Roles of bacteria in colon cancer

Patients with an inherited form of colon cancer harbor two bacterial species that lead to development of the disease, and the same species have been found in people who develop a sporadic form of colon cancer, a study led by a Johns Hopkins Bloomberg~Kimmel Institute for Cancer Immunotherapy research team finds.

A second study by the same researchers shows a possible mechanism behind how one of these species spurs a specific type of immune response, promoting-instead of inhibiting the formation of malignant tumors. Together, these findings could lead to new ways to more effectively screen for and ultimately prevent colon cancer.

The Science findings describe a process in which these bacteria invade the protective mucus layer of the colon and collude to create a microenvironment-complete with nutrients and everything the bacteria need to survive that induces chronic inflammation and subsequent DNA damage that supports tumor formation.

These findings suggest a change in the standard of care for people who carry both types of bacteria. "More frequent colon cancer screening than the currently recommended once every 10 years should be considered," says Drew Pardoll, M.D., Ph.D., director of the Bloomberg~Kimmel Institute for Cancer Immunotherapy. Ultimately, once better understood, administering drugs or vaccines to prevent colonization of the bacteria in the colon, and potentially even probiotics to chase the bugs from the colon, are preventive measures that could be explored to interrupt the cancer-promoting process.

These new findings shows that particular strains of bacteria can invade the colon mucus in some patients who get colon cancer but who have no inherited predisposition for the disease. Unlike most bacteria, which do not make it past the colon's protective mucus layer, these communities of bacteria that invade the mucus form a sticky biofilm right next to the colon epithelial cells that line the colon, where colon cancer usually originates.

About 5 percent of colon cancers are caused by a hereditary syndrome called familial adenomatous polyposis (FAP), in which an inherited mutation launches a series of genetic changes that develop over time and eventually prompt the epithelial cells to turn malignant. However, it was unclear whether ETBF or other bacteria played a role in the progression to colon cancer in FAP patients.

To investigate the relationship between the bacteria-caused biofilms and cancer formation, researchers examined colon tissue removed from six FAP patients. Tests showed patchy sections of biofilms distributed along the colon's length in about 70 percent of the patients. The researchers used gene probes to identify the particular bacterial species and found that the biofilms consisted mainly of two types, Bacteroides fragilis and Escherichia coli, a surprising finding since the colon contains at least 500 different types of bacteria.

Tests on 25 additional colon samples from FAP patients showed that the B. fragilis strain was a subtype, called ETBF, which makes a toxin that triggers certain oncogenic, or cancer-promoting, pathways in colon epithelial cells and causes colon inflammation. The E. coli strain produced a substance called colibactin (synthesized by a set of genes in the bacterial genome called the PKS island), which causes DNA mutations.

FAP is a devastating disease that ultimately results in surgical removal of the colon, a Currently, using colonoscopy to monitor for the formation of precancerous tumors, called polyps, is the standard of care. Using a mouse model of colon cancer, the researchers found that animals whose colons were colonized with just one of these species developed few or no tumors. However, when their colons were colonized with both species simultaneously, they developed many tumors, suggesting a synergy between the two types of bacteria.

An earlier study suggested a unique type of immune response producing an inflammatory protein called IL-17-was key to ETBF-induced tumor formation. In order to prove the importance of IL-17 in the cancer-promoting effects of the bacterial combination, they used a mouse model in which the IL-17 gene was genetically deleted so it could not make IL-17, and colonized the mice with both ETBF and PKS+E. coli. Unlike animals that readily made IL-17, the genetically altered mice didn't form colon tumors, confirming the importance of this protein in bacterial-driven colon cancer.

However, in addition to IL-17, the studies showed that ETBF digested the mucus layer, enabling the PKS+ E. coli to adhere in larger numbers to the colon mucosa where together the bacteria induced increased DNA damage, a step preceding the gene mutations that underlie colon tumor formation. The complementary findings in Cell Host & Microbe demonstrate how ETBF's toxin prompts colon cancer to develop. Using a different mouse model of colon cancer, the researchers colonized the animals' colons with ETBF and then performed a series of tests to monitor the resulting cellular and molecular changes.

Their results revealed that ETBF's toxin spurs a cascade of events that promote colon inflammation that feeds back to act on the colon epithelial cells. First, the toxin triggers colon immune cells to produce IL-17. This inflammatory molecule then acts directly on the colon epithelial cells to trigger activation of a protein complex involved in promoting further inflammation, known as NFkappaB. NFkappaB in turn induces the colon epithelial cells to produce several signaling molecules that recruit more immune cells, called myeloid cells, to the colon.

