"Recent Breakthrough in Protein Interaction Mapping Leads to Cancer Cell Therapeutic Discovery" by Defne Alpdogan
In most cases, cancer cell biology and its interaction intracellular and extracellular are not only interesting but also fundamental to the diagnosis and prognosis of treatment. In a current discovery, researchers have mapped out protein to protein interactions in common head and neck cancers. In their discoveries and findings, they used specific and recent technological advancements to help map the interactions between the proteins. This is extremely important in understanding cancer cell biology because mechanisms as delicate as protein interactions and one simple mutation and or pathways signal change can lead to the growth of cancerous cells and or oncogenes. This multi- study approach also was able to have significant breakthroughs in treatment. For example, in one of the studies, the researchers were able to identify an effective treatment for individuals with head and neck cancers that stem from the mutation in the PIK3CA gene.
In this interaction with the drug, the investigators do not block the actual coding of PIK3CA or the interaction with other signals but rather block HER3. By disrupting HER3, researchers were able to prove that there was a backdoor way of blocking the actions of the mutant PIK3CA. Utilizing the information from the map interactions, researchers were able to delinage this information and can even use it for the future as it allows investigators to create therapeutic agents that are unconventional. Targeting just cancer cell oncogenes and protooncogenes with various chemotherapeutic sources might be effective but the current approach or the new approach would be to look through the proteins and find ways to limit the interaction between them that can create a positive outcome for the patient and treatment.
This article and this recent multi- research approach has been extremely pivotal for the study of biology. It illustrates how macromolecules are quintessential to the interactions of diseases and even the smallest mechanisms are not only interconnected but can lead to better reagents and treatments in the near future. Specific targeted therapies to genes like EGFR, HER2, and BRAF and many others demonstrate how essential molecular biology is to the scientific community. In most cases, cellular biology is very complicated and not only deals with mechanisms but electron transports and coenzymes which is the next wave of medical research shift.
Source: https://www.cancer.gov/news-events/cancer-currents-blog/2021/protein-interactions-mapping-cancer-pathways
In most cases, cancer cell biology and its interaction intracellular and extracellular are not only interesting but also fundamental to the diagnosis and prognosis of treatment. In a current discovery, researchers have mapped out protein to protein interactions in common head and neck cancers. In their discoveries and findings, they used specific and recent technological advancements to help map the interactions between the proteins. This is extremely important in understanding cancer cell biology because mechanisms as delicate as protein interactions and one simple mutation and or pathways signal change can lead to the growth of cancerous cells and or oncogenes. This multi- study approach also was able to have significant breakthroughs in treatment. For example, in one of the studies, the researchers were able to identify an effective treatment for individuals with head and neck cancers that stem from the mutation in the PIK3CA gene.
In this interaction with the drug, the investigators do not block the actual coding of PIK3CA or the interaction with other signals but rather block HER3. By disrupting HER3, researchers were able to prove that there was a backdoor way of blocking the actions of the mutant PIK3CA. Utilizing the information from the map interactions, researchers were able to delinage this information and can even use it for the future as it allows investigators to create therapeutic agents that are unconventional. Targeting just cancer cell oncogenes and protooncogenes with various chemotherapeutic sources might be effective but the current approach or the new approach would be to look through the proteins and find ways to limit the interaction between them that can create a positive outcome for the patient and treatment.
This article and this recent multi- research approach has been extremely pivotal for the study of biology. It illustrates how macromolecules are quintessential to the interactions of diseases and even the smallest mechanisms are not only interconnected but can lead to better reagents and treatments in the near future. Specific targeted therapies to genes like EGFR, HER2, and BRAF and many others demonstrate how essential molecular biology is to the scientific community. In most cases, cellular biology is very complicated and not only deals with mechanisms but electron transports and coenzymes which is the next wave of medical research shift.
Source: https://www.cancer.gov/news-events/cancer-currents-blog/2021/protein-interactions-mapping-cancer-pathways
What are the effects of obesity on the physiological nature of the brain? by Sabrina Salman
Obesity is a common disease that affects almost 300 million people in the United States per year, and identified as a condition where an individual has excessive body fat which increases the risk of other major health problems. It has been discovered previously that obesity can result in many phenotypic changes to the individual, and that obesity can induce heart disease and diabetes, as well as many other medical conditions; however, when considering the underlying effects on body organs, many will not account for possible physiological changes in the brain. If obesity affects every major organ including the heart then wouldn’t it cause problems in the brain too? The answer to that question is: Yes. Through the contributions of recent neurological research studies, it has been concluded that there is a major correlation between obese individuals will face structural brain changes and will be predisposed mental conditions such as anterograde dementia.
In a 2019 study, researches compared the MRI scans to healthy non-obese individuals, and healthy obese individuals. It was deducted that the brains of the obese individuals lacked gray matter around certain areas of the brain, primarily the prefrontal cortex located in the frontal lobe. Gray matter on an MRI shows the nuclei and cell bodies of nervous cells in the brain, whereas white matter shows axon tails of neurons. Gray matter is dominant in the outer regions of the brain throughout the neocortex, and white matter is seen in the inner regions of the brain, for example the brain stem. The frontal lobe of the brain is responsible for higher level executive functions, such as planning, decision making, motor skills, problem solving, and social interaction. A lack of gray matter in this area of the brain reveals a lack of cognitive function in that area. This cognitive decline can cause severe mental dysfunctions such as dementia. The study also announced changes to the anterior cingulate gyrus, hippocampus, and thalamus. Researchers recently announced how biological gender can also play a significant role in determining the cognitive effects of obesity. In a study of all middle aged participants, female individuals who were diagnosed with obesity had more extensive gray matter volume reductions as compared to men.
The overall reason for this became clear from a 2013 study regarding correlational research with obesity and the FTO gene. The FTO gene (fat mass and obesity associated gene), or alpha-ketoglutarate-dependent dioxygenase, is an enzyme identified in the FTO gene which is located on chromosome 16 in humans. This gene is seen more frequently activated in females compared to males, the reason is not entirely concluded upon thus far. However, those who are affected by an activated state of the FTO gene are predisposed to obesity and increase the likelihood of cognitive decline and dementia. The FTO gene is most highly expressed in the cerebral cortex of the brain, and even a singular risk allele can be the cause of predetermined obesity due to even a slight over abnormal BMI, as the gene is highly responsive at activation. FTO will interfere with ghrelin and leptin hormones which are associated with food-intake balance, suppressing the amount of leptin and increasing ghrelin in the body, causing the individual to become more susceptible to binge on unhealthy foods.
Not only is obesity a physiological disorder in the human body but it can also be categorized as a mental disorder. The FTO gene will suppress impulse control within the prefrontal cortex when the individual comes into contact with food, and it is also commonly associated with altering dopamine signaling pathways. With the interference of dopamine pathways with increased food intake, this puts obesity as an additive mental disorder as much as it is a physiological one. With the individual unable to control how much food is being consumed and will go through strong withdrawal symptoms when those needs are unable to be met, obesity can be an extremely mentally straining condition.
Although there are several concerns in cogntive functioning for obese individuals, the effects can possibly be reversible. In a 2003 study, researchers Gustafson et al. analyzed 12 studies which resulted in the conclusion that weightloss has correlated with an increase of gray matter in the neocortex of the brain from predetermined obese patients. This links a healthy diet and exercise regularity with stronger cognitive function in individuals rather than the weight loss aspect of the study. If an individual contributes to a healthy meal plan, regular active exercise in any form (preferably 30 minutes each day) and receives 7-8 hours of sleep, can form increased gray matter volume in the brain, specifically in the frontal lobe strengthening neural connections. Overall, if all humans contribute to a healthy lifestyle with the aforementioned necessities and target aspects, there will be no risk of obesity in any individual and this nationwide epidemic can finally be suppressed.
Sources:
Melhorn, Susan J, et al. “FTO Genotype Impacts Food Intake and Corticolimbic Activation.” The American Journal of Clinical Nutrition, Oxford University Press, 1 Feb. 2018, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6454473/.
TEDEducation. “What Is Obesity? - Mia Nacamulli.” YouTube, YouTube, 30 June 2016, https://www.youtube.com/watch?v=-vNVG7XJpVE.
“Appetite, Obesity, and the Brain.” YouTube, YouTube, 1 July 2016, https://www.youtube.com/watch?v=Qbcr9RAOWtM.
Sui, Sophia X, and Julie A Pasco. “Obesity and Brain Function: The Brain-Body Crosstalk.” Medicina (Kaunas, Lithuania), MDPI, 24 Sept. 2020, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7598577/.
“How Might Obesity Affect the Brain?” Medical News Today, MediLexicon International, https://www.medicalnewstoday.com/articles/325054#More-body-fat,-less-gray-matter-volume
.
“The Effects of Obesity on Brain Structure and Size.” Practical Neurology, Bryn Mawr Communications, https://practicalneurology.com/articles/2013-july-aug/the-effects-of-obesity-on-brain-structure-and-size.
Obesity is a common disease that affects almost 300 million people in the United States per year, and identified as a condition where an individual has excessive body fat which increases the risk of other major health problems. It has been discovered previously that obesity can result in many phenotypic changes to the individual, and that obesity can induce heart disease and diabetes, as well as many other medical conditions; however, when considering the underlying effects on body organs, many will not account for possible physiological changes in the brain. If obesity affects every major organ including the heart then wouldn’t it cause problems in the brain too? The answer to that question is: Yes. Through the contributions of recent neurological research studies, it has been concluded that there is a major correlation between obese individuals will face structural brain changes and will be predisposed mental conditions such as anterograde dementia.
In a 2019 study, researches compared the MRI scans to healthy non-obese individuals, and healthy obese individuals. It was deducted that the brains of the obese individuals lacked gray matter around certain areas of the brain, primarily the prefrontal cortex located in the frontal lobe. Gray matter on an MRI shows the nuclei and cell bodies of nervous cells in the brain, whereas white matter shows axon tails of neurons. Gray matter is dominant in the outer regions of the brain throughout the neocortex, and white matter is seen in the inner regions of the brain, for example the brain stem. The frontal lobe of the brain is responsible for higher level executive functions, such as planning, decision making, motor skills, problem solving, and social interaction. A lack of gray matter in this area of the brain reveals a lack of cognitive function in that area. This cognitive decline can cause severe mental dysfunctions such as dementia. The study also announced changes to the anterior cingulate gyrus, hippocampus, and thalamus. Researchers recently announced how biological gender can also play a significant role in determining the cognitive effects of obesity. In a study of all middle aged participants, female individuals who were diagnosed with obesity had more extensive gray matter volume reductions as compared to men.
The overall reason for this became clear from a 2013 study regarding correlational research with obesity and the FTO gene. The FTO gene (fat mass and obesity associated gene), or alpha-ketoglutarate-dependent dioxygenase, is an enzyme identified in the FTO gene which is located on chromosome 16 in humans. This gene is seen more frequently activated in females compared to males, the reason is not entirely concluded upon thus far. However, those who are affected by an activated state of the FTO gene are predisposed to obesity and increase the likelihood of cognitive decline and dementia. The FTO gene is most highly expressed in the cerebral cortex of the brain, and even a singular risk allele can be the cause of predetermined obesity due to even a slight over abnormal BMI, as the gene is highly responsive at activation. FTO will interfere with ghrelin and leptin hormones which are associated with food-intake balance, suppressing the amount of leptin and increasing ghrelin in the body, causing the individual to become more susceptible to binge on unhealthy foods.
Not only is obesity a physiological disorder in the human body but it can also be categorized as a mental disorder. The FTO gene will suppress impulse control within the prefrontal cortex when the individual comes into contact with food, and it is also commonly associated with altering dopamine signaling pathways. With the interference of dopamine pathways with increased food intake, this puts obesity as an additive mental disorder as much as it is a physiological one. With the individual unable to control how much food is being consumed and will go through strong withdrawal symptoms when those needs are unable to be met, obesity can be an extremely mentally straining condition.
Although there are several concerns in cogntive functioning for obese individuals, the effects can possibly be reversible. In a 2003 study, researchers Gustafson et al. analyzed 12 studies which resulted in the conclusion that weightloss has correlated with an increase of gray matter in the neocortex of the brain from predetermined obese patients. This links a healthy diet and exercise regularity with stronger cognitive function in individuals rather than the weight loss aspect of the study. If an individual contributes to a healthy meal plan, regular active exercise in any form (preferably 30 minutes each day) and receives 7-8 hours of sleep, can form increased gray matter volume in the brain, specifically in the frontal lobe strengthening neural connections. Overall, if all humans contribute to a healthy lifestyle with the aforementioned necessities and target aspects, there will be no risk of obesity in any individual and this nationwide epidemic can finally be suppressed.
Sources:
Melhorn, Susan J, et al. “FTO Genotype Impacts Food Intake and Corticolimbic Activation.” The American Journal of Clinical Nutrition, Oxford University Press, 1 Feb. 2018, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6454473/.
TEDEducation. “What Is Obesity? - Mia Nacamulli.” YouTube, YouTube, 30 June 2016, https://www.youtube.com/watch?v=-vNVG7XJpVE.
“Appetite, Obesity, and the Brain.” YouTube, YouTube, 1 July 2016, https://www.youtube.com/watch?v=Qbcr9RAOWtM.
Sui, Sophia X, and Julie A Pasco. “Obesity and Brain Function: The Brain-Body Crosstalk.” Medicina (Kaunas, Lithuania), MDPI, 24 Sept. 2020, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7598577/.
“How Might Obesity Affect the Brain?” Medical News Today, MediLexicon International, https://www.medicalnewstoday.com/articles/325054#More-body-fat,-less-gray-matter-volume
.
“The Effects of Obesity on Brain Structure and Size.” Practical Neurology, Bryn Mawr Communications, https://practicalneurology.com/articles/2013-july-aug/the-effects-of-obesity-on-brain-structure-and-size.
"Discovery in HIV Treatments" By Defne Alpdogan
A recent discovery may have found a link between the transcription factor CREB1 and human immunodeficiency virus 1 vaccine induced immunity. In this, CREB1 is a transcription factor that has been widely studied and it is a cAMP depended element binding protein that when active can have a positive effect against HIV-1 and decrease the viral development in humans. This induced immunity and or discovery was first seen on non-human primates and while the studies were approved for primates, they are recently being studied in humans but so far there is a positive outcome in the results that Tomalka, et al are finding. Currently, the human trial has 16,000 volunteers with the ALVAC-HIV and AIDSVAX B/E and will continued to be monitored for the next three years post vaccination with these two different strains. What Tomalka et al found was with their experimentations would be that they located the target genes of the transcription factor after the vaccination of the two strains and looked at the induced immunity and performed antibody tests to see if there are antibodies being created and or expressed. Furthermore, they found that the CREB1 target genes indicated a lower risk of HIV-1 development and the authors also expressed that most of these genes expressed these traits of immunity, as early as 24h after the vaccination of the subjects.
This discovery was maintained by the group through their persistent efforts and methods to explain that the CREB1 target genes and the activation they cause can lead to increased immunity for HIV-1 vaccination induced immunities. For example, to directly illustrate the regions of the genes, the author perfumed “chromatin immunoprecipitation” which then was able to depict the overlap between the genes of the vaccination and the genes of the CREB1 activated and bound to. Their discoveries with the molecular mechanisms and pathways that can be seen with the interactions between the CREB1 target genes, the ALVAC immunity (the vaccines that were given to the correspondents of the study) and HIV-1 induced immunity could help create a new transition state to a better vaccination and a vaccination for HIV-1. This information continues to lay the foundation necessary for immunologists to utilize test trails to create specific medications or target specific pathways to induce a response to then aid people in their disease transgression.
The final mechanism the authors proposed utilizes, cGAS, cGAMP and the activation of T cells, B cells and VREB1. Further research into cytokines and their affect on this pathway can help express the missing link to formulate and generate a better therapeutic approach to HIV-1.
Source: https://www.nature.com/articles/s41590-021-01018-9
A recent discovery may have found a link between the transcription factor CREB1 and human immunodeficiency virus 1 vaccine induced immunity. In this, CREB1 is a transcription factor that has been widely studied and it is a cAMP depended element binding protein that when active can have a positive effect against HIV-1 and decrease the viral development in humans. This induced immunity and or discovery was first seen on non-human primates and while the studies were approved for primates, they are recently being studied in humans but so far there is a positive outcome in the results that Tomalka, et al are finding. Currently, the human trial has 16,000 volunteers with the ALVAC-HIV and AIDSVAX B/E and will continued to be monitored for the next three years post vaccination with these two different strains. What Tomalka et al found was with their experimentations would be that they located the target genes of the transcription factor after the vaccination of the two strains and looked at the induced immunity and performed antibody tests to see if there are antibodies being created and or expressed. Furthermore, they found that the CREB1 target genes indicated a lower risk of HIV-1 development and the authors also expressed that most of these genes expressed these traits of immunity, as early as 24h after the vaccination of the subjects.
This discovery was maintained by the group through their persistent efforts and methods to explain that the CREB1 target genes and the activation they cause can lead to increased immunity for HIV-1 vaccination induced immunities. For example, to directly illustrate the regions of the genes, the author perfumed “chromatin immunoprecipitation” