This document summarizes research on telomeres and telomerase and their role in aging and cancer. It discusses how telomeres protect chromosome ends from degradation but shorten with each cell division, acting as a mitotic clock. The enzyme telomerase prevents shortening by adding telomere repeats. While telomerase is inactive in most somatic cells, leading to senescence, it is active in cancer and stem cells, allowing unlimited proliferation. Shortened telomeres are associated with human aging and disease. Inhibiting telomerase is a potential anti-cancer therapy since cancer cells must maintain telomeres to proliferate indefinitely.
TA 65 - Telomeres and Telomerase - Los Angeles 2015telomerescience
This document provides an overview of a workshop on telomeres and telomerase activation held in Los Angeles in 2015. It discusses telomere biology, factors that impact telomere length, lifestyle interventions and supplements that may help maintain telomere length, and clinical evidence on the effects of telomerase activation. Specifically, it summarizes evidence that telomerase activation through supplements like TA-65 has been shown to reverse cellular aging in mice and improve immune function, metabolic health, and psychological outcomes in human studies. It also discusses how stress, lifestyle factors, and diseases like depression are associated with shorter telomere length.
Telomeres, lifestyle, cancer, and agingHasnat Tariq
Telomeres are DNA-protein structures that protect chromosome ends from damage. Telomere length decreases with each cell division and critically short telomeres cause cell senescence or death. Certain lifestyle factors like smoking, obesity, stress, and diets low in antioxidants can accelerate telomere shortening and aging. Maintaining healthy habits like exercise, dietary restriction, and antioxidant-rich diets may help preserve telomeres and reduce cancer risk. Cancer cells maintain telomere length through high telomerase activity, making telomerase a potential target for cancer treatments.
This study explored the relationship between physical activity levels, telomere length, and telomerase activity in immune cells of older adults. The researchers found that moderate physical activity was associated with longer telomere length compared to low and high activity levels. No relationship was observed between activity level and telomerase enzyme activity. Additionally, individuals with the hTERT TT genotype had greater telomerase activity than other genotypes, and the TT genotype combined with high activity was associated with even greater telomerase activity. The findings suggest moderate physical activity may benefit telomere length while higher levels may not provide the same benefits.
Telomeres play an important role in cellular aging and division. A study found that women with phobic anxiety had shorter telomeres, suggesting anxiety is a risk factor for accelerated aging. In cancer cells, telomerase remains active, allowing indefinite division by regenerating telomeres. Researchers discovered a protein complex that normally inhibits telomerase; in cancer it is delayed, allowing telomerase to extend telomeres and confer immortality. Understanding these processes may lead to new prevention and treatment strategies for diseases of aging and cancer.
1) Telomeres are protective nucleoprotein structures at the ends of chromosomes that shorten with each cell division due to the end replication problem.
2) Telomerase is an enzyme that adds telomeric repeats to chromosome ends to counteract shortening and allow indefinite cell division.
3) Telomerase activation allows cancer cells to avoid replicative senescence and become immortalized, while preceding telomere shortening provides a mechanism for genetic instability and tumor progression.
Telomerase Activation: The Key to Unlocking the Aging Puzzle
The presentation discusses telomeres and telomerase, and their role in cellular aging and longevity. It notes that telomeres protect chromosome ends and shorten with each cell division, acting as a biological clock for aging. Telomerase is an enzyme that can rebuild telomere length, counteracting their shortening. Studies show telomerase activation can rejuvenate cells and tissues in mice, reducing biomarkers of aging without increasing cancer risk. Preliminary human studies suggest telomerase activation may provide benefits like improved immunity and bone density. The presentation promotes further research on telomerase activation as a way to potentially treat aging and age-related diseases
Different researches shows that, g-quadruplex- kind of tandem repeats are present in vivo,
Telomeres having tandem repeats of d(TTAGGG) , herein G is either anti or sync.
5’- UTR (untranslated region) of mRNA (U–U–U–U tetrads, as well as G- and U-containing octads)
Promoter region of c-myc , c-kit and variant bcl-2 oncogenes.
inferior oncogenic expression & veiled binding target of telomere associated proteins ( TRF1, POT1) may help to combat the uncontrolled cellular growth by inducing apoptosis & inhibit the telomerase overactivity.
The presentation discusses telomeres and telomerase in the context of cancer. It begins by defining telomeres as repetitive DNA sequences that cap the ends of chromosomes and shorten each time a cell divides. Telomerase is an enzyme that adds telomeric repeats and prevents shortening. In cancer cells, telomerase remains active and prevents telomere shortening, allowing unlimited cell division. Measuring telomerase may help detect and treat cancer by inducing senescence, though blocking it could also impair normal cell functions. The conclusion is that while inhibiting telomerase shows promise against cancer, more research is needed to minimize side effects.
TA 65 - Telomeres and Telomerase - Los Angeles 2015telomerescience
This document provides an overview of a workshop on telomeres and telomerase activation held in Los Angeles in 2015. It discusses telomere biology, factors that impact telomere length, lifestyle interventions and supplements that may help maintain telomere length, and clinical evidence on the effects of telomerase activation. Specifically, it summarizes evidence that telomerase activation through supplements like TA-65 has been shown to reverse cellular aging in mice and improve immune function, metabolic health, and psychological outcomes in human studies. It also discusses how stress, lifestyle factors, and diseases like depression are associated with shorter telomere length.
Telomeres, lifestyle, cancer, and agingHasnat Tariq
Telomeres are DNA-protein structures that protect chromosome ends from damage. Telomere length decreases with each cell division and critically short telomeres cause cell senescence or death. Certain lifestyle factors like smoking, obesity, stress, and diets low in antioxidants can accelerate telomere shortening and aging. Maintaining healthy habits like exercise, dietary restriction, and antioxidant-rich diets may help preserve telomeres and reduce cancer risk. Cancer cells maintain telomere length through high telomerase activity, making telomerase a potential target for cancer treatments.
