Chromosome Length May Indicate Development of Respiratory Infection

The rate of experimentally induced upper respiratory infection increased in healthy adults with shorter telomere length (a structure at the end of a chromosome) in specific leukocytes, according to research in JAMA. The results were identified in comparison to participants with longer telomeres.

Telomeres, DNA-protein complexes at the end regions of chromosomes, decrease in length with every cell division.

“Telomere shortening in leukocytes (white blood cells) has implications for immunocompetence and is associated with increased synthesis of proinflammatory cytokines and poorer antibody response to vaccines,” according to background information accompanying the article. “Shorter leukocyte telomere length also is associated with aging-related morbidity and mortality from conditions with immune system involvement, including infectious diseases, cancer, and cardiovascular disease.”

Investigators assessed telomere length in 152 healthy adults, then quarantined participants to administer nasal drops containing a common cold virus; participants were then monitored for 5 days for development of infection and clinical illness.

Among all patients, 69% developed respiratory infections and 22% developed a cold. An association was seen between those with shorter telomere lengths in all 4 cell types and increased odds of infection following exposure to the virus.

Those with the shortest CD8CD28 telomere length had a rate of infection of 77%, compared to 50% for those in the group with the longest telomeres. Among participants with the shortest telomeres, 26% became clinically ill. The rate for clinical illness was 13% for those in the group with the longest telomeres.

“In this study of healthy young and midlife adults, shorter CD8CD28 cell telomere length was associated with upper respiratory tract infection and clinical illness following experimental exposure to rhinovirus,” the authors concluded. “Because these data are preliminary, their clinical implications are unknown.”

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Biomarkers found for lymph node metastasis in oral cancer

Two biomarkers are heritable DNA changes while three are somatic DNA alterations

By looking out for five biomarkers, it is now possible to tell in advance if a person with oral cancer of the gum and cheek has lymph node metastasis even before surgery is undertaken, a study has found. The ability to correctly predict absence/presence of lymph node metastasis in oral cancer patients is 80-90% based on the five biomarkers, a team has found.

As a result, an oral cancer patient can be spared of a neck dissection to investigate if the cancer has spread to the lymph nodes in case the five biomarkers are absent. Lymph node dissection increases morbidity. However, if the patient tests positive for even one biomarker then an aggressive treatment would be required. An oral cancer patient with cancer spread to the lymph node has a 50% lower chance of survival for five years or more compared with patients in whom it has not spread to the lymph node.

Hypothesis

In oral cancer patients, the cancer cells tend to commonly spread to the lymph node in the neck. But not all oral cancer patients have the tendency for the cancer to spread to other organs (metastasis). “We posited that oral cancer patients who have lymph node metastasis possess DNA alterations in specific genes that provide cancer cells the ability to spread. These DNA alterations are different from those that cause the primary cancer, and these alterations arise independent of the stage of cancer,” says the Prof.

So in some patients, the cancer would have spread to the lymph node even at an early stage of oral cancer, while in some patients with advanced (T4 stage) oral cancer, the cancer would not have spread.

To find out what determines lymph node metastasis in oral cancer patients, the team studied two groups of patients — those with lymph node metastasis and those with advanced oral cancer but without lymph node metastasis. Totally, 72 patients belonging to these two groups were studied by a team.

Five genomic biomarkers

The team found that lymph node metastasis was associated with five genomic biomarkers. 


There are five genomic features or biomarkers of lymph node metastasis in oral cancer patients. Two of these are rare, heritable DNA changes in BRCA2 and FAT1 genes. The remaining three are non-heritable (somatic) DNA alterations. The somatic DNA alterations can occur in genes belonging to three different pathways — mitotic G2/M cell-cycle pathway, homologous recombination (HR) and non-homologous end joining (NHEJ) DNA-repair pathways.

