, unlike luminal breast cancer cells, which tend to remain in the non-CSC state.
The scientists determined that the difference in ZEB1’s effects is due to the way the gene is marked in the two types of cancers. This work is supported the Advanced Medical Research Foundation (AMRF), Breast Cancer Research Foundation, and National Institutes of Health (NIH) grants HG002668 and CA146445.
Robert Weinberg’s primary affiliation is with Whitehead Institute for Biomedical Research, where his laboratory is located and all his research is conducted. Christine L Chaffer (1*), Nemanja D Marjanovic (1*), Tony Lee (1), George Bell (1), Celina G Kleer (2), Ferenc Reinhardt (1), Ana C D’Alessio (1), Richard A Young (1,3), and Robert A Weinberg (1,4).
Whitehead Institute is a world-renowned non-profit research institution dedicated to improving human health through basic biomedical research. This is a carefully controlled process that allows the body to grow, and to replace lost or damaged cells during adult life.
However, a new study by researchers at Weill Cornell Medical College has found that even smokers who seem healthy have damaged airway cells, with characteristics similar to cells found in aggressive lung cancer. The smokers' cells showed early signs of impairment, similar to that found in lung cancer -- providing evidence that smoking causes harm, even when there is no clinical evidence that anything is wrong.

These are genes that are normally expressed in developing embryos -- soon after eggs are fertilized -- before cells are programmed with their specific assignment. Although all of the body's cells contain the same genes, genes are only "turned on" for each cell's defined task. It doesn't necessarily mean you will develop cancer, but that the soil is fertile to develop cancer", says Dr.
All individuals were evaluated at Weill Cornell's Clinical and Translational Science Center and Department of Genetic Medicine Clinical Research Facility. Understanding these very early events will give us clues and help us develop ways to protect the lungs." said Dr. In the case of ZEB1, it has an important role in the so-called epithelial-to-mesenchymal transition (EMT), during which epithelial cells acquire the traits of mesenchymal cells. Now Chaffer and Nemanja Marjanovic have pinpointed ZEB1, a key player in the EMT, as a gene critical for this conversion in breast cancer cells. More broadly these groups can be subdivided into the less aggressive ‘luminal’ subgroup or more aggressive ‘basal’ subgroup. In luminal breast cancer cells, the ZEB1 gene is occupied with modifications that shut it down.
Wholly independent in its governance, finances, and research programs, Whitehead shares a close affiliation with Massachusetts Institute of Technologythrough its faculty, who hold joint MIT appointments. The cancer stem cell theory could explain how some cancers work and why patients suffer relapses. In cancer, cells divide in an uncontrolled way, eventually forming an abnormal mass of cells called a tumour. According to the stochastic model, tumor cells are biologically equivalent but their behavior is influenced by intrinsic and extrinsic factors and is therefore both variable and unpredictable. Therefore, healthy lung cells only express genes related to lung function, while brain cells express brain-specific genes. By sending a thin tube called a bronchoscope and a fine brush into the lungs, investigators gently brushed the inside of the airways to collect cells from the airway's lining. The difference in ZEB1’s effects is due to the way the gene is marked in the two types of cancers. According to a 2011 epidemiological study, the 5-year survival rate for patients with basal breast cancer is 76%, compared with a roughly 90% 5-year survival rate among patients with other forms of breast cancer.
Unlike the tightly-packed epithelial cells that stick to one another, mesenchymal cells are loose and free to move around a tissue. The aggressive basal-type breast cancers often metastasize, seeding new tumors in distant parts of the body. But in basal breast cancer cells, ZEB1’s state is more tenuous, with repressing and activating markers coexisting on the gene. Thus, tumor-initiating activity cannot be enriched by sorting cells based on intrinsic characteristics. Researchers examined these cells, called the airway epithelium, which come into contact with cigarette smoke and are where cancer begins, Dr.
Previous work in the Weinberg lab showed that adult cancer cells passing through an EMT are able to self-renew and to seed new tumors with high efficiency, hallmark traits of CSCs.

Patients with basal breast cancer generally have a poorer prognosis than those with the less aggressive luminal-type breast cancer. When these cells are exposed to certain signals, including those from TGF?, the repressive marks are removed and ZEB1 is expressed, thereby converting the basal non-CSCs into CSCs. Mutations accumulate as our cells divide and age, but certain combinations of genetic mutations can lead to cancer.How tumours growDespite intense research into cancer, it is not clear exactly how tumours grow.
In contrast, the hierarchy model postulates the existence of biologically distinct classes of cells with differing functional abilities and behavior. Only a subset of cells has the ability to initiate tumor growth; these cancer stem cells possess self-renewal and give rise to nontumorigenic progeny that make up the bulk of the tumor. Some cells divide repeatedly, while others appear to develop into more mature cell types that no longer divide.
This model predicts that tumor-initiating cells can be identified and purified from the bulk nontumorigenic population based on intrinsic characteristics.
The stochastic model says that tumour growth is a random process to which all cells can contribute.The cancer stem cell theory suggests that tumours grow like normal tissues of the body, with stem cells at the starting point of an organised system that produces new cells to make a tissue grow.
According to this idea, tumours contain:Cancer stem cells that divide and feed tumour growth.
This theory argues that all cancer cells have the same potential to grow and divide, but each cell chooses at random between self-renewal and differentiation.
The cells in a tumour are not in an organised system – any cell has the same intrinsic potential to contribute to tumour growth.Different types of cancer may work in different ways, so it is possible that both of these theories are right. Perhaps they apply to different cancers or different stages of tumour development.Evidence for cancer stem cellsThere is no definitive proof in favour of either theory of cancer growth. However, an increasing amount of evidence suggests that the cancer stem cell theory holds true in some cases. Researchers found that only a subset of leukaemic cells can cause leukaemia when transplanted into a healthy body, the key characteristic of cancer stem cells.Since that discovery, many researchers have found cells with cancer stem cell characteristics in a great variety of human and mouse cancers, including breast, brain, skin, prostate and colonic cancers. In other types of cancer, such as melanoma, a very large number of the tumour cells have cancer stem cell characteristics.Cancer stem cells are controversialThe cancer stem cell theory is controversial because evidence for the existence of cancer stem cells relies solely on experiments that involve breaking down a tumour, taking out particular cells and then transplanting them. To prove that the transplanted cells are really cancer stem cells, scientists will need to look at individual cells and find direct evidence that the cells do indeed feed tumour growth within the natural environment of the body.Cancer stem cells and future therapiesThe cancer stem cell concept has important implications for cancer therapy. Understanding how cancer stem cells resist medical therapy could lead to the development of new, more efficient cancer treatments.Current researchMany questions remain to be answered about cancer.
More studies are needed to determine precisely how different cancers grow and how they resist medical therapy. Does the tumour’s immediate surroundings, or ‘microenvironment’, affect how cancer stem cells behave?

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