1) Researchers discovered a new class of DNA regions called early replicating fragile sites (ERFSs) that are prone to damage during cell division.
2) ERFSs overlap significantly with DNA alterations found in B cell lymphoma, suggesting they contribute to mutations in this cancer.
3) Understanding how these fragile sites lead to DNA breaks could enable better treatments for cancers like B cell lymphoma.
The document discusses two recent discoveries that could improve cancer treatment: 1) the discovery of a protein called XPD that acts as a scanner to recognize specific damaged locations in DNA sequences and help repair them, and 2) the identification of early replicating fragile sites (ERFSs) in DNA that are particularly vulnerable to damage and associated with a type of blood cancer. These findings provide new tools for understanding DNA damage and vulnerabilities that can be exploited to develop better targeted cancer therapies.
This document discusses two recent discoveries that could lead to improved cancer treatments: 1) the discovery of a protein called XPD that acts as a "scanner" to recognize and mark locations of damaged DNA, and 2) the identification of early replicating fragile sites (ERFSs) in DNA that are particularly vulnerable to damage and associated with a type of blood cancer. These findings provide new insights into DNA vulnerability and damage recognition that may help enhance cancer therapies by directly manipulating DNA to make it more resistant to damage and tumors.
July’s SHOW will focus on the genetic pathways that drive the development of cancer. Specifically, we will look at melanoma, an aggressive form of skin cancer, which has been on the rise of late. Though making up only five percent of skin cancers cases, melanoma is responsible for a large number of the deaths associates with skin cancers, having a particularly poor prognosis when diagnosed in its later stages. Our special guest speaker, Dr. Craig J. Ceol has been working to identify the genetic defects responsible for the growth of tumors, specifically malignant melanoma.
1) Cancer arises from DNA damage in fragile sites in the genome like repetitive sequences that occur during DNA replication.
2) Early replicating fragile sites that are AID-independent contribute to DNA breaks and alterations in B cells lymphoma.
3) Discovering new classes of damage-prone DNA regions could help scientists develop improved cancer treatments by better understanding how DNA replication errors lead to cancer and resistance to chemotherapy.
Cancer arises from DNA damage in fragile sites in the genome like repetitive sequences. B cells have a higher risk of DNA damage because they divide rapidly. Early replicating fragile sites are also associated with DNA breaks in B cells and are a principal cause of alterations in B cell lymphomas. The discovery of these early replicating fragile sites could lead to better cancer treatments by helping scientists understand cancer mechanisms and failures in current treatments in order to develop new treatment methods.
The document discusses two recent discoveries: 1) Scientists elucidated the structure of SMC-kleisin proteins, which help hold chromosomes together by wrapping around DNA. This ensures orderly DNA packaging and transcription. 2) Researchers found that the XPD protein acts as a scanner to detect damaged DNA, which could lead to new cancer therapies by targeting recognition of genetic defects in different tissues. Overall, understanding how proteins interact with DNA has implications for processes like cell replication and may help explain genetic transmission from parents to children as well as approaches to improving cancer treatment.
This document discusses two research articles about DNA repair mechanisms. The first article finds that sister chromatid exchanges occur in cells irradiated during the G2 phase as a means of repairing DNA double strand breaks. The second article examines polymorphisms in the DNA repair genes XPD and XRCC1 and their association with age-related cataracts, finding females are at higher risk due to increased UV light exposure and certain gene variants. Understanding DNA repair is important for detecting diseases and potential treatments by manipulating cells. The document emphasizes continuing research on the DNA basis of life and disease prevention.
This document discusses two recent studies on DNA repair mechanisms and their implications for cancer research and treatment. The first study found a higher incidence of germline mutations in DNA repair genes in men with metastatic prostate cancer compared to localized disease, which could enable more personalized cancer therapies. The second study was able to film the enzymes involved in DNA repair, providing insights into the repair process that may help counter cancer's resistance to chemotherapy and develop new treatments. Both studies increase understanding of cancer at the molecular level and open doors to improved early detection and more targeted therapies.
The document discusses two recent discoveries that could improve cancer treatment: 1) the discovery of a protein called XPD that acts as a scanner to recognize specific damaged locations in DNA sequences and help repair them, and 2) the identification of early replicating fragile sites (ERFSs) in DNA that are particularly vulnerable to damage and associated with a type of blood cancer. These findings provide new tools for understanding DNA damage and vulnerabilities that can be exploited to develop better targeted cancer therapies.
This document discusses two recent discoveries that could lead to improved cancer treatments: 1) the discovery of a protein called XPD that acts as a "scanner" to recognize and mark locations of damaged DNA, and 2) the identification of early replicating fragile sites (ERFSs) in DNA that are particularly vulnerable to damage and associated with a type of blood cancer. These findings provide new insights into DNA vulnerability and damage recognition that may help enhance cancer therapies by directly manipulating DNA to make it more resistant to damage and tumors.
July’s SHOW will focus on the genetic pathways that drive the development of cancer. Specifically, we will look at melanoma, an aggressive form of skin cancer, which has been on the rise of late. Though making up only five percent of skin cancers cases, melanoma is responsible for a large number of the deaths associates with skin cancers, having a particularly poor prognosis when diagnosed in its later stages. Our special guest speaker, Dr. Craig J. Ceol has been working to identify the genetic defects responsible for the growth of tumors, specifically malignant melanoma.
1) Cancer arises from DNA damage in fragile sites in the genome like repetitive sequences that occur during DNA replication.
2) Early replicating fragile sites that are AID-independent contribute to DNA breaks and alterations in B cells lymphoma.
3) Discovering new classes of damage-prone DNA regions could help scientists develop improved cancer treatments by better understanding how DNA replication errors lead to cancer and resistance to chemotherapy.