This study explored the relationship between physical activity levels, telomere length, and telomerase activity in immune cells of older adults. The researchers found that moderate physical activity was associated with longer telomere length compared to low and high activity levels. No relationship was observed between activity level and telomerase enzyme activity. Additionally, individuals with the hTERT TT genotype had greater telomerase activity than other genotypes, and the TT genotype combined with high activity was associated with even greater telomerase activity. The findings suggest moderate physical activity may benefit telomere length while higher levels may not provide the same benefits.
Telomeres play an important role in cellular aging and division. A study found that women with phobic anxiety had shorter telomeres, suggesting anxiety is a risk factor for accelerated aging. In cancer cells, telomerase remains active, allowing indefinite division by regenerating telomeres. Researchers discovered a protein complex that normally inhibits telomerase; in cancer it is delayed, allowing telomerase to extend telomeres and confer immortality. Understanding these processes may lead to new prevention and treatment strategies for diseases of aging and cancer.
1) Telomeres are protective nucleoprotein structures at the ends of chromosomes that shorten with each cell division due to the end replication problem.
2) Telomerase is an enzyme that adds telomeric repeats to chromosome ends to counteract shortening and allow indefinite cell division.
3) Telomerase activation allows cancer cells to avoid replicative senescence and become immortalized, while preceding telomere shortening provides a mechanism for genetic instability and tumor progression.
Telomerase Activation: The Key to Unlocking the Aging Puzzle
The presentation discusses telomeres and telomerase, and their role in cellular aging and longevity. It notes that telomeres protect chromosome ends and shorten with each cell division, acting as a biological clock for aging. Telomerase is an enzyme that can rebuild telomere length, counteracting their shortening. Studies show telomerase activation can rejuvenate cells and tissues in mice, reducing biomarkers of aging without increasing cancer risk. Preliminary human studies suggest telomerase activation may provide benefits like improved immunity and bone density. The presentation promotes further research on telomerase activation as a way to potentially treat aging and age-related diseases
Different researches shows that, g-quadruplex- kind of tandem repeats are present in vivo,
Telomeres having tandem repeats of d(TTAGGG) , herein G is either anti or sync.
5’- UTR (untranslated region) of mRNA (U–U–U–U tetrads, as well as G- and U-containing octads)
Promoter region of c-myc , c-kit and variant bcl-2 oncogenes.
inferior oncogenic expression & veiled binding target of telomere associated proteins ( TRF1, POT1) may help to combat the uncontrolled cellular growth by inducing apoptosis & inhibit the telomerase overactivity.
The presentation discusses telomeres and telomerase in the context of cancer. It begins by defining telomeres as repetitive DNA sequences that cap the ends of chromosomes and shorten each time a cell divides. Telomerase is an enzyme that adds telomeric repeats and prevents shortening. In cancer cells, telomerase remains active and prevents telomere shortening, allowing unlimited cell division. Measuring telomerase may help detect and treat cancer by inducing senescence, though blocking it could also impair normal cell functions. The conclusion is that while inhibiting telomerase shows promise against cancer, more research is needed to minimize side effects.
Telomerase Inhibition as Novel Cancer Therapeutic MethodVincensanicko
Telomere in cancerous cells is conserved even after several rounds of cell division. By identifying the responsible protein in this process, i.e. telomerase, researchers have utilised it as a novel target for cancer treatment. So, how is the telomerase targetted? Are you ready to discover the truth?
Telomeres and the telomerase enzyme play important roles in cellular aging and cancer development. In cancer cells, telomerase is abnormally overexpressed, allowing cells to overcome the Hayflick limit and become immortal. The telomerase enzyme maintains telomere length through its reverse transcriptase activity, using an RNA component as a template. Several approaches are being explored to develop telomerase inhibitors as anti-cancer drugs, including targeting the enzyme's components or using them together with conventional chemotherapy to increase treatment effectiveness against various cancer types. By inhibiting telomerase, cells would be unable to maintain telomere length and would eventually senesce or die.
Telomeres are repetitive nucleotide sequences at the end of chromosomes that protect them from deterioration. Telomerase is an enzyme that adds telomere repeats and maintains telomere length. As cells divide, telomeres shorten due to the end replication problem. This eventual telomere shortening leads to cell senescence and aging. Diseases such as cancer, cardiovascular disease, and various progerias are associated with abnormal telomere shortening or maintenance by telomerase. Understanding telomeres and telomerase may help treat aging and age-related diseases.
Telomerase its role in aging and cancerHimadri Nath
Telomeres are repetitive DNA sequences at the ends of chromosomes that protect chromosomal DNA from degradation. Telomerase is an enzyme that adds telomere repeats to the ends of chromosomes to overcome replication-induced shortening. In normal cells, telomerase is inactive and telomeres shorten with each cell division, eventually leading to senescence. Cancer cells maintain telomere length through telomerase reactivation, allowing unlimited proliferation. Studies found telomerase expressed in 90% of human tumors but not normal tissues, supporting its role in immortality.
Telomeres are repetitive DNA sequences at the ends of chromosomes that protect cellular DNA from degradation. Telomere shortening is linked to cellular aging and is thought to be a root cause of age-related diseases. Telomerase is an enzyme that adds telomere repeats to chromosome ends and counteracts telomere shortening during cell division. Studies have shown that activating telomerase can prolong cellular lifespan, rejuvenate cells, and delay age-related changes in animals. Preliminary studies in humans using TA-65, a molecule that activates telomerase, have shown benefits such as reduced levels of senescent immune cells and lengthened short telomeres without safety issues.
Dr Una L Fairbrother
Telomere length: a 21st century biomarker" discusses DNA structure and the nature of telomeres. This talk explains the importance of telomere length and the impact of this feature on human health. The talk finishes describing the exciting work being carried out in London Metropolitan University to help develop this measure as a 21st century biomarker.
It describes about Structure and function of telomere, Telomerase enzyme, How does telomerase works?, Telomere replication, What happens to telomeres as we age?, Factors contribute to telomere shortening
Dr. Al Sears explains the Nobel Prize winning breakthrough telomere technology. This opened the way for Harvard researcher, Dr. Ronal DePinho to find a way to activate telomerase. Telomerase is the enzyme that signals your telomeres to grow longer, unfortunately, it shuts down while you are still in your mother's womb.
