Cancers are primarily an environmental disease
with 90–95% of cases attributed to environmental factors
and 5–10% due to genetics.
with 90–95% of cases attributed to environmental factors
and 5–10% due to genetics.
Cancer is ultimately the result of cells that uncontrollably grow and do
not die.
Normal cells in the body follow an orderly path of growth, division, and death.
Programmed cell death is called apoptosis, and when this process breaks down, cancer begins to form. Unlike regular cells, cancer cells do not experience programmatic death and instead continue to grow and divide. This leads to a mass of abnormal cells that grows out of control.
Carcinogenesis or oncogenesis or tumorigenesis is literally the creation of cancer.
Normal cells in the body follow an orderly path of growth, division, and death.
Programmed cell death is called apoptosis, and when this process breaks down, cancer begins to form. Unlike regular cells, cancer cells do not experience programmatic death and instead continue to grow and divide. This leads to a mass of abnormal cells that grows out of control.
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| Cancer cells can spread through the body in a process
known as metastasis. This cancer cell is moving down a pore in a filter.
The
image was taken at Cancer Research UK, where the spread of cancer is
studied in the hope of finding a cure. (©Anne Weston )
|
It is a process by which normal cells are transformed into cancer cells.
It is characterized by a progression of changes at the cellular, genetic and epigenetic level
that ultimately reprogram a cell to undergo uncontrolled cell division, thus forming a malignant mass.
It is characterized by a progression of changes at the cellular, genetic and epigenetic level
that ultimately reprogram a cell to undergo uncontrolled cell division, thus forming a malignant mass.
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Cancers are caused by a series of mutations.
Each mutation alters
the behavior of the
cell somewhat.
image credit:http://en.wikipedia.org
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There are five broad groups that are used to classify cancer.
- Carcinomas are characterized by cells that cover internal and external parts of the body such as lung, breast, and colon cancer.
- Sarcomas are characterized by cells that are located in bone, cartilage, fat, connective tissue, muscle, and other supportive tissues.
- Lymphomas are cancers that begin in the lymph nodes and immune system tissues.
- Leukemias are cancers that begin in the bone marrow and often accumulate in the bloodstream.
- Adenomas are cancers that arise in the thyroid, the pituitary gland, the adrenal gland, and other glandular tissues.
Cancers are often referred to by terms that contain a prefix related to
the cell type in which the cancer originated and a suffix such as
-sarcoma, -carcinoma, or just -oma. Common
prefixes include:
- Adeno- = gland
- Chondro- = cartilage
- Erythro- = red blood cell
- Hemangio- = blood vessels
- Hepato- = liver
- Lipo- = fat
- Lympho- = white blood cell
- Melano- = pigment cell
- Myelo- = bone marrow
- Myo- = muscle
- Osteo- = bone
- Uro- = bladder
- Retino- = eye
- Neuro- = brain
A protein that can mean life or death for cells: Sep. 17, 2013 — Each cell in an organism has a
sensor that measures the health of its "internal" environment. This
"alarm" is found in the endoplasmic reticulum (ER), which is able to
sense cellular stress and trigger either rescue responses or the death
of the cell. A team from the Institute for Research in Biomedicine
(IRB), in Barcelona, has discovered that the protein Mitofusin 2 (Mfn2)
plays a crucial role in correctly measuring stress levels, and also
makes sure the pathways of cell repair or cell death are effective. The researchers reveal some of the molecular mechanisms that connect
Mfn2 to endoplasmic reticulum stress in the latest edition of the
scientific journal, EMBO Journal, from the Nature Group, published by the European Molecular Biology Organization.
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In the image, the ER of a
cell with the Mfn2 protein (left)
and
without it. On the right,
the ER form vesicles which
indicates that the
organelle is
completely disorganized and
unable to respond correctly
to
cellular stress.
(Credit: JP Muñoz)
|
When the scientists removed Mfn2 from the cell under conditions of cell
stress, the endoplasmic reticulum responded by over-activating the
repair pathways. By doing so, it contradictorily functioned worse,
reducing the capacity of cells to overcome the stress insult and
promoting to a lesser degree apoptotic cell death. "When Mfn2 is
removed, the cellular stress response pathways are completely
disrupted," says Antonio Zorzano, coordinator of IRB's Molecular
Medicine Programme and leader of the group "Heterogenic and polygenic
diseases."
"The fact that we can modulate cell damage response with Mfn2 opens a
wide window of possible therapeutic avenues for further study," says
Muñoz. The Chilean scientist at IRB explains that tumour cells don't
activate cell death properly and proliferate uncontrolled. "Cancer cells
have already been noted to have low Mfn2 levels, and if we could
increase such levels, we would be able to promote apoptosis," he
continues. According to this, other research teams have already
published work indicating that the overexpression of Mfn2 induce
apoptosis.
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Professor Per Hall. (Credit: Gustav Mårtensson) |
Genetic 'Spelling Mistakes' that increase risk of common cancers determined:
Mar. 27, 2013
More
than 80 'genetic mistakes' that can increase the risk of breast,
prostate and ovarian cancer have found in a large, international
research study within the framework of the EU network COGS. For the
first time, researchers also have a relatively clear picture of the
total number of genetic alternations that can be linked to these
cancers. Ultimately the researchers hope to be able to calculate the
individual risk of cancer, to better understand how these cancers
develop and and to be able to generate new treatments.
The
scientists performed genetic analyses on all study participants. The
composition of nitrogen bases A, G, C and T was studied on 200,000
selected sections of the DNA strand. When cancer patients had
significantly different compositions compared to healthy control
subjects, the difference were considered to be relevant to risk of
disease. The alternations can be described as a genetic 'spelling
mistake', where A, G, C or T have been replaced with another letter.
This spelling mistake is called Single Nucleotide Polymorphis, (SNP) -
pronounced 'snip'. "COGS is the largest genotyping project in the world
targeting identification of alterations that influence the risk of
common cancers. The collaborative efforts have been tremendous and key
to success," says COGS coordinator Per Hall.
Decoded: Molecular messages that tell prostate and breast cancers to spread:
Apr. 30, 2013
Cancer
cells are wily, well-traveled adversaries, constantly side-stepping
treatments to stop their spread. But for the first time scientists at
the University of Michigan have decoded the molecular chatter that ramps
certain cancer cells into overdrive and can cause tumors to metastasize
throughout the body.
Russell Taichman, a professor at the U-M
School of dentistry and research associate Younghun Jung lookes at
prostate and breast tumors. Their study, "Recruitment of mesenchymal
stem cells into prostate tumors promotes metastasis," appears April 30
in the online journal Nature Communications.
Tumor cells secrete signals that
call in wound healing cells to
the
tumor site. In the process,
the normal wound healing cells
make the
tumor cells more
aggressive and able to metastasize.
(Credit: Image
courtesy of University of Michigan)
call in wound healing cells to
the tumor site. In the process,
the normal wound healing cells
make the tumor cells more
aggressive and able to metastasize.
(Credit: Image courtesy of University of Michigan)
Consider that a tumor is a wound that won't heal. To that end, both
cancerous and benign tumors emit distress signals and messages to
recruit healing-type cells, called mesenchymal stem cells, or MSCs,
Taichman said.
"Now we know what messages (tumors) send to recruit and alter those
healing cells, and we can take steps to block those messages," said
Taichman, the study's principal investigator. To that end,
Taichman said he was surprised at the large role played by
the protein CXCL16 in altering the healing type cells in such a way that
they revved the cancer cells into overdrive.
Life style changes may lengthen telomeres a measure of cell aging: Sep. 16, 2013 — A small pilot study shows for the first time that changes in diet, exercise, stress management and social support may result in longer telomeres, the parts of chromosomes that affect aging. The study will be published online on Sept. 16, 2013 in The Lancet Oncology.
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Three-dimensional representation
of the molecular structure of a
telomere (G-quadruplex).
picture credit:http://en.wikipedia.org
|
 | |
The greenish-yellow tips on
this human chromosome (No. 16)
are telomeres.
Scientists claim they have evidence
that explains why lifestyle changes
known to be good for you —
low-fat diets, exercise,
reducing stress —
can lengthen
your life.
picture credit: http://www.npr.org
|
In recent years, shorter telomeres have become associated with a broad
range of aging-related diseases, including many forms of cancer, stroke,
vascular dementia, cardiovascular disease, obesity, osteoporosis and
diabetes.
For five years, the researchers followed 35 men with localized,
early-stage prostate cancer to explore the relationship between
comprehensive lifestyle changes, and telomere length and telomerase
activity. All the men were engaged in active surveillance, which
involves closely monitoring a patient's condition through screening and
biopsies.
Ten of the patients embarked on lifestyle changes that included: a
plant-based diet (high in fruits, vegetables and unrefined grains, and
low in fat and refined carbohydrates); moderate exercise (walking 30
minutes a day, six days a week); stress reduction (gentle yoga-based
stretching, breathing, meditation). They also participated in weekly
group support.
They were compared to the other 25 study participants who were not asked to make major lifestyle changes.
The group that made the lifestyle changes experienced a "significant"
increase in telomere length of approximately 10 percent. Further, the
more people changed their behavior by adhering to the recommended
lifestyle program, the more dramatic their improvements in telomere
length, the scientists learned.
Telomere nucleotide sequences for human and mouse is TTAGGG, i.e.Telomeric repeat (5' to 3' toward the end).#consulted & shared thankfully from: http://www.sciencedaily.com, http://www.npr.org , http://en.wikipedia.org, http://www.medicalnewstoday.com
Notes on Carcinogens:
Procarcinogen
A procarcinogen is a precursor to a carcinogen. One example is nitrites when taken in by the diet. They are not carcinogenic themselves, but turn into nitrosamines in the body, which are carcinogenic.Common carcinogens
Occupational carcinogens
Occupational carcinogens are agents that pose a risk of cancer in several specific work-locations:| Carcinogen | Associated cancer sites or types | Occupational uses or sources |
|---|---|---|
| Arsenic and its compounds |
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| Asbestos | Not in widespread use, but found in:
|
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| Benzene |
|
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| Beryllium and its compounds |
|
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| Cadmium and its compounds | ||
| Hexavalent chromium(VI) compounds |
|
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| IC engine exhaust gas |
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| Ethylene oxide |
|
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| Nickel |
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| Radon and its decay products |
|
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| Vinyl chloride |
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| Shift work that involves circadian disruption | ||
| Involuntary smoking (Passive smoking) |
|
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| Radium-226, Radium-224, Plutonium-238 , Plutonium-239 and other alpha particle emitters with high atomic weight |
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Others
- Gasoline (contains aromatics)
- Lead and its compounds
- Alkylating antineoplastic agents (e.g. mechlorethamine)
- Other alkylating agents (e.g. dimethyl sulfate)
- Ultraviolet radiation from the sun and UV lamps
- Alcohol (causing head and neck cancers)
- Other ionizing radiation (X-rays, gamma rays, etc.)
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