Tuesday, December 3, 2013

Cancer: reasons behind unruly behaviour of a single cell

Cancers are primarily an environmental disease 
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.
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


Carcinogenesis or oncogenesis or tumorigenesis is literally the creation of cancer. 
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.
Cancers are caused by a series of mutations. 
Each mutation alters 
the behavior of the 
cell somewhat.
image credit:http://en.wikipedia.org

There are five broad groups that are used to classify cancer.
  1. Carcinomas are characterized by cells that cover internal and external parts of the body such as lung, breast, and colon cancer.
  2. Sarcomas are characterized by cells that are located in bone, cartilage, fat, connective tissue, muscle, and other supportive tissues.
  3. Lymphomas are cancers that begin in the lymph nodes and immune system tissues.
  4. Leukemias are cancers that begin in the bone marrow and often accumulate in the bloodstream.
  5. 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.
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.

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)


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, 2013A 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.
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
Telomeres are the protective caps on the ends of Telomeres are the protective caps on the ends of chromosomes that affect how quickly cells age. They are combinations of DNA and protein that protect the ends of chromosomes and help them remain stable. As they become shorter, and as their structural integrity weakens, the cells age and die quicker.
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
  • Alloys
  • Electrical and semiconductor devices
  • Medications (e.g. melarsoprol)
  • Herbicides
  • Fungicides
  • Animal dips
  • Drinking water from contaminated aquifers.
Asbestos Not in widespread use, but found in:
  • Constructions
  • Roofing papers
  • Floor tiles
  • Fire-resistant textiles
  • Friction linings (only outside Europe)
  • Replacement friction linings for automobiles still may contain asbestos
Benzene
Beryllium and its compounds
  • Lung
  • Missile fuel
  • Lightweight alloys
  • Aerospace applications
  • Nuclear reactors
Cadmium and its compounds
Hexavalent chromium(VI) compounds
  • Lung
  • Paints
  • Pigments
  • Preservatives
IC engine exhaust gas
Ethylene oxide
  • Leukemia
  • Ripening agent for fruits and nuts
  • Rocket propellant
  • Fumigant for foodstuffs and textiles
  • Sterilant for hospital equipment
Nickel
  • Nose
  • Lung
  • Nickel plating
  • Ferrous alloys
  • Ceramics
  • Batteries
  • Stainless-steel welding byproduct
Radon and its decay products
  • Lung
  • Uranium decay
  • Quarries and mines
  • Cellars and poorly ventilated places
Vinyl chloride
Shift work that involves circadian disruption
Involuntary smoking (Passive smoking)
  • Lung

Radium-226, Radium-224,
Plutonium-238
, Plutonium-239
and other alpha particle
emitters with high atomic weight

Others

#consulted & shared thankfully from: http://www.sciencedaily.com,  http://www.npr.org , http://en.wikipedia.org, http://www.medicalnewstoday.com

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