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article imageEssential Science: Researchers locate the origin of cancer

By Tim Sandle     Jan 25, 2016 in Science
In groundbreaking research, scientists have pinpointed how developing cells switch to a specialized state and how the process might go wrong in cancer. Digital Journal investigates further.
Cancer cells begin as normal cells. They go awry through an incorrect developmental step. The human body is composed of trillions of cells (somewhere, according to recent estimates, around 39 trillion.) From this vast number of cells, cancer begins with changes in one cell or a small group of cells.
When growing, cells produce signals. These signals control by how much and how often cells divide. When a signal is faulty, this can lead to cells growing and multiplying too much. When a series of cells in close proximity do this they can form a mass which is termed a tumor. The base where cancer starts is referred to as the primary tumor. Not all cancers are associated with a tumor (leukaemia, for example, is associated with blood and bone marrow.)
The most common reason signals are incorrect is due to mutations, which affect the genes within cells. Mutations can either occur by chance; through particular genes; or through external factors (like the chemicals in tobacco smoke). This is not a single event, for there needs to be around six or more different mutations before a normal cell transforms into a cancer cell. The formation of a tumor normally takes a long period of time; sometimes it takes several years for a tumor large enough to be detected on a scan to form.
The video below explains the process in more detail:
It is with the starting point for cancerous cells that researchers have gained a new insight. Although tumors are well characterized, the early beginnings remains an area about which there remains a lot to learn.
With the research, the science team used fruit flies. Fruit flies are often used in scientific research. Although fruit flies are generally regarded as a nuisance in homes, restaurants, and other areas where food is served, they have a number of useful scientific applications. The fruit fly is, for example, a model organism for genetic analysis. Some new research has taken an applied tract. Scientists have discovered that the sense of smell that the fly uses to seek out fruit can be used to sense drugs and explosives.
Outside of its role in laboratory studies, the fruit fly (Drosophila melanogaster) is an interesting insect. The eye of the fruit fly, for instance, is made up of 760 mini-eyes, making it one of the most complex organs in nature. In the research discussed in this article, it is the cells within the eyes of the fruit fly that scientists have examined cancer formation.
With the new research, scientists examined the cellular behavior of fruit fly eye cells. At the genetic level there are sufficient similarities between fruit fly cells and human cells. The cells of a fruit fly are very compact and they grow much faster than human cells.
Through these observations the medical scientists noted that a protein called Yan acted in a strange way as the fruit fly cells switched from a primitive stem-like state into a more specialized state. Here when Yan cells fluctuated, variations determined whether or not a cell advanced to the next state. As a cell does so, a receptor called EGFR stabilized the variation. In some cases, when the EGFR receptor did not receive the signal to stabilize the effect of the Yan, the cell remained in an uncontrolled state. This is a potential precursor to cancer.
Further study allowed the researchers to measure the concentration of the Yan protein and assess how it fluctuated. With the rapidly growing fruit fly cells, which can take as little as 15 hours to develop fully, the Yan protein fluctuated (or remained "noisy") for between six to eight hours.
Yan is not present in human cells. However, there is a near identical equivalent called Tel-1 protein transcription factor. In cancers like leukaemia, Tel-1 is often found to be mutated and the gene is said to be overexpressed. When Tel-1 is functioning normally it instructs cells to turn into white blood cells. Fluctuations with Tel-1 are controlled by a cell receptor called Her-2 (the equivalent to the EGFR receptor; the name is an abbreviation for human epidermal growth factor receptor 2). Thus the mechanism is sufficiently similar to be of research interest in relation to cancer formation.
It is hoped the new insight will be the basis for identifying a new target against cancer. At the very least it provides a new research tranche for cancer scientists.
The research was led by Richard W. Carthew at Northwestern University. The study is published in the journal eLife. The paper is titled "Dynamics and heterogeneity of a fate determinant during transition towards cell differentiation."
This article is part of Digital Journal's Essential Science series. Other articles in the series are:
"Space-food for astronauts made from bacteria";
"Health effects of antibiotic use";
"Graphene makes improved night vision tech";
"Personalized medicines, the health innovation”;
Power paper can store electricity”;
"Why some rainbows are completely red";
"Bright white light affects animal reproduction";
"Low cost device restores speech to patients";
"Learn about the new field of neurogastronomy";
"How implanted coils help to fight lung disease."
More about cancer origin, Cancer, Cancer cells, Tumor
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