These immune cells are involved in the inflammatory response and are known to support tumor growth. This process culminates in tumors forming in the colon. Additional experiments showed that a protein known as STAT3, which was previously shown to play a role in regulating cancer and inflammatory genes, is also necessary for tumor formation.
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Nicotine in E-cigarettes may cause cancer

The nicotine in e-cigarettes seems to damage DNA in ways that may increase cancer risk, the damage was seen both to DNA and its ability to repair itself, making cells more likely to mutate and develop into cancer, said lead researcher Moon-shong Tang, a professor of environmental medicine at New York University School of Medicine.

Reseachers exposed laboratory mice to e-cigarette vapor, which contains both nicotine and liquid solvents. They also exposed mice to the nicotine and the solvents separately. The vapors were produced using 4.2 volts of electricity, at or below the level at which most commercial e-cigarettes function.

Prior studies have shown that e-liquid heated using higher levels of electricity could produce harmful chemicals. This research team wanted to investigate the risk posed to people using a typical e-cigarette. They found the solvent alone does not cause DNA damage, nicotine with e-cigarette solvent caused the same damage as nicotine alone. The researchers also exposed cultured human lung and bladder cells to nicotine, and found the same effects-DNA damage and suppressed DNA repair.
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How alcohol damages DNA and causes cancer

Scientists have shown how alcohol damages DNA in stem cells, helping to explain why drinking increases the risk of cancer, according to latest research. Researchers used mice to show how alcohol exposure leads to permanent genetic damage. Scientists at the MRC Laboratory of Molecular Biology, Cambridge, gave diluted alcohol, chemically known as ethanol, to mice.

They then used chromosome analysis and DNA sequencing to examine the genetic damage caused by acetaldehyde, a harmful chemical produced when the body processes alcohol. They found that acetaldehyde can break and damage DNA within blood stem cells leading to rearranged chromosomes and permanently altering the DNA sequences within these cells.

It is important to understand how the DNA blueprint within stem cells is damaged because when healthy stem cells become faulty, they can give rise to cancer. These new findings therefore help us to understand how drinking alcohol increases the risk of developing 7 types of cancer including common types like breast and bowel.

Some cancers develop due to DNA damage in stem cells while some damage occurs by chance. The study also examined how the body tries to protect itself against damage caused by alcohol. The first line of defence is a family of enzymes called aldehyde dehydrogenases (ALDH). These enzymes break down harmful acetaldehyde into acetate, which our cells can use as a source of energy.

In the study, when mice lacking the critical ALDH enzyme - ALDH2 - were given alcohol, it resulted in four times as much DNA damage in their cells compared to mice with the fully functioning ALDH2 enzyme. The second line of defence used by cells is a variety of DNA repair systems which, most of the time, allow them to fix and reverse different types of DNA damage. But they don't always work and some people carry mutations which mean their cells aren't able to carry out these repairs effectively.

The study highlights that not being able to process alcohol effectively can lead to an even higher risk of alcohol-related DNA damage and therefore certain cancers. But it's important to remember that alcohol clearance and DNA repair systems are not perfect and alcohol can still cause cancer in different ways, even in people whose defence mechanisms are intact.
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Parabens can reduce sperm quality

According to the latest research, chemicals found in soap and plastic can reduce sperm quality. Hormone-disrupting chemicals, known as parabens, are significantly associated with an increased number of abnormally sized and shaped sperm, which has previously been linked to infertility.

Parabens, which are also found in certain foods, drugs and cosmetics can also cause DNA damage in sperm, which may hinder a woman's ability to conceive. Exposure to such chemicals also reduces sperms' mobility, making it more difficult for ejaculate to reach an egg. Parabens cause slow-moving sperm of an abnormal size

The researchers analysed the urine samples of men who attended a fertility clinic. The samples' paraben concentrations were assessed. The participants were also interviewed and provided semen, saliva and blood samples.

Results reveal the presence of parabens in urine are significantly associated with an increase number of sperm of an abnormal size and shape, which has previously been linked to infertility.
Parabens are also linked to DNA damage in sperm.

A particular type of the chemical, known as butyl paraben, was found to be particularly associated with reducing sperm quality. Parabens are widely-used preservatives in cosmetic products, including soaps, moisturisers and make-up. They are also found in certain drugs, pesticides, plastics, detergents, foods, toys and flame retardants.

The most common forms of the chemical are methylparaben, propylparaben and butylparaben. Parabens are sometimes combined to increase their effectiveness. Parabens may have developmental, reproductive, neurological and immune-system side effects.
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Better cancer treatment

Cancer patients can now have better and safer treatment by the use of less toxic drug for cancer treatment.
 Synthetic lethal interactions could inhibit the growth of tumors in mesenchymal cells, cells that develop into connective tissue such as those found in bones, soft tissues, and the central nervous system.

Presently, chemotherapy is the only available treatment for persistent cancers known as alternative lengthening telomere ALT cancers.
In healthy stem cell reproduction, the enzyme telomerase prevents the shortening of linear DNA ends called telomeres with each replication.