Heritable DNA changes

The protein product of FAT1 gene functions as an adhesion molecule that keeps the cells together. In the case of cancer, cellular adhesion property is sometimes lost and the cells tend to spread. “Our finding that rare alterations in FAT1 are found in metastatic oral cancer is comprehensible, but new,” Prof. says. “Also, our finding that some rare alterations in BRCA2, which cause breast cancer, can also cause metastasis is novel.”

A cell duplicates to produce two daughter cells. Many genes are involved in this cell-cycle pathway, called mitotic G2/M pathway. If DNA of one or more genes of this pathway is altered, then many adverse cellular events take place. Most importantly, chromosomes become unstable and abnormal chromosomal changes occur, eventually leading to metastasis. “We have mapped DNA alterations in genes that belong to the mitotic G2/M pathway in oral cancer patients and have found that altered genes of this pathway promote lymph node metastasis,” says the first author of the paper.

Two pathways

When two major pathways — homologous recombination and non-homologous end joining — of DNA damage repair machinery gets perturbed, cells tend to behave abnormally. “We have found that DNA alterations in oral cancer patients that can be mapped to these pathways promote lymph node metastasis,” Prof. says. “So, metastasis in oral cancer is not promoted by a unique event.”

“The results have to be validated in a larger patient cohort,” says the Dr. “We have enrolled many patients to validate the results of this study. Besides TMC, the validation has to be done at other centres in India too.”

“We have found that a patient who presents without lymph node metastasis survives longer disease-free after standard treatment for oral cancer than one with metastasis of the lymph node. Therein lies the importance of our work,” says the Prof. 

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Australian researchers discover how a baby's sex is determined

While it is known that the sex of a baby is determined by its chromosome make-up at conception, new research has identified a "regulator" that increases or decreases the activity of genes which decide if we become male or female.

"These regulatory segments of DNA are called enhancers," said lead author of the study.

"If these enhancers that control testis genes are disrupted it may lead to a baby being born with a disorder of sex development," Sinclair said. 

While an embryo with two X chromosomes will become a girl, an embryo with an X-Y combination results in a boy. But the Y chromosome carries a critical gene, called SRY, which acts on another gene called SOX9 to start the development of testes in the embryo, explained a researcher.

"High levels of the SOX9 gene are needed for normal testis development," he added. 

This study,  sought to understand how the SOX9 gene was regulated by enhancers and whether disruption of the enhancers would result in disorders of sex development.

"We discovered three enhancers that, together ensure the SOX9 gene is turned on to a high level in an XY embryo, leading to normal testis and male development," he said.

"Importantly, we identified XX patients who would normally have ovaries and be female but carried extra copies of these enhancers, (high levels of SOX9) and instead developed testes," Sinclair said.
"In addition, we found XY patients who had lost these SOX9 enhancers, (low levels of SOX9) and developed ovaries instead of testes," Sinclair added.

Croft said human sex reversal such as seen in these cases is caused by gain or loss of these vital enhancers that regulate the SOX9 gene.

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Gene mutation behind deadly skin cancer identified

Researchers have identified gene mutation that is responsible for a hereditary form of skin cancer melanoma.

The study has found that people with specific mutations in the POT1 gene were extremely likely to develop melanoma and these mutations deactivate the gene that protects the ends of our chromosomes from damage.

Researchers revealed that the inactivation of POT1 caused by these mutations leads to longer and potentially unprotected telomeres, regions at the end of our chromosomes that protect chromosomes from damage.

Dr David Adams, co-senior author from the Wellcome Trust Sanger Institute, said that with this discovery, they should be able to determine who in a family is at risk, and in turn, who should be regularly screened for early detection.

According to the research team, there were also cases of other cancer types in families with these hereditary mutations such as leukaemias and brain tumours and the mutations that deactivate the POT1 gene may underlie other cancers, not just melanoma.

The scientists are currently working on developing cells and mice with an inactive POT1 gene, which will be used to test potential drug therapies that alter telomere metabolism. 

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Positive lifestyle changes linked to reversed aging process

Positive lifestyle changes, such as adopting a healthy diet and moderate exercise, may reverse the ageing process, according to a study.

Researchers have discovered that certain lifestyle changes may increase the length of telomeres.