Once Nobel Prize winning research identified that telomeres are the protective tips at each end of the strands of your DNA, and as your cells replicate, gradully your telomeres grow shorter. They are the "aging-clocks" inside your DNA.
Once Dr. DePinho found a way to reactivate the telomerase enzyme, he turned old mice into young mice again.
Not long after, scientists discovered ways to do this in humans as well, and today, the discovery of the telomere and telomerase are the most important anti-aging breakthrough of our time.
Telomeres are protective caps on the ends of chromosomes that shorten with each cell division. When telomeres become too short, cells enter a permanent non-dividing state called replicative senescence. Telomerase is an enzyme that adds DNA repeats to telomeres to counteract their shortening. Telomerase is active in stem cells and early development but inactive in most adult tissues, leading to age-related telomere shortening. Shorter telomere length is associated with increased risk of aging, disease, and mortality. Lifestyle factors like exercise, stress reduction, and antioxidants may help slow telomere shortening. A small molecule called TA-65 was found to activate telomerase
Telomere, Functions & Role in Aging & CancerZohaib HUSSAIN
Telomeres cap the ends of chromosomes and protect them from degradation during cell division. As cells divide, telomeres shorten due to the inability of DNA replication enzymes to fully copy chromosome ends. This limits a cell to around 50-70 divisions before entering senescence. Cancer cells activate telomerase to maintain telomere length, allowing unlimited division. Telomeres play a key role in both aging and cancer - their shortening limits the lifespan of normal cells but cancer cells overcome this via telomerase to achieve immortality and uncontrolled growth. Measuring and targeting telomerase may provide new strategies for cancer detection and treatment.
Telomeres are repetitive DNA sequences at the ends of chromosomes that protect them from deterioration. Each time a cell divides, the telomeres shorten due to an inability to fully replicate chromosome ends. When telomeres become too short, the cell can no longer divide and becomes senescent or dies, contributing to aging. A recent study found that people who drank sugar-sweetened soda daily had shorter telomeres, equivalent to faster aging of around 2.9 years. Maintaining longer telomeres through diet and lifestyle factors like exercise may help slow the aging process.
The document summarizes a webinar presentation about telomere shortening and its relationship to human disease and cancer. The presentation discusses how telomeres shorten with cell division, potentially leading to diseases like dyskeratosis congenita and acquired aplastic anemia. It shows that some patients with acquired aplastic anemia have mutations in the telomerase gene TERT that cause shorter telomeres, increased chromosomal instability, and worse outcomes. Telomere length may be a predictor of relapse and survival in aplastic anemia patients.
Telomeres are repeating DNA sequences at the tip of chromosomes that protect chromosome ends from deterioration or fusion with neighboring chromosomes. They are composed of double-stranded DNA with single-stranded overhangs and their functions include capping chromosome ends, controlling cell division, and potentially holding secrets to aging and cancer development. The length of telomeres is the most accurate indicator of a person's aging rate, though it remains unclear if shorter telomeres cause or just indicate the aging process.
This presentation describes the structure and function of telomeres ,their role in various disease.The structure and function of telomerase is also described ,together with its possible role in therapy .
Telomeres are protective structures at the end of chromosomes that shorten each time a cell divides. Telomerase is an enzyme that adds DNA bases to telomeres and maintains their length. In cancer cells, telomerase is often overexpressed, allowing cells to proliferate indefinitely by preventing telomere shortening. Maintaining telomere length through telomerase activity is key to cellular immortality and unchecked growth, making telomerase a potential target for anti-cancer therapies.
Learning and understanding the correlation between telomere shortening and disease is the most important principal to stop the aging process. Dr Sears is one of the worlds most respected and renown Anti-Aging physicians in the world. Please visit our website at www.alsearsmd.com or www.searwellnesscenter.com for tons of great free information.
TA-65 Telomerase Activator - Is it a key to unlocking the longevity puzzle?Ivan Joksimovic
TA-65 is a natural supplement without any active ingredients added. The only way to lengthen telomeres is through the activation of an enzyme called telomerase. Currently the only way to activate telomerase is to take TA-65 supplement. The telomerase-activating potency of TA-65 has been independently proven in rigorous tests by Geron and Sierra Sciences, two biotech companies specializing in telomere biology.
Telomeres are protective pieces of DNA material at the ends of chromosomes. Like the plastic tips on shoelaces, telomeres prevent chromosome ends from fraying and sticking to each other, which would damage genetic information to cause cancer, other diseases or premature ageing.
Evidence clearly shows that people with long telomeres age healthier and live longer.
Every time a cell divides, the telomeres get shorter. After they get too short, the cell no longer can divide and becomes inactive or dies. This process is related with aging and age related diseases.
Without telomeres, the protective caps at the chromosome - the part containing genes essential for life - would get shorter each time a cell divides. Cell division is needed so we can grow new skin, blood, bone and other cells when needed.
The only way to lengthen telomeres is through the activation of an enzyme called telomerase. Currently the only way to activate telomerase is to take TA-65 supplement.
Telomerase is natural enzyme that stabilizes telomere length by adding DNA repeats (TTAGGG) onto the telomeric ends of the chromosomes, thus compensating for the loss of telomeres when cell divide.
Buy TA-65 now for the best price!
http://www.ta65doctor.com/products-page/
www.ta65doctor.com
Majority of cancer lead by point mutation in p53 gene. which is also known as "guardian of genome". this mutation leads conversion of normal cell into cancerous cell.
Telomerase Inhibition as Novel Cancer Therapeutic MethodVincensanicko
Telomere in cancerous cells is conserved even after several rounds of cell division. By identifying the responsible protein in this process, i.e. telomerase, researchers have utilised it as a novel target for cancer treatment. So, how is the telomerase targetted? Are you ready to discover the truth?
Telomeres and the telomerase enzyme play important roles in cellular aging and cancer development. In cancer cells, telomerase is abnormally overexpressed, allowing cells to overcome the Hayflick limit and become immortal. The telomerase enzyme maintains telomere length through its reverse transcriptase activity, using an RNA component as a template. Several approaches are being explored to develop telomerase inhibitors as anti-cancer drugs, including targeting the enzyme's components or using them together with conventional chemotherapy to increase treatment effectiveness against various cancer types. By inhibiting telomerase, cells would be unable to maintain telomere length and would eventually senesce or die.
Telomeres are repetitive nucleotide sequences at the end of chromosomes that protect them from deterioration. Telomerase is an enzyme that adds telomere repeats and maintains telomere length. As cells divide, telomeres shorten due to the end replication problem. This eventual telomere shortening leads to cell senescence and aging. Diseases such as cancer, cardiovascular disease, and various progerias are associated with abnormal telomere shortening or maintenance by telomerase. Understanding telomeres and telomerase may help treat aging and age-related diseases.
Telomerase its role in aging and cancerHimadri Nath
Telomeres are repetitive DNA sequences at the ends of chromosomes that protect chromosomal DNA from degradation. Telomerase is an enzyme that adds telomere repeats to the ends of chromosomes to overcome replication-induced shortening. In normal cells, telomerase is inactive and telomeres shorten with each cell division, eventually leading to senescence. Cancer cells maintain telomere length through telomerase reactivation, allowing unlimited proliferation. Studies found telomerase expressed in 90% of human tumors but not normal tissues, supporting its role in immortality.
Telomeres are repetitive DNA sequences at the ends of chromosomes that protect cellular DNA from degradation. Telomere shortening is linked to cellular aging and is thought to be a root cause of age-related diseases. Telomerase is an enzyme that adds telomere repeats to chromosome ends and counteracts telomere shortening during cell division. Studies have shown that activating telomerase can prolong cellular lifespan, rejuvenate cells, and delay age-related changes in animals. Preliminary studies in humans using TA-65, a molecule that activates telomerase, have shown benefits such as reduced levels of senescent immune cells and lengthened short telomeres without safety issues.
Dr Una L Fairbrother
Telomere length: a 21st century biomarker" discusses DNA structure and the nature of telomeres. This talk explains the importance of telomere length and the impact of this feature on human health. The talk finishes describing the exciting work being carried out in London Metropolitan University to help develop this measure as a 21st century biomarker.
It describes about Structure and function of telomere, Telomerase enzyme, How does telomerase works?, Telomere replication, What happens to telomeres as we age?, Factors contribute to telomere shortening
Dr. Al Sears explains the Nobel Prize winning breakthrough telomere technology. This opened the way for Harvard researcher, Dr. Ronal DePinho to find a way to activate telomerase. Telomerase is the enzyme that signals your telomeres to grow longer, unfortunately, it shuts down while you are still in your mother's womb.
Once Nobel Prize winning research identified that telomeres are the protective tips at each end of the strands of your DNA, and as your cells replicate, gradully your telomeres grow shorter. They are the "aging-clocks" inside your DNA.
Once Dr. DePinho found a way to reactivate the telomerase enzyme, he turned old mice into young mice again.
Not long after, scientists discovered ways to do this in humans as well, and today, the discovery of the telomere and telomerase are the most important anti-aging breakthrough of our time.
Telomeres are protective caps on the ends of chromosomes that shorten with each cell division. When telomeres become too short, cells enter a permanent non-dividing state called replicative senescence. Telomerase is an enzyme that adds DNA repeats to telomeres to counteract their shortening. Telomerase is active in stem cells and early development but inactive in most adult tissues, leading to age-related telomere shortening. Shorter telomere length is associated with increased risk of aging, disease, and mortality. Lifestyle factors like exercise, stress reduction, and antioxidants may help slow telomere shortening. A small molecule called TA-65 was found to activate telomerase
Telomere, Functions & Role in Aging & CancerZohaib HUSSAIN
Telomeres cap the ends of chromosomes and protect them from degradation during cell division. As cells divide, telomeres shorten due to the inability of DNA replication enzymes to fully copy chromosome ends. This limits a cell to around 50-70 divisions before entering senescence. Cancer cells activate telomerase to maintain telomere length, allowing unlimited division. Telomeres play a key role in both aging and cancer - their shortening limits the lifespan of normal cells but cancer cells overcome this via telomerase to achieve immortality and uncontrolled growth. Measuring and targeting telomerase may provide new strategies for cancer detection and treatment.
Telomeres are repetitive DNA sequences at the ends of chromosomes that protect them from deterioration. Each time a cell divides, the telomeres shorten due to an inability to fully replicate chromosome ends. When telomeres become too short, the cell can no longer divide and becomes senescent or dies, contributing to aging. A recent study found that people who drank sugar-sweetened soda daily had shorter telomeres, equivalent to faster aging of around 2.9 years. Maintaining longer telomeres through diet and lifestyle factors like exercise may help slow the aging process.
The document summarizes a webinar presentation about telomere shortening and its relationship to human disease and cancer. The presentation discusses how telomeres shorten with cell division, potentially leading to diseases like dyskeratosis congenita and acquired aplastic anemia. It shows that some patients with acquired aplastic anemia have mutations in the telomerase gene TERT that cause shorter telomeres, increased chromosomal instability, and worse outcomes. Telomere length may be a predictor of relapse and survival in aplastic anemia patients.
Telomeres are repeating DNA sequences at the tip of chromosomes that protect chromosome ends from deterioration or fusion with neighboring chromosomes. They are composed of double-stranded DNA with single-stranded overhangs and their functions include capping chromosome ends, controlling cell division, and potentially holding secrets to aging and cancer development. The length of telomeres is the most accurate indicator of a person's aging rate, though it remains unclear if shorter telomeres cause or just indicate the aging process.
This presentation describes the structure and function of telomeres ,their role in various disease.The structure and function of telomerase is also described ,together with its possible role in therapy .