Cancer arises from DNA damage in fragile sites in the genome like repetitive sequences. B cells have a higher risk of DNA damage because they divide rapidly. Early replicating fragile sites are also associated with DNA breaks in B cells and are a principal cause of alterations in B cell lymphomas. The discovery of these early replicating fragile sites could lead to better cancer treatments by helping scientists understand cancer mechanisms and failures in current treatments in order to develop new treatment methods.
The document discusses two recent discoveries: 1) Scientists elucidated the structure of SMC-kleisin proteins, which help hold chromosomes together by wrapping around DNA. This ensures orderly DNA packaging and transcription. 2) Researchers found that the XPD protein acts as a scanner to detect damaged DNA, which could lead to new cancer therapies by targeting recognition of genetic defects in different tissues. Overall, understanding how proteins interact with DNA has implications for processes like cell replication and may help explain genetic transmission from parents to children as well as approaches to improving cancer treatment.
This document discusses two research articles about DNA repair mechanisms. The first article finds that sister chromatid exchanges occur in cells irradiated during the G2 phase as a means of repairing DNA double strand breaks. The second article examines polymorphisms in the DNA repair genes XPD and XRCC1 and their association with age-related cataracts, finding females are at higher risk due to increased UV light exposure and certain gene variants. Understanding DNA repair is important for detecting diseases and potential treatments by manipulating cells. The document emphasizes continuing research on the DNA basis of life and disease prevention.
This document discusses two recent studies on DNA repair mechanisms and their implications for cancer research and treatment. The first study found a higher incidence of germline mutations in DNA repair genes in men with metastatic prostate cancer compared to localized disease, which could enable more personalized cancer therapies. The second study was able to film the enzymes involved in DNA repair, providing insights into the repair process that may help counter cancer's resistance to chemotherapy and develop new treatments. Both studies increase understanding of cancer at the molecular level and open doors to improved early detection and more targeted therapies.
Seminário Nacional do Benzeno (5 e 6 dez/12) - Derivação de Limites de Exposição Ocupacional para Substâncias Carcinogênicas e
Mutagênicas - Experiências Internacionais e Nacional
Secrets of parasites' replication unraveledcarito40
This document discusses various topics related to DNA replication and genetic diseases. It describes how origin of replication (ORI) proteins recognize the origin of replication site to initiate DNA duplication. It also discusses alternative treatments for diseases caused by parasites like Trypanosoma brucei that cause sleeping sickness. Finally, it mentions how understanding genetic causes of diseases like Meier-Gorlin syndrome could allow for preventative genetic therapies in the future.
The document summarizes key components of nucleic acids including phosphates, sugars, and nitrogenous bases. It also describes the primary, secondary, and tertiary structural levels of nucleic acids. Additionally, it discusses the discovery of a ring-shaped SMC-kleisin protein complex that ensures order in DNA packaging during cell division. Disruption of this complex can lead to disorders like cancer and genetic defects. The document also summarizes an article about the discovery of fragile sites in DNA that contribute to damage in B-cell lymphoma and how this finding could help develop new cancer treatments.
This document discusses lessons learned from building cancer models and realities around sharing, rewards, and affordability. It notes that oncogenes only make good targets in particular molecular contexts, as seen with the EGFR story. Predicting treatment response to known oncogenes is complex and requires detailed understanding of how different genetic backgrounds function. It also discusses preliminary probabilistic models being used to identify genes causal for disease. Extensive publications now substantiate the scientific approach of using probabilistic causal bionetwork models for diseases like metabolism, cardiovascular disease, and bone diseases. Sage Bionetworks is working to build an information commons for biological functions through collaborative disease maps and data repositories to better relate genetic features of cancer to drug efficacy and
1. Researchers have discovered a new four-stranded quadruple helix DNA structure called G-quadruplexes that exists in human genomes, particularly in regions rich in guanine. These quadruplexes are more common in rapidly dividing cells like cancer cells.
2. A separate study identified new sites in cells where DNA breaks early in the replication process. These break sites correlate with damage seen in cancers like diffuse large B cell lymphoma. Comparing mouse and human cells, both exhibit similar trends of genome instability at these sites.
3. Discoveries of DNA structures and break sites help understand the origins of diseases and cancer, offering new treatment approaches through stopping replication in cancer cells or addressing instability.
DNA repair mechanisms are indispensable for cell maintenance. The most common repair mechanisms are base excision repair (BER) and nucleotide excision repair (NER). Deficiencies in repair can lead to diseases like cancer or myelodysplastic syndrome. Studies have found that some viruses like murine polyomavirus activate DNA damage repair proteins like ATR and MRE11 to promote viral replication. Understanding DNA repair is important for developing new treatments for diseases linked to repair deficiencies and viral infections.
This document discusses the relationship between cell cycle mechanisms and cancer. It focuses on mammalian cell cycle checkpoints and their role in maintaining DNA stability when exposed to genotoxic stress. Key points covered include: 1) Heritable human cancer syndromes often have defects in DNA damage response pathways and cell cycle checkpoints. 2) Ataxia telangiectasia is caused by defects in the ATM gene and results in impaired DNA damage checkpoints. 3) Retinoblastoma involves defects in the Rb gene and disruption of cell cycle control. 4) Li-Fraumeni syndrome involves germline p53 mutations and loss of p53-mediated checkpoints and apoptosis.
The DNA is the most important part of the cell, as it contains all the information needed for cell maintenance, functioning, and life. Checkpoints in the cell cycle ensure this DNA is accurately replicated and passed to daughter cells. Failure of these mechanisms can lead to DNA damage and diseases like cancer. The document discusses DNA repair mechanisms like sister chromatid exchange and non-homologous end joining that help repair breaks, and how certain agents like radiation differently impact these processes. It also examines how polymorphisms in DNA repair genes may increase risk of diseases like cataracts by impacting the ability to repair UV damage.
1. Bronchogenic carcinoma, also known as lung cancer, is the leading cause of cancer death in the United States. The main cell types are adenocarcinoma, squamous cell carcinoma, undifferentiated large cell carcinoma, and small cell carcinoma.