 The enzyme can also be re-activated to promote genetic stability and immortality in many cancer cells. While many cancers that multiple through telomerase re-activation may be treated with therapies other than chemotherapy, ALT cancer cells lack telomerase and few treatment options have been developed to inhibit their proliferation.

 ALT cancer cells account for fifteen percent of cancer cases, these incidences include some of the most deadly cancers like glioblastoma.

Researchers investigated three human genes associated with cancer development: FANCM mutations of which are associated with blood cancers), BRCA1 (mutations of which are commonly found in patients with breast and ovarian cancers), and BLM (mutations of which cause a variety of cancers).

FANCM, known to repair DNA damage where two DNA strands have been incorrectly linked, was removed from cells also deficient of BRCA1 or BLM. As a result, the team found that simultaneous inactivation of BLM and FANCM or of BRCA1 and FANCM resulted in dramatic increases of unrepaired DNA damages, preventing the cancerous cells from further reproducing.

 Their discoveries suggest that if drugs are developed to simultaneously inhibit BLM and FANCM, or BRCA1 and FANCM, they should kill the ALT cancers without posing the same toxic effects as the conventional chemotherapy drugs.
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Watercress boosts sperm counts

Watercress is a good source of vitamins B1, B2, B6, C, E, manganese, and carotenes. It is also a good source of calcium, fiber, iron and copper.

Watercress reduces stress, prevents pressure, tension and maintains the sperm count in men. Poor diet and obesity contribute to the drop in sperm levels, eating watercress regularly can destroy the effects of stress on sperm counts.

It is a good source of age-defying antioxidants that may prevent or slow the oxidative stress induced by free radical damage.

Regular intake of watercress increases counts and quality of sperm. It also prevents DNA damage that can lead to testicular cancer.

Apart from watercress these foods can also boost sperm counts - Banana, Walnut, Egg, Spinach, Dark chocolate, Asparagus, Broccoli, Pomegranate, Oyster, Garlic and Beans.
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Facts about cancer

Cancer is a condition where cells in a particular part of the body develop and reproduce uncontrollably. Cells can
experience uncontrolled growth if there are mutations to DNA, and it alters genes involved in cell division.

Cancer occurs when a cell's gene mutations make the cell unable to correct DNA damage. Normal cells in the body follow grow, divide and die.
Cancerous cells can destroy other healthy tissue and organs in the body, cancer can grow in any part of the body.
There are over 220 different types of cancer.

It alters normal cells division to form lumps or masses of tissue known as tumors. Tumors interfere with the digestive, nervous, and circulatory systems, and release hormones that alter proper body functions. Metastasis is multiplication and spread of cancers to other parts of the body to invade and destroy other healthy tissues.

Cancer is considered to be one of the leading causes of morbidity and mortality worldwide. Carcinogens are tobacco, asbestos, arsenic, radiation such as gamma and x-rays, the sun, and compounds in car exhaust fumes are all examples of carcinogens.

 When our bodies are exposed to carcinogens, free radicals are formed that try to steal electrons from other molecules in the body. Theses free radicals damage cells and affect their ability to function normally.

Cancer can be the result of a genetic predisposition that is inherited from family members. It is possible to be born with certain genetic mutations or a fault in a gene that makes one more likely to develop cancer later in life.

African Americans are more likely to die of cancer than people of any other race. Risk of cancer can be reduced by avoiding tobacco, limiting alcohol intake, limiting UV ray exposure from the sun and tanning, eating healthy diet, and regular medical check.

There is an increase in the number of possible cancer-causing mutations in our DNA as we get older. Some viruses like human papillomavirus, hepatitis B and C and E, Human immunodeficiency virus and any disease that suppresses the immune system increases the risk of developing cancer.

There is an increase in the number of possible cancer-causing mutations in our DNA as we get older. Some viruses like human papillomavirus, hepatitis B and C and E, Human immunodeficiency virus and any disease that suppresses the immune system increases the risk of developing cancer.

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New drug for ovarian cancer

The drug, known as ONX-0801 in the phase 1 clinical trial, was tested in 15 women with advanced ovarian cancer as part of a wider trial run by the Institute of Cancer Research (ICR) and the Royal Marsden NHS Foundation Trust in London.

The aim was to test its safety, but the results were so good that researchers are keen to move the drug to the next stage of research.

ONX-0801 is the first in a new class of drugs discovered at the ICR.
It attacks ovarian cancer by mimicking folic acid to enter the cancer cells.

The drug  kills these cells by blocking a molecule called thymidylate synthase, thereby causing irreparable DNA damage.

Ovarian cancer cells have an abnormally large number of receptors for folic acid, called alpha folate receptors. This means these cancer cells respond particularly well to the treatment.

The drug targeted cancer cell with little side-effects, making it a kinder treatment for ovarian cancer patients.