Telomeres are protective structures at the end of chromosomes that shorten each time a cell divides. Telomerase is an enzyme that adds DNA bases to telomeres and maintains their length. In cancer cells, telomerase is often overexpressed, allowing cells to proliferate indefinitely by preventing telomere shortening. Maintaining telomere length through telomerase activity is key to cellular immortality and unchecked growth, making telomerase a potential target for anti-cancer therapies.
Learning and understanding the correlation between telomere shortening and disease is the most important principal to stop the aging process. Dr Sears is one of the worlds most respected and renown Anti-Aging physicians in the world. Please visit our website at www.alsearsmd.com or www.searwellnesscenter.com for tons of great free information.
TA-65 Telomerase Activator - Is it a key to unlocking the longevity puzzle?Ivan Joksimovic
TA-65 is a natural supplement without any active ingredients added. The only way to lengthen telomeres is through the activation of an enzyme called telomerase. Currently the only way to activate telomerase is to take TA-65 supplement. The telomerase-activating potency of TA-65 has been independently proven in rigorous tests by Geron and Sierra Sciences, two biotech companies specializing in telomere biology.
Telomeres are protective pieces of DNA material at the ends of chromosomes. Like the plastic tips on shoelaces, telomeres prevent chromosome ends from fraying and sticking to each other, which would damage genetic information to cause cancer, other diseases or premature ageing.
Evidence clearly shows that people with long telomeres age healthier and live longer.
Every time a cell divides, the telomeres get shorter. After they get too short, the cell no longer can divide and becomes inactive or dies. This process is related with aging and age related diseases.
Without telomeres, the protective caps at the chromosome - the part containing genes essential for life - would get shorter each time a cell divides. Cell division is needed so we can grow new skin, blood, bone and other cells when needed.
The only way to lengthen telomeres is through the activation of an enzyme called telomerase. Currently the only way to activate telomerase is to take TA-65 supplement.
Telomerase is natural enzyme that stabilizes telomere length by adding DNA repeats (TTAGGG) onto the telomeric ends of the chromosomes, thus compensating for the loss of telomeres when cell divide.
Buy TA-65 now for the best price!
http://www.ta65doctor.com/products-page/
www.ta65doctor.com
Majority of cancer lead by point mutation in p53 gene. which is also known as "guardian of genome". this mutation leads conversion of normal cell into cancerous cell.
The document discusses the tumor suppressor protein p53, known as "the guardian of the genome". It describes p53's history of identification in 1979 and role in regulating cell growth and proliferation. P53 prevents unrestrained cell division after DNA damage by initiating growth arrest, DNA repair, or apoptosis. The document outlines p53's structure and domains, and mechanism of action in normal cells where it is kept at low levels through degradation by Mdm2. When DNA is damaged, p53 is stabilized and can activate repair proteins, growth arrest, or apoptosis if damage cannot be repaired. The role and significance of p53 in cancer treatment, potential therapeutic uses, and future trends are also summarized.
Molecular biology of oral cancer
The document discusses the molecular basis of oral cancer through three main points:
1) It describes common genetic alterations in oral cancer such as overexpression of oncogenes like EGFR and mutations in tumor suppressor genes like p53.
2) It explains how alterations in proto-oncogenes and oncogenes lead to uncontrolled cell growth and proliferation through signaling pathways and transcription factors.
3) It discusses how defects in DNA repair genes can cause genomic instability, a hallmark of cancer, through increased mutations that evade cell cycle checkpoints and apoptosis.
1. Tumor markers are substances produced by cancer cells or the body's response to cancer that can be detected and measured in blood, urine, or tissue samples.
2. Common tumor markers include CEA, AFP, CA19-9, CA125, PSA, and HER2/neu. They are used to help diagnose cancer, determine prognosis, guide treatment decisions, and monitor response to treatment.
3. However, tumor marker levels can also be elevated in non-cancerous conditions, so they are not definitive cancer diagnoses on their own and must be interpreted along with other clinical information.
This document discusses Dave McClure's investment thesis and experience in venture capital. It provides an overview of 500 Startups, including its history, strategy of making many small investments, and how it invests through its accelerator program and seed/follow-on funding. Details are given around 500's investment criteria, portfolio diversification approach, and generating deal flow through its brand and network.
Telomeres are protective structures at the end of chromosomes that shorten each time a cell divides. This eventual shortening leads to cellular senescence or death. Telomerase is an enzyme that adds DNA bases to telomeres and maintains their length, allowing cells to avoid senescence and continue dividing. In cancer cells, telomerase is often reactivated, allowing tumors to grow indefinitely by preventing telomere shortening. Maintaining telomere length through telomerase is important for cellular immortality and is a hallmark of cancer.
1) Telomeres are nucleoprotein structures at the ends of chromosomes that protect them from degradation. Telomerase is an enzyme that elongates telomeres by adding DNA repeats.
2) Telomerase activity is observed in over 80% of cancers and helps cancer cells proliferate indefinitely by maintaining telomere length.
3) In normal cells, telomeres shorten with each cell division due to the end-replication problem until cells enter senescence. Rare cells can reactivate telomerase to immortalize.
Telomeres are repetitive DNA sequences at the ends of chromosomes that protect them from deterioration during cell division. Telomeres shorten each time a cell divides, acting as a biological clock. When telomeres become too short, cells can no longer divide and become senescent. Telomerase is an enzyme that adds telomeric repeats to chromosome ends, counteracting shortening and allowing cells to avoid senescence. Cancer cells express high levels of telomerase, allowing them to divide indefinitely. Drugs are being developed to inhibit telomerase as a cancer treatment, though they can also damage telomeres in normal cells. Future research aims to specifically target the telomerase expression in cancer cells.