2. Adenocarcinoma accounts for about 50% of cases and typically presents as a solitary peripheral nodule or mass. It is characterized microscopically by the formation of glands and papillary structures.
3. Cigarette smoking is the most important risk factor, responsible for 80-90% of lung cancer deaths. Other risk factors include exposure to radon, asbestos, and other occupational carcinogens.
Chapter 5 -repair or radiation damage and dose-rate effect - jtlJohn Lucas
The document summarizes various pathways for repairing DNA damage from radiation: base excision repair removes inappropriate bases; nucleotide excision repair removes bulky adducts like pyrimidine dimers. Mismatch repair fixes base-base mismatches. Non-homologous end joining and homologous recombination repair double-strand breaks, with the former being error-prone and active in G1, and the latter being error-free using a sister chromatid template and most active in G2 phase. Certain syndromes like ataxia-telangiectasia and LIG4 syndrome result from defects in these pathways and cause radiation sensitivity.
This document summarizes the current state of induced pluripotent stem cell (iPS cell) research and commercialization efforts. While iPS cells avoid ethical issues associated with embryonic stem cells and hold promise for disease modeling and drug screening, fundamental questions remain about reprogramming and differentiation. Several companies are working to develop iPS cell production kits, cell lines, and disease models. Intellectual property around iPS cell patents is still unclear, but many patent applications have been filed. Collaboration between research and industry aims to advance the technology and its applications.
This article discusses recent developments in induced pluripotent stem cell (iPS) research and commercialization efforts. It notes that while iPS cells avoid ethical issues associated with embryonic stem cells, fundamental questions remain about reprogramming and differentiation. Specifically, the presence of integrated vectors used to generate iPS cells poses risks for clinical application. Additionally, epigenetic variability between iPS cell lines from different donors and culture conditions can impact differentiation potential. The article also discusses ongoing research to replace integrating vectors with small molecules or proteins to induce pluripotency and intellectual property issues as numerous patents have been filed but none issued yet.
DNA polymerases play an important role in DNA replication and repair. There are 15 known DNA polymerases that fall into different families based on their structure and function. The main DNA polymerases involved in chromosomal replication are polymerases α, δ, ε and γ. Errors during DNA replication and repair can lead to mutations, some of which may cause cancer. DNA damage is repaired through several pathways including direct reversal, base excision repair, nucleotide excision repair, mismatch repair, and double strand break repair. Specialized translesion polymerases like pol η, κ, and ζ are involved in translesion synthesis to tolerate DNA damage. Overexpression of some error-prone polymerases has been associated with increased mutations
“The data presented here and in the literature are consistent with the hypothesis that at least one cancer, retinoblastoma, can be caused by two mutations…. One of these mutations may be inherited as a result of a previous germinal mutation…. Those patients that inherit one mutation develop tumors earlier than do those who develop the nonhereditary form of the disease; in a majority of cases those who inherit a mutation develop more than one tumor.
The document discusses the cell cycle, which is a programmed series of events that allows a cell to duplicate its contents and divide into two daughter cells. It describes the stages of the cell cycle including gap phases, DNA synthesis, and mitosis. Checkpoint controls ensure each step is completed before advancing to the next. Cancer cells often lose these checkpoint controls, allowing uncontrolled cell division. The roles of cyclins, CDKs, and inhibitors like pRb in regulating the cell cycle are also summarized. Understanding the cell cycle can aid developing anticancer drugs that target specific regulatory proteins.
1) The study analyzed satellite data on changes in Earth's gravity field to measure mass changes in glaciers and ice caps globally between 2003-2010.
2) Unexpectedly, the results found the contribution of glaciers and ice caps to sea level rise during this period was less than half of previous estimates.
3) Mass loss in the Himalayan and surrounding regions was insignificant, in contrast to previous estimates that were over ten times larger.
Stephen Friend NIH PPP Coordinating Committee Meeting 2012-02-16Sage Base
The document discusses using networked team approaches and integrating omics data to build better disease maps through public-private partnerships like CTCAP and Arch2POCM. It proposes sharing clinical and genomic data from comparator arms of trials to create models and de-risking novel drug targets through developing test compounds in a precompetitive space to accelerate new therapies.
Perrault & Hahn 2014 Addressing the Instability of DNA Nanostrctures in Tissu...Steven Perrault
This study characterized the stability of DNA nanostructures in tissue culture conditions. Three nanostructure designs - a DNA nano-octahedron, nanotube, and nanorod - were tested. The nano-octahedron and nanorod showed signs of denaturation in standard tissue culture medium, which has low magnesium levels, but remained stable when medium was adjusted to 6 mM magnesium. The nanotube appeared less sensitive to magnesium levels. Digestion by nucleases in fetal bovine serum, a common tissue culture supplement, also threatened nanostructure integrity over 24 hours. Adjustments like heat-inactivating serum or including actin protein could prevent this. The findings have implications for reliable experiments using DNA nanostructures with cells.
A method of DNA repair called Break-induced Replication (BIR) is more likely to cause genetic mutations than normal DNA synthesis, being up to 2,800 times more mutagenic. BIR occurs when a broken DNA piece invades another chromosome during replication, which happens in the wrong place and time, losing accuracy. There are several changes to the replication machinery that make BIR highly mutagenic. Neutron scattering experiments provide information about how DNA strands separate at different temperatures during denaturation, observing the first stage of separation before the strands become disordered. Understanding DNA repair mechanisms and structure allows for medical advances in addressing genetic diseases and conditions like cancer.
This document summarizes two scientific articles. The first article discusses how the condensin protein folds chromosome arms during cell division in yeast, helping prevent errors. The second article discusses how scientists identified molecular mechanisms behind DNA breakage, a hallmark of cancer cells, finding some DNA regions are more susceptible to damage and cancer results when repair mechanisms fail. The document discusses potential medical applications, like developing new treatments that target these molecules to help prevent genetic disorders and cancers.