Telomeres are DNA-protein complexes found at the end of chromosomes that control the ageing process. They protect the end of the chromosomes from becoming damaged. If the telomeres are shortened or damaged, the cells age and die quicker, triggering the ageing process.

Biological age can be predicted by the length of our telomeres, the researchers say. Shorter telomeres are linked to higher risk of premature death and age-related diseases, including many cancers (breast, prostate, colorectal and lung), heart disease, vascular dementia and obesity.

For the study, the researchers analyzed two groups of men who had been diagnosed with low-risk prostate cancer. Both groups had no conventional treatments, such as surgery or radiation, for the cancer.

The first group was required to make comprehensive lifestyle changes. These included:

Adopting a whole foods with plant-based diet

Carrying out moderate exercise

Adopting stress management techniques, such as meditation and yoga, and

Adopting greater intimacy and social support.

The second group was not asked to make any lifestyle changes.

The researchers measured the length of the men's telomeres at the beginning of the study and again at the end, 5 years later.

Positive lifestyle changes increase telomere length

Findings of the study revealed that the group who made lifestyle changes showed an increased telomere length of 10%, while the men who did not make any lifestyle changes showed a decreased telomere length of 3%.

Additionally, the more the participants enrolled in positive changes to their lifestyle, the higher the increase in their telomere length.

The study authors say:

"After 5 years, relative telomere length had increased in the lifestyle intervention group and decreased in the control group; the difference between the two groups was significant.

We also found a correlation between the degree of adherence to the lifestyle changes and the extent of change in relative telomere length."

The researchers say that although the study was not conducted to determine how lifestyle changes would affect participants' prostate cancer, a previous study revealed that positive lifestyle changes may delay the progression of the cancer in its early stages.

The effects of this relatively small pilot study may go beyond men with prostate cancer.

If proved by large-scale randomized controlled trials, these positive lifestyle changes may significantly reduce the risk of a wide variety of diseases and premature mortality. Our genes, and our telomeres, are a predisposition, but they are not necessarily our fate.

The researchers say that more trials involving larger and varied populations would be useful in determining how lifestyle affects telomere length.

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Men may inherit a form of heart disease from their fathers via Y chromosome

Although heart disease is the leading killer of women as well as of men, two heart disease patients out of every three are male, and heart disease strikes men 10 to 15 years earlier than it does women. No one really knows why.

Now, a new study reports that part of the answer may lie in the Y chromosome, the one chromosome unique to men.

In the study, published on Wednesday in The Lancet, researchers found that nearly all British men have one of two variants of a cluster of genes on their Y chromosome. Those with one of the variants had a 50 per cent increased risk of heart disease compared with men with the other variants. This risk was independent of traditional factors like cholesterol, smoking and diabetes.

The study needs to be replicated, researchers say, and while it raises intriguing hypotheses, it is not definitive.

The researchers also do not yet know which individual genes in the cluster are responsible for the increased risk, nor do they know why the genes have this effect. 

Everyone knows men who did all the wrong things — ignored their cholesterol levels, smoked — and yet were spared heart disease. And everyone knows men who were careful about their diet, controlled their cholesterol levels and blood pressure and did not smoke, yet died young from heart attacks.

The message of the new study, was that for some of those unlucky men, “yes indeed, they did have inheritable factors that independently caused death.” And when a screening test is developed to find those Y chromosome gene clusters, and researchers have a better understanding of how they act, it may be possible to protect some of them from having heart attacks.

A heart disease researcher  said it was also possible that simply having a Y chromosome instead of two X chromosomes, as women have, increased heart disease risk. The extra X could be protective.

Heart disease researchers have generally ignored the role of the Y chromosome, assuming it was mostly involved in determining malenes . He suggested the cluster of genes on the Y chromosome of the men with lower risk may help control inflammation, a process that is part of the formation of atherosclerotic plaques.

 A lot more work needs to be done on the gene cluster. The association between the gene cluster and heart disease risk needed to be confirmed.