Telomeres are repetitive DNA sequences located at the ends of chromosomes that protect genetic material during cell division. As cells divide, telomeres slowly shorten due to the inability of DNA replication to fully copy chromosome ends. Eventually telomeres become so short that cells can no longer divide, leading to cellular aging. In most human cells, the enzyme telomerase is turned off, contributing to telomere shortening with each cell division. However, telomerase is active in approximately 90% of cancer cells, allowing them to divide indefinitely and overcome the natural limits of cellular replication. Telomere shortening may promote cancer by causing chromosome instability when telomeres become dysfunctional. Maintaining telomere length through telomerase
Telomeres are repetitive DNA sequences at the ends of chromosomes that prevent shortening as cells divide. Their length declines with age, potentially contributing to aging. Telomerase is an enzyme that adds telomere sequences, counteracting shortening. Studies link both short telomeres and high telomerase to cancer by affecting cell division limits. Researchers are exploring using telomerase to potentially prevent aging, but it may also promote immortality in cancer cells, so more study is needed to safely apply these findings.
BTE101 assignment--Telomere and telomeraseSamiya Yesmin
This document discusses telomeres and telomerase. It begins by explaining that telomeres are repetitive DNA sequences at the ends of chromosomes that protect them from deterioration. Telomerase is an enzyme that adds DNA repeats to the ends of chromosomes to replace sequences lost during cell division, thereby preventing shortening of chromosomes over time. The document then covers how telomerase works, the role of telomeres and aging, and potential anti-aging applications of telomerase research and supplements. It concludes by stating that while aging processes are still being researched, telomerase holds promise for slowing cellular aging and potentially extending lifespan.
In this way, you can take care of your health and learn more about telomeres. Consider telomere testing and talk to medical experts who focus on telomere research. By working together, we can unlock the mysteries of aging and create a world where healthy longevity is the norm.
Telomeres are repetitive DNA sequences at the ends of chromosomes that protect chromosomal integrity. Each cell division causes telomeres to shorten as DNA replication cannot fully copy chromosome ends. When telomeres become too short, cells stop dividing or die. Telomerase is an enzyme that adds telomeric DNA to chromosome ends and counteracts shortening. While most somatic cells lack telomerase, its presence allows cancer cells and germ cells to avoid replicative aging. Maintaining telomere length through telomerase overexpression is a hallmark of cancer cells and targeting this process may lead to new anticancer therapies.
Telomere maintenance as a target for drug discoveryDavid Wallace
This document discusses targeting telomere maintenance as an approach for cancer drug discovery. It notes that telomerase, the enzyme responsible for telomere maintenance, is upregulated in 80-90% of cancer cells but absent in healthy cells, making it an attractive drug target. Efforts to target telomerase include inhibiting its enzymatic function, using immunotherapy targeting its catalytic subunit hTERT, and using hTERT promoters to drive gene therapy. Telomeres themselves have also been targeted. The document reviews different strategies for targeting telomere maintenance and telomerase in cancer cells.
Telomeres Relation with Cell Division and Aging.pptNABIHANAEEM2
Telomeres are repetitive DNA sequences at the ends of chromosomes that protect them from deterioration. Each time a cell divides, the telomeres shorten due to an inherent problem with DNA replication. When telomeres reach a critically short length, the cell can no longer divide and becomes senescent. Telomerase is an enzyme that can add DNA sequences back to telomeres, compensating for their shortening and allowing cells to avoid senescence. Telomerase activity allows stem cells and cancer cells to avoid senescence through repeated cell division by maintaining telomere length.
Aging and the telomere connection dr. Jerry w. Shay - april 2012Life Length
1. Telomeres are repetitive DNA sequences at the ends of chromosomes that protect chromosomal DNA from deterioration. Each cell division, telomeres shorten until they reach a critical length that causes cells to stop dividing.
2. Short telomere length is associated with aging and age-related diseases by limiting tissue regeneration abilities. Telomere length measurements provide insight into overall health and longevity.
3. Environmental stressors like smoking can accelerate telomere shortening, while behaviors like exercise may help slow the rate of shortening. Quantitative telomere tests are being developed to monitor health and the effects of therapies on telomere biology.
The document discusses telomeres and telomere-binding proteins. It begins by introducing telomeres as the protective ends of chromosomes, and the shelterin protein complex that binds telomeres. It then describes telomerase, the enzyme that elongates telomeres. The objective is to discuss the roles of telomeric proteins in cancer and aging by regulating telomere length, protection, and gene expression. Key points covered include how telomerase and shelterin influence telomere function, the mechanisms by which telomere dysfunction can cause genomic instability and cancer, and potential applications of targeting telomerase for cancer treatment.
Dr. Elizabeth Blackburn gives a lecture on telomeres and telomerase, and their implications for aging and age-related diseases. She explains that telomeres are repetitive DNA sequences that cap the ends of chromosomes and protect genetic material. Telomerase is an enzyme that adds telomere sequences to chromosomes to maintain their length during cell division. Studies show genetics play a role in longevity, and stress and caregiving can impact telomere length by reducing telomerase activity and increasing oxidative stress. Shorter telomeres are associated with increased mortality and disease susceptibility.
Telomeres are repetitive nucleotide sequences located at the ends of chromosomes that protect them from deterioration. They consist of the sequence TTAGGG repeated hundreds to thousands of times. Each time a cell divides, the telomeres shorten due to an inability to fully replicate chromosome ends. This represents a biological clock for cell division. Telomerase is an enzyme that adds telomere sequences and prevents shortening, allowing cells to avoid replicative senescence or death. In cancer cells, telomerase is often reactivated, allowing unlimited cell division by maintaining telomere length. Telomeres play a key role in cellular aging and are also implicated in many diseases.
What is the consequence when a chromosome loses its telomeresSol.pdfarchiesgallery
Loss of telomeres on chromosomes can have significant consequences. Telomeres normally protect the ends of chromosomes and prevent them from fusing. Without telomeres, chromosomes will fuse with each other, leading to aneuploidy and cell death. Rare cells may survive if they regain the ability to maintain telomere length through telomerase or recombination. Spontaneous telomere loss can also initiate breakage-fusion-bridge cycles that result in DNA mutations like amplifications and translocations on the affected chromosome. These telomere acquisitions through translocation or duplication can stabilize the chromosome but also threaten genome stability overall. Loss of a telomere from a donor chromosome during these cycles can further cause
The connection between Telomeres and Aging-Dr. Patana teng-umnuayLife Length
Telomeres are protective caps on the ends of chromosomes that play an important role in the aging process. As cells divide and replicate over time, telomeres gradually shorten until they reach a length where the cells can no longer divide properly. This contributes to aging at both the cellular and organismal levels and is linked to increased risk for age-related diseases like cancer, cardiovascular disease, and diabetes. Lifestyle factors like stress, poor nutrition, smoking, and lack of exercise can accelerate telomere shortening, while a healthy lifestyle and certain supplements may help slow this process. Measuring telomere length provides insights into biological aging and can help identify individuals at higher risk for developing age-related diseases at an earlier stage
The document discusses telomere-binding proteins in humans. It describes the Shelterin complex, which comprises six subunits (TRF1, TRF2, TIN2, POT1, TPP1, RAP1) that provide protection to chromosome ends. It also discusses the telomerase complex, which contains TERT and TR components and maintains telomere length. The CST complex plays a role in telomere protection and DNA metabolism. Diseases caused by impaired telomere maintenance are called "telomeropathies". Certain cancers have shown links to telomere-binding proteins like increased TERF2 expression in skin tumors and oral cancers.
Telomere is the end part of a chromosome.its length is maintained by na enzyme called telomerase.if telomerase is lacking,many genetic diseases may result( like progeria)
1. 2013 ASEE Northeast Section Conference Norwich University
Reviewed Paper March 14-16, 2013
A TALE OF LOBSTERS :
TELOMERE AND TELOMERASE
Nmereole Chibueze1
, Christian Bach2
Abstract – Lobsters don't appear to age. How can we be more like lobsters. Immortality can be
decoded by understanding telomere and telomerase clinically and biologically. In this paper, we
will review the current knowledge of telomere and telomerase and their influence on cellular
senescence, cell proliferation, cancer therapy, tumor and laying emphasis on human aging.
Preventing our telomeres from shorting will prevent us from disease and increase our life span.
Deactivation of the enzyme telomerase in tumor and cancerous cells will be an alternative to
chemotherapy or treatment for cancer and tumor cells.
Keywords: telomere, telomerase, aging, cancer, tumor.
INTRODUCTION
The tip of a eukaryotic chromosome has a special structure called the telomere. They are
Repetitive DNA sequences at the ends of all human chromosomes. They consist of repeats of the
DNA sequence TTAGGG and some proteins [1] They protects the chromosomes from
enzymatic end degradation and keeps their stability [2] . They achieve this by effectively
"capping" the end of a chromosome in a manner similar to the way the plastic on the ends of our
shoelaces "caps" and protects the shoelaces from unraveling. Without telomeres, the ends of the
chromosomes would be "repaired", leading to chromosome fusion and massive genomic
instability. Telomeres not only give stabilization and protection of the chromosome, their
structure allows the tip of linear DNA to be replicated completely, thus, Telomeres are also
thought to be the "clock" that regulates how many times an individual cell can divide. Telomeric
sequences shorten each time the DNA replicates. When the replication of linear chromosome is
taking place, the DNA polymerase will replicate DNA termini in 5’ to 3’ direction using an RNA
primer for the initiation. The RNA primer is removed after the DNA has replicated, then the
telomeric DNA sequence is lost from the ends [2]. Telomere length varies within species. In
humans the length of the telomere is 8- 14 kilobasepairs and in mice they have as much as 150
kilobasepairs [1]. The mechanism of DNA replication differs for the leading and the lagging
DNA Strand. The leading strand replicates continually and for the lagging strand to replicate,
DNA polymerization have to start with several RNA primers which elongates to produce a DNA
fragment called Okazaki fragments. The RNA sequence will later be degraded and replaced by
DNA sequence.
1
University of Bridgeport, 113 Austin St, Bridgeport, CT. 06604, cnmereol@bridgeport.edu
2
University of Bridgeport, 221 University Ave., Bridgeport, CT. 06604 cbach@bridgeport.edu
2. 2013 ASEE Northeast Section Conference Norwich University
Reviewed Paper March 14-16, 2013
TELOMERASE
Telomerase is a ribonucleoproteic enzymatic complex and it catalyzes the addition of telomeric
repeats to the tip of chromosomes DNA [3]. This makes them to prevent the loss of telomeric
sequence that occur normally at each cell division. Whenever there is telomerase activity, there is
stabilization of the chromosome length, replication of the cell is not limited and cells are
immortal. Telomerase is an enzyme needed for continuous growth of the cell [4]. It is inactivated
in most of the somatic cells except for cells that reproduce rapidly (Proliferating cells) and
telomerase is activated in 85% of the human cancer tissues. Its activity is needed as a cancer
detecting marker in some of the cancers. It is also a useful Prognostic detector in cancel cells in
which it has become unregulated from the progression of tumor. Telomerase activity at the
telomere is also regulated at the level of telomerase recruitment to the telomere [5]. But the
mechanism in which it recruits telomere is not fully known, but is likely a part of negative feed
back loop caused by shelterin proteins that bound at the telomere as act as negative regulators of
telomerase extension of telomere. Inhibition of telomerase has the features to be used as a
selective anti can therapy that stops the multiplication capacity of telomerase positive cancer
cells.
CELL PROLIFERATION
Proliferation competent somatic cell don't show any noticeable telomerase activity in them and
their telomere shorten with each cell division [6] In cancer and stem cells of renewal tissues,
telomerase activity levels correspond with the rapid reproduction state of the cells. The presence
of this telomerase enzyme is needed for unlimited proliferation (immortality) and it's absence
leads to a finite life span (senescence).
CELLULAR SENESCENCE
Olovnikov in 1971 proposed that the loss of telomeric DNA through the end replication process
could serve as the mitotic clock, and this induces senescence once a shortening to a certain value
has reached [7]. He states that telomere shorten as somatic cells divides. This was supported by
the measurement of telomeres in different cell types which was done indirectly. We cannot
measure telomere directly in most organism including humans because their telomeric repeats
and subtelomeric DNA don't have a recognition site for any known restriction enzyme. When
telomeres get damaged and fail to function, it leads to DNA damage. This DNA damage is
characterized by the binding of DNA damage response proteins to the uncapped telomere [8].
Considering the cell type, genetic information and level of the telomeric damage, the cell can
enter permanent cell cycle arrest which is senescence. These cellular responses may have
important effects on the organism, especially for complex eukaryotic organism that have both
mitotic and post mitotic cells. The most important effect of the telomere dysfunction is
carcinogenesis which comes from mitotic cells.
HUMAN AGING
3. 2013 ASEE Northeast Section Conference Norwich University
Reviewed Paper March 14-16, 2013
Shortening of the telomere is followed by human aging and there is also some premature aging
diseases that is associated with short telomere. From this you can note that telomere length
directly influences longevity [9]. No other Chromosome has been linked to major human health
issues expect telomere and this has to do with their length. Telomere length is now taking to be
the reference point for anyone discussing the impact of any factor into human fitness. Short
telomeres has been said to be associated with aging, high risk of premature death and
development of vascular and colon disease. For us to decide if shorten of telomere is really the
cause of many vascular disease that is linked to aging or short life span is not an easy thing to do.
The presence of short telomere starts cell senescence in vivo, and this affects organ and tissue
function. Senescence can be caused by other factors and not only telomere shortening, it marks a
need to for us to study more on this. A recent study with baboons shows that the first time their
telomere is being seen as damaged, it increases with age in the skin whereby this increase is not
present in muscle cells. This supports the notion that telomere shortening is highly responsible
for cell senescence in organs with high proliferative potential. This is also seen in aged humans.
It has been seen that telomere length is an indication of biological aging [2]. The incomplete
replication of linear chromosomes by DNA polymerase, telomeric repeats at the end are lost each
time there is a cell division. This dysfunction of telomere is has associated itself with the
pathogenesis of many age related diseases. Telomere length can be changed by nutrition in
human and animals.
ANTI CANCER THERAPY
The telomeres of mortal cells shorten during each round of cell division, cancer cells don't and
they possess indefinite growth capacity and maintain their telomeres [10]. We see immortality
of these cells as an escape from senescence, deregulation of cell cycle and proliferation of the
cells. Telomerase has been suggested as an important target for the production of new anti cancer
drugs. Processes based on the reversal of tumor growth by telomerase inhibition. A therapeutic
anticancer approach is needed that will inhibit telomerase function will be able to deny unlimited
progeny [11]. Telomerase contain a catalytic protein unit, human telomerase reverse
transcriptase (hTERT) and the human telomerase RNA (hTR) and they provide the template for
the telomeric repeat sequence. Telomerase is found at the 3' telomere end and they add new
sequence by the release of DNA according to the RNA template. Using telomerase inhibition as
a cancer treatment has a limitation. It takes weeks for telomeres at the lag phase to shorten to a
critical value and start the cellular senescence. Telomerase inhibition is a new method of cancer
treatment and there are also several potential targets acting in either stabilization of the telomere
end protective structures or proteins involved in telomerase activity regulation. In the process of
carcinogenesis, there is activation of telomerase at different stages [12]. Sometimes, they are
activated gradually through out the progression of the cancer where in some other instances the
enzyme is expressed in precancerous stages and this affects the clinical utilization of telomerase
as a diagnostic marker. Most cells exhibit telomerase activity and this make it difficult to know if
the telomerase activity is coming from the tumor cells. To over come this, an in situ TRAP assay
that employs fluorescent dyes and microscopy to visualize telomerase activity in the nuclei of
cells being investigated is required to determine if the telomerase expression seen is gotten from
normal telomerase positive cells or malignant cells. Since telomerase activity is also detected in
premalignant tissue, it is important for physicians to noted that testing for telomerase activity is
4. 2013 ASEE Northeast Section Conference Norwich University
Reviewed Paper March 14-16, 2013
important for detection of cancer in high risk patients. hTR subunit is found in all cells and its
expression in cancer cells are high. hTERT expression correlates with telomerase activity since
its presence is needed for enzymatic activity. From this we can see that early detection of hTERT
mRNA is needed for the detection of cancer cells in clinical samples.
TUMOUR
Tumors require telomeric consistency to maintain viability conferred by adequate length of
telomeric DNA replenished by telomerase and binding of telomere binding proteins (TBPs) [13].
Levels of TBPs in tumor tissue might have effects for drug development if they make some
cancers more sensitive or resistant to telomere targeted agents. In contrast to somatic cells, 85 -
90% tumor cells have telomerase enzyme over expressed and activated. In some other tumors an
alternative recombination mechanism (ALT) maintains telomere length [14]. However the
maintenance of telomere length is important for the survival of tumor cells and any means of
stopping this process is an important new approach to the therapy [13].
CONCLUSION
Telomere and Telomerase are important in somatic cells. This review has helped us to
understand that telomere shortening are the most causes of aging and some other vascular
disease. When multiple cell divisions take places, the telomere is shorten to a critical length in
which it cannot divide again. At this time, senescence or apoptosis takes effect. Telomerase
activation leads to the integrity of telomeres and causes cell proliferation which is the hallmark
of carcinogenesis and tumorgenesis. Inhibition of telomerase enzyme in somatic cells will be the
hallmark for anti cancer therapy drugs. Changing our lifestyle by eating right, and exercising will
help in maintaining a healthy telomere length, there reducing the shorting of telomere length and
making human somatic cells immortal and increasing long life span.
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Nmereole Chibueze
Chibueze graduated from Abia State University, Uturu Abia State, Nigeria with a Bachelor's in
food science and technology in 2008. He is currently pursuing his Masters degree in Biomedical
Engineering at the University of Bridgeport. He is expected to graduate in December 2013.
Christian Bach
Christian Bach holds academic honors as: PhD in Information Science and executive MBA at the
University at Albany/SUNY. His multidiscipline research approach is aimed to integrate in
particular marketing research and information effectiveness.