Seminário Nacional do Benzeno (5 e 6 dez/12) - Derivação de Limites de Exposição Ocupacional para Substâncias Carcinogênicas e
Mutagênicas - Experiências Internacionais e Nacional
Secrets of parasites' replication unraveledcarito40
This document discusses various topics related to DNA replication and genetic diseases. It describes how origin of replication (ORI) proteins recognize the origin of replication site to initiate DNA duplication. It also discusses alternative treatments for diseases caused by parasites like Trypanosoma brucei that cause sleeping sickness. Finally, it mentions how understanding genetic causes of diseases like Meier-Gorlin syndrome could allow for preventative genetic therapies in the future.
The document summarizes key components of nucleic acids including phosphates, sugars, and nitrogenous bases. It also describes the primary, secondary, and tertiary structural levels of nucleic acids. Additionally, it discusses the discovery of a ring-shaped SMC-kleisin protein complex that ensures order in DNA packaging during cell division. Disruption of this complex can lead to disorders like cancer and genetic defects. The document also summarizes an article about the discovery of fragile sites in DNA that contribute to damage in B-cell lymphoma and how this finding could help develop new cancer treatments.
This document discusses lessons learned from building cancer models and realities around sharing, rewards, and affordability. It notes that oncogenes only make good targets in particular molecular contexts, as seen with the EGFR story. Predicting treatment response to known oncogenes is complex and requires detailed understanding of how different genetic backgrounds function. It also discusses preliminary probabilistic models being used to identify genes causal for disease. Extensive publications now substantiate the scientific approach of using probabilistic causal bionetwork models for diseases like metabolism, cardiovascular disease, and bone diseases. Sage Bionetworks is working to build an information commons for biological functions through collaborative disease maps and data repositories to better relate genetic features of cancer to drug efficacy and
1. Researchers have discovered a new four-stranded quadruple helix DNA structure called G-quadruplexes that exists in human genomes, particularly in regions rich in guanine. These quadruplexes are more common in rapidly dividing cells like cancer cells.
2. A separate study identified new sites in cells where DNA breaks early in the replication process. These break sites correlate with damage seen in cancers like diffuse large B cell lymphoma. Comparing mouse and human cells, both exhibit similar trends of genome instability at these sites.
3. Discoveries of DNA structures and break sites help understand the origins of diseases and cancer, offering new treatment approaches through stopping replication in cancer cells or addressing instability.
DNA repair mechanisms are indispensable for cell maintenance. The most common repair mechanisms are base excision repair (BER) and nucleotide excision repair (NER). Deficiencies in repair can lead to diseases like cancer or myelodysplastic syndrome. Studies have found that some viruses like murine polyomavirus activate DNA damage repair proteins like ATR and MRE11 to promote viral replication. Understanding DNA repair is important for developing new treatments for diseases linked to repair deficiencies and viral infections.
This document discusses the relationship between cell cycle mechanisms and cancer. It focuses on mammalian cell cycle checkpoints and their role in maintaining DNA stability when exposed to genotoxic stress. Key points covered include: 1) Heritable human cancer syndromes often have defects in DNA damage response pathways and cell cycle checkpoints. 2) Ataxia telangiectasia is caused by defects in the ATM gene and results in impaired DNA damage checkpoints. 3) Retinoblastoma involves defects in the Rb gene and disruption of cell cycle control. 4) Li-Fraumeni syndrome involves germline p53 mutations and loss of p53-mediated checkpoints and apoptosis.
The DNA is the most important part of the cell, as it contains all the information needed for cell maintenance, functioning, and life. Checkpoints in the cell cycle ensure this DNA is accurately replicated and passed to daughter cells. Failure of these mechanisms can lead to DNA damage and diseases like cancer. The document discusses DNA repair mechanisms like sister chromatid exchange and non-homologous end joining that help repair breaks, and how certain agents like radiation differently impact these processes. It also examines how polymorphisms in DNA repair genes may increase risk of diseases like cataracts by impacting the ability to repair UV damage.
1. Bronchogenic carcinoma, also known as lung cancer, is the leading cause of cancer death in the United States. The main cell types are adenocarcinoma, squamous cell carcinoma, undifferentiated large cell carcinoma, and small cell carcinoma.
2. Adenocarcinoma accounts for about 50% of cases and typically presents as a solitary peripheral nodule or mass. It is characterized microscopically by the formation of glands and papillary structures.
3. Cigarette smoking is the most important risk factor, responsible for 80-90% of lung cancer deaths. Other risk factors include exposure to radon, asbestos, and other occupational carcinogens.
Chapter 5 -repair or radiation damage and dose-rate effect - jtlJohn Lucas
The document summarizes various pathways for repairing DNA damage from radiation: base excision repair removes inappropriate bases; nucleotide excision repair removes bulky adducts like pyrimidine dimers. Mismatch repair fixes base-base mismatches. Non-homologous end joining and homologous recombination repair double-strand breaks, with the former being error-prone and active in G1, and the latter being error-free using a sister chromatid template and most active in G2 phase. Certain syndromes like ataxia-telangiectasia and LIG4 syndrome result from defects in these pathways and cause radiation sensitivity.
This document summarizes the current state of induced pluripotent stem cell (iPS cell) research and commercialization efforts. While iPS cells avoid ethical issues associated with embryonic stem cells and hold promise for disease modeling and drug screening, fundamental questions remain about reprogramming and differentiation. Several companies are working to develop iPS cell production kits, cell lines, and disease models. Intellectual property around iPS cell patents is still unclear, but many patent applications have been filed. Collaboration between research and industry aims to advance the technology and its applications.
This article discusses recent developments in induced pluripotent stem cell (iPS) research and commercialization efforts. It notes that while iPS cells avoid ethical issues associated with embryonic stem cells, fundamental questions remain about reprogramming and differentiation. Specifically, the presence of integrated vectors used to generate iPS cells poses risks for clinical application. Additionally, epigenetic variability between iPS cell lines from different donors and culture conditions can impact differentiation potential. The article also discusses ongoing research to replace integrating vectors with small molecules or proteins to induce pluripotency and intellectual property issues as numerous patents have been filed but none issued yet.
DNA polymerases play an important role in DNA replication and repair. There are 15 known DNA polymerases that fall into different families based on their structure and function. The main DNA polymerases involved in chromosomal replication are polymerases α, δ, ε and γ. Errors during DNA replication and repair can lead to mutations, some of which may cause cancer. DNA damage is repaired through several pathways including direct reversal, base excision repair, nucleotide excision repair, mismatch repair, and double strand break repair. Specialized translesion polymerases like pol η, κ, and ζ are involved in translesion synthesis to tolerate DNA damage. Overexpression of some error-prone polymerases has been associated with increased mutations
“The data presented here and in the literature are consistent with the hypothesis that at least one cancer, retinoblastoma, can be caused by two mutations…. One of these mutations may be inherited as a result of a previous germinal mutation…. Those patients that inherit one mutation develop tumors earlier than do those who develop the nonhereditary form of the disease; in a majority of cases those who inherit a mutation develop more than one tumor.
The document discusses the cell cycle, which is a programmed series of events that allows a cell to duplicate its contents and divide into two daughter cells. It describes the stages of the cell cycle including gap phases, DNA synthesis, and mitosis. Checkpoint controls ensure each step is completed before advancing to the next. Cancer cells often lose these checkpoint controls, allowing uncontrolled cell division. The roles of cyclins, CDKs, and inhibitors like pRb in regulating the cell cycle are also summarized. Understanding the cell cycle can aid developing anticancer drugs that target specific regulatory proteins.
1) The study analyzed satellite data on changes in Earth's gravity field to measure mass changes in glaciers and ice caps globally between 2003-2010.
2) Unexpectedly, the results found the contribution of glaciers and ice caps to sea level rise during this period was less than half of previous estimates.
3) Mass loss in the Himalayan and surrounding regions was insignificant, in contrast to previous estimates that were over ten times larger.
Stephen Friend NIH PPP Coordinating Committee Meeting 2012-02-16Sage Base
The document discusses using networked team approaches and integrating omics data to build better disease maps through public-private partnerships like CTCAP and Arch2POCM. It proposes sharing clinical and genomic data from comparator arms of trials to create models and de-risking novel drug targets through developing test compounds in a precompetitive space to accelerate new therapies.
Perrault & Hahn 2014 Addressing the Instability of DNA Nanostrctures in Tissu...Steven Perrault
This study characterized the stability of DNA nanostructures in tissue culture conditions. Three nanostructure designs - a DNA nano-octahedron, nanotube, and nanorod - were tested. The nano-octahedron and nanorod showed signs of denaturation in standard tissue culture medium, which has low magnesium levels, but remained stable when medium was adjusted to 6 mM magnesium. The nanotube appeared less sensitive to magnesium levels. Digestion by nucleases in fetal bovine serum, a common tissue culture supplement, also threatened nanostructure integrity over 24 hours. Adjustments like heat-inactivating serum or including actin protein could prevent this. The findings have implications for reliable experiments using DNA nanostructures with cells.
A method of DNA repair called Break-induced Replication (BIR) is more likely to cause genetic mutations than normal DNA synthesis, being up to 2,800 times more mutagenic. BIR occurs when a broken DNA piece invades another chromosome during replication, which happens in the wrong place and time, losing accuracy. There are several changes to the replication machinery that make BIR highly mutagenic. Neutron scattering experiments provide information about how DNA strands separate at different temperatures during denaturation, observing the first stage of separation before the strands become disordered. Understanding DNA repair mechanisms and structure allows for medical advances in addressing genetic diseases and conditions like cancer.
This document summarizes two scientific articles. The first article discusses how the condensin protein folds chromosome arms during cell division in yeast, helping prevent errors. The second article discusses how scientists identified molecular mechanisms behind DNA breakage, a hallmark of cancer cells, finding some DNA regions are more susceptible to damage and cancer results when repair mechanisms fail. The document discusses potential medical applications, like developing new treatments that target these molecules to help prevent genetic disorders and cancers.
The document discusses tumor viruses, oncogenes, and tumor suppressor genes. It summarizes key findings such as:
1. Peyton Rous discovered viruses can cause cancer in chickens in 1910. Retroviruses like Rous sarcoma virus carry oncogenes that can transform infected cells.
2. Oncogenes were first discovered in viruses and called viral oncogenes. Their normal cellular counterparts are called proto-oncogenes, which regulate cell growth. Activation of proto-oncogenes into oncogenes, such as via mutation, can accelerate cell growth and division leading to cancer.
3. Tumor suppressor genes are normal genes that protect the cell. Their absence can allow
This document discusses carcinogenesis and the molecular basis of tumor development. It covers several theories of carcinogenesis, including genetic damage to oncogenes, tumor suppressor genes, genes regulating apoptosis, and DNA repair genes. It also discusses various carcinogenic agents and the multi-step process of carcinogenesis, including initiation, promotion, and progression. Finally, it provides examples of different types of neoplasms and tumors, along with their characteristics.
This document discusses a study examining the roles of the transcriptional repressors Snail and Slug in mediating radioresistance and chemoresistance in ovarian cancer cells. The study finds that Snail and Slug contribute to resistance by 1) repressing p53-mediated apoptosis and 2) promoting the acquisition of stem-like characteristics in ovarian cancer cells. This allows cancer cells to survive radiation/chemotherapy stress and take on properties associated with cancer stem cells that can regenerate tumors. The study identifies many new direct gene targets of Snail and Slug through various genomic analyses and validates their roles in mediating resistance in ovarian cancer cell models.
The document discusses two scientific articles:
1) Mutation rates in cancer cells are strongly linked to how chromatin, the protein-DNA complex, is organized in the cell nucleus. The study provides new insights into the causes of cancer that may help understand why some genomic regions mutate faster than others.
2) Microbiologists studied how T. brucei, the parasite that causes sleeping sickness, organizes key proteins to replicate its mitochondrial DNA. Understanding these survival mechanisms could provide tools to more effectively treat parasitic diseases while minimizing effects on the host.
This document discusses using gold nanoparticles for breast cancer gene therapy. It provides background on breast cancer, gene therapy, and nanoparticles. It describes how gold nanoparticles can be used to deliver tumor suppressor genes or siRNA to cancer cells via gene therapy to treat breast cancer. Gold nanoparticles are promising for cancer therapy due to their ability to bind drugs and proteins and target cancer cells. The document envisions future prospects for improving siRNA delivery and developing multifunctional gold nanoparticles for combined imaging and targeted drug/gene delivery to treat breast cancer.
Scientists have identified molecular bases for DNA breakage, a hallmark of cancer cells. Studying DNA replication in fragile sites could provide insights into cancer development. Understanding weak areas in the DNA that are prone to breakage may help advise new therapeutic interventions and allow modification of cancer progression. More accurate DNA testing techniques in laboratories could help physicians improve cancer diagnosis and treatment.
Eukaryotic DNA is organized differently than prokaryotes, containing multiple chromosomes made of linear DNA molecules packaged around histone proteins to form chromatin. The cell cycle regulates cell division, ensuring daughter cells receive a full copy of the genome through DNA replication and cell growth or repair. Researchers found inhibiting signaling pathways in brain cancer cells stopped their reproduction and migration, making them more sensitive to chemotherapy. Studying chromatin remodeling genes in pancreatic cancer showed restoring expression of missing genes slowed cancer cell growth and induced senescence.
Eukaryotic DNA is organized differently than prokaryotes, containing multiple chromosomes made of linear DNA molecules packaged around histone proteins to form chromatin. The cell cycle regulates cell division, ensuring daughter cells receive a full copy of the genome through DNA replication and cell growth or repair. Researchers found inhibiting signaling pathways in brain cancer cells stopped their reproduction and migration, making them more sensitive to chemotherapy. Studying chromatin remodeling genes in pancreatic cancer showed restoring expression of missing genes slowed cancer cell growth and induced senescence.
Eukaryotic DNA is organized differently than prokaryotic DNA, containing multiple chromosomes made of linear DNA molecules packaged around histone proteins to form chromatin. The cell cycle regulates cell division, ensuring daughter cells receive a complete copy of the genome through DNA replication and cell growth or repair. Researchers found inhibiting signaling pathways in brain cancer cells stopped their reproduction and migration, making them more sensitive to chemotherapy. Studying chromatin remodeling genes in pancreatic cancer showed restoring expression of missing genes slowed cancer cell growth and induced senescence.
This document provides an overview of oral cancer and carcinogenesis. It discusses the molecular pathogenesis of cancer including oncogenes, tumor suppressor genes, and mechanisms of carcinogenesis. It describes the stages of chemical carcinogenesis as initiation and promotion. Physical carcinogens like ultraviolet light and ionizing radiation can damage DNA. Viruses can also cause cancer. Over 95% of oral cancers are squamous cell carcinomas, which have a high worldwide incidence, particularly in India, Australia, and parts of Africa. Oral cancer represents a major health problem in many developing countries.
This document discusses the molecular genetics of cancer. It explains that cancer arises from the accumulation of genetic changes over time that allow cells to proliferate uncontrollably. Key genes involved include oncogenes, which promote growth when mutated, and tumor suppressor genes, which normally inhibit growth but cannot when inactivated. The "two-hit hypothesis" proposes that both copies of a tumor suppressor gene must be inactivated for cancer to develop. Telomerase activity allows cancer cells to proliferate indefinitely by maintaining telomere length. DNA mismatch repair genes normally correct replication errors but cannot when mutated, allowing more mutations to accumulate and potentially cause cancer. Metastasis is the spread of cancer from the primary site to other parts of
The central-dogma-oh-genetic-informationDaniel Madrid
The central dogma of genetics describes the flow of genetic information from DNA to RNA to proteins. Two articles discuss cancer-causing mechanisms related to this dogma. One found that the enzyme APOBEC3G can induce mutations during DNA replication that lead to cancer. The other identified that cancer cells rely on the protein SMARCAL1 to resolve replication stress and maintain telomere length through the ALT pathway. Further research is needed to identify targets of these carcinogenic processes to develop new treatment strategies.
The document discusses research into controlling inflammatory and immune responses through proteins like STAT 3 and GR. It also discusses the potential medical applications of studying the genetics of sea urchins, which share over 7,000 genes with humans. Researchers hope to better understand transcription factors and how genetic expression is regulated in order to develop new treatments for diseases. Studying other species like sea urchins and sponges that can return cells to a stem cell state may also provide insights into how humans can fight diseases through genetic manipulation and therapy.
DNA repair mechanisms are developed by cells to repair various types of DNA damage induced by chemicals, radiation, and other factors. These repair mechanisms include base excision repair, nucleotide excision repair, strand break repair, and mismatch repair. Recent studies have found new enzymes and gene switches that may play an important role in DNA repair and preventing cancer by contributing to accurate chromosome segregation and reducing genome instability. Understanding DNA repair pathways could provide opportunities to develop new cancer therapies by preventing initial DNA damage or enhancing the body's natural repair processes.
Scientists have discovered seven new DNA regions that are linked to an increased risk of prostate cancer. A study of prostate cancer patients found variants in these DNA regions that are associated with carcinogenesis. This discovery may help explain the 25% risk of familial prostate cancer. Identifying the specific genes influencing prostate cancer risk can lead to new prevention techniques.
Promoting Wellbeing - Applied Social Psychology - Psychology SuperNotesPsychoTech Services
A proprietary approach developed by bringing together the best of learning theories from Psychology, design principles from the world of visualization, and pedagogical methods from over a decade of training experience, that enables you to: Learn better, faster!
ABDOMINAL TRAUMA in pediatrics part one.drhasanrajab
Abdominal trauma in pediatrics refers to injuries or damage to the abdominal organs in children. It can occur due to various causes such as falls, motor vehicle accidents, sports-related injuries, and physical abuse. Children are more vulnerable to abdominal trauma due to their unique anatomical and physiological characteristics. Signs and symptoms include abdominal pain, tenderness, distension, vomiting, and signs of shock. Diagnosis involves physical examination, imaging studies, and laboratory tests. Management depends on the severity and may involve conservative treatment or surgical intervention. Prevention is crucial in reducing the incidence of abdominal trauma in children.
TEST BANK For Community Health Nursing A Canadian Perspective, 5th Edition by...Donc Test
TEST BANK For Community Health Nursing A Canadian Perspective, 5th Edition by Stamler, Verified Chapters 1 - 33, Complete Newest Version Community Health Nursing A Canadian Perspective, 5th Edition by Stamler, Verified Chapters 1 - 33, Complete Newest Version Community Health Nursing A Canadian Perspective, 5th Edition by Stamler Community Health Nursing A Canadian Perspective, 5th Edition TEST BANK by Stamler Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Pdf Chapters Download Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Pdf Download Stuvia Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Study Guide Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Ebook Download Stuvia Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Questions and Answers Quizlet Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Studocu Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Quizlet Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Stuvia Community Health Nursing A Canadian Perspective, 5th Edition Pdf Chapters Download Community Health Nursing A Canadian Perspective, 5th Edition Pdf Download Course Hero Community Health Nursing A Canadian Perspective, 5th Edition Answers Quizlet Community Health Nursing A Canadian Perspective, 5th Edition Ebook Download Course hero Community Health Nursing A Canadian Perspective, 5th Edition Questions and Answers Community Health Nursing A Canadian Perspective, 5th Edition Studocu Community Health Nursing A Canadian Perspective, 5th Edition Quizlet Community Health Nursing A Canadian Perspective, 5th Edition Stuvia Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Pdf Chapters Download Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Pdf Download Stuvia Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Study Guide Questions and Answers Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Ebook Download Stuvia Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Questions Quizlet Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Studocu Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Quizlet Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Stuvia
8 Surprising Reasons To Meditate 40 Minutes A Day That Can Change Your Life.pptxHolistified Wellness
We’re talking about Vedic Meditation, a form of meditation that has been around for at least 5,000 years. Back then, the people who lived in the Indus Valley, now known as India and Pakistan, practised meditation as a fundamental part of daily life. This knowledge that has given us yoga and Ayurveda, was known as Veda, hence the name Vedic. And though there are some written records, the practice has been passed down verbally from generation to generation.
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
Does Over-Masturbation Contribute to Chronic Prostatitis.pptxwalterHu5
In some case, your chronic prostatitis may be related to over-masturbation. Generally, natural medicine Diuretic and Anti-inflammatory Pill can help mee get a cure.
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
share - Lions, tigers, AI and health misinformation, oh my!.pptxTina Purnat
• Pitfalls and pivots needed to use AI effectively in public health
• Evidence-based strategies to address health misinformation effectively
• Building trust with communities online and offline
• Equipping health professionals to address questions, concerns and health misinformation
• Assessing risk and mitigating harm from adverse health narratives in communities, health workforce and health system
share - Lions, tigers, AI and health misinformation, oh my!.pptx
Fragile sites in the cancer
1. DISCOVERY OF NEW CLASS OF DAMAGE-
PRONE DNA REGIONS COULD LEAD TO
BETTER CANCER TREATMENTS AND A NEW
MECHANISM THAT CONTRIBUTES TO
EVOLUTION OF CANCER
Ángela Maria Aragon Canencio
Medicine Student -III Semester.
Universidad Pontificia Bolivariana
Molecular Biology- february 18 2013
2. MEDICAL UTILITY BIBLIOGRAPHY MOLECULAR BIOLOGY
MARTINEZ S, Lina Maria. Biología DISCOVERY OF NEW CLASS
Molecular. 5 ed Medellin: UPB OF DAMAGE-PRONE DNA
Fac. Medicina REGIONS COULD LEAD TO
BETTER CANCER
Discovery of New Class of TREATMENTS AND A NEW
Damage-Prone DNA Regions MECHANISM THAT
Could Lead to Better Cancer CONTRIBUTES TO
Treatments, Science daily. EVOLUTION OF CANCER
( jan 24 2013)
The findings could lead A New Mechanism That
to the development of Contributes to the Evolution of
more effective Cancer, science daily.
(jan 31 2013)
treatments for B cell
lymphoma, know Ángela Maria Aragon
Canencio
better the causes of Medicine Student -III
cancer, allow the Semester.
Universidad Pontificia
creation of news Bolivariana
treatments for these Molecular Biology-
february 18 2013
3. DISCOVERY OF NEW CLASS A NEW MECHANISM
INTRODUCTION
OF DAMAGE-PRONE DNA THAT CONTRIBUTES TO
REGIONS COULD LEAD TO EVOLUTION OF CANCER
BETTER CANCER
The fragile sites are regions of
chromosome likely to break or TREATMENTS
separate by certain cell activities
like replication and division.
Consist of repeated sequences
when DNA is replicated in cell Cancer arises from the
of CGG. division can take damage in
accumulation of mutations
places that are known as
and structural changes in
fragile sites for double-strand
break chromosomes , this tend
to lose or duplicate entire
regions
Cancer is a DNA damage disease
associated with replication. Also
accumulation of mutations and B cells divide rapidly and so
structural changes in are at greater risk, in this
chromosomes. Is for that reason
tthat the study of fragile sites study described their
provides to the understanding of instability
cancer and the possibility of
better treatment
4. INTRODUCTION Cancer becomes in a public health
The fragile sites are regions of
problem due to of its high incidence
chromosome likely to break or in recent years. The increase was
separate by certain cell activities
like replication and division. influenced by environmental factors,
Consist of repeated
genetic and lifestyle. Therefore the
sequences of CGG.
need was created by the scientific
community to find an effective
treatment, thus decreasing possible
side effects of treatments allowing
better quality of life for these
patients
Cancer is a DNA damage disease
associated with replication. Also
accumulation of mutations and
structural changes in
chromosomes. Is for that reason
that the study of fragile sites
provides to the understanding of
cancer and the possibility of
better treatment
5. DISCOVERY OF NEW CLASS DISCOVERY OF NEW CLASS OF DAMAGE-PRONE
OF DAMAGE-PRONE DNA DNA REGIONS COULD LEAD TO BETTER CANCER
REGIONS COULD LEAD TO
BETTER CANCER TREATMENTS TREATMENTS
when DNA is replicated in cell
division can take damage in
places that are known as
fragile sites for double-strand
break
B cells are leukocytes which depends
B cells divide rapidly and so
are at greater risk, in this
mediated immunity with antibodies
study described their specific activity of antigen binding.
instability
6. DISCOVERY OF NEW CLASS OF DAMAGE-PRONE DNA REGIONS COULD LEAD TO
BETTER CANCER TREATMENTS
a somatic cell of the
body undergoes a
division called mitosis
and it results in two
haploid daughter
cells, this process has
four steps are:
prophase, metaphase, a
naphase and telophase
and result is the
cells called B cell lymphocytes are among development of the
the most rapidly dividing cells, they are at organism
great risk for replication-induced DNA
damage.
7. DISCOVERY OF NEW CLASS OF DAMAGE-PRONE
DNA REGIONS COULD LEAD TO BETTER CANCER
TREATMENTS
FRAGILES SITES
The fragile sites are specific
loci that show fractures
during karuoyping perform
under specific, the fragiles
sites have provided insight
into understanding of the
effects of replicative stress on
DNA damage and genomic
instability in cancer cells.
8. DISCOVERY OF NEW CLASS OF DAMAGE-PRONE
DNA REGIONS COULD LEAD TO BETTER CANCER
TREATMENTS
In this study the
team uncovered an AID-
independent source of DNA
breaks associated with
replication called early
replicating fragile sites (ERFSs).
these sites overlapped
significantly with DNA
alterations associated with B
cell lymphoma, suggesting that
ERFSs are a major feature of
the mutational landscape of
this type of cancer and possibly
other cancers.
9. OBSERVATION
I think that this is so
importan because
undertand how
replication hanppen
in the B cells we will
do more specific
treatment
10. A NEW MECHANISM THAT A NEW MECHANISM THAT CONTRIBUTES
CONTRIBUTES TO TO EVOLUTION OF CANCER
EVOLUTION OF CANCER
Cancer arises from the Cancer is a disease caused by a group
accumulation of of cells that grow and multiply
mutations and uncontrollably autonomously,
structural changes in invading other tissues locally and
chromosomes , this remotely.
tend to lose or duplicate
entire regions
11. Cancer occurs after the appearance
of mutations and chromosome
changes, lost or duplicated
chromosomes entire regions
the cancer cells are not divide as
normal cells of the body, these cells
can produce up to 5 daughters, the
different process of this division
causes the daughters have more or
fewer chromosomes than a normal
one leading to aneuploidy
A NEW MECHANISM THAT CONTRIBUTES
TO EVOLUTION OF CANCER
12. A NEW MECHANISM THAT CONTRIBUTES TO
EVOLUTION OF CANCER
It was thought that
the problems
originated in parts
difficult to
duplicate but this
study found that
areas that replicate
quickly also are
prone
13. A NEW MECHANISM THAT CONTRIBUTES TO
EVOLUTION OF CANCER
"In these cases, the
collision between the
two machineries, the
duplication machine
and the transcription
machine, can be
responsible for
generating
chromosomal
alterations that are
deadly for cells," says
ndez‐Capetillo
14. OBSERVATION
The importance of this research is
the knowlodge of the mechanisms
that explain the cromosomal
alteration furthemore the study
help us to understand the changes
in the genome throughout
evolution.
15. MEDICAL UTILITY
with this new knowledge about
cancer, you can make new and
better treatments to treat and
prevent so many deaths from
this disease.
The findings could lead to
the development of more
effective treatments for B
cell lymphoma, know better
the causes of cancer, allow
the creation of news
treatments for these
desease.
MEDICAL UTILITY
16. MEDICAL UTILITY
how advanced the how is the chromosome
disease division
according to this
what is the right in what time should be
treatment applied
17. MEDICAL UTILITY
is very important for science
continue investigating causes
of this disease, as this not
only affects the person
suffering but also his entire
family circle and bring this
allows for a better way, just
because you can explain it
better the patient is
happening inside.
18. MEDICAL UTILITY
knowing that fragile
sites are easily
damaged in the
division and that
cancer is a disease
that occurs when
there is
accumulation of
mutations may start
thinking that
decreasing fragile
sites can reach
decreser disease
19. BIBLIOGRAPHY
•MARTINEZ S, Lina Maria. Biología Molecular. 5 ed
Medellin: UPB Fac. Medicina
•Discovery of New Class of Damage-Prone DNA
Regions Could Lead to Better Cancer Treatments,
Science daily.
( jan 24 2013)
•A New Mechanism That Contributes to the
Evolution of Cancer, science daily.
(jan 31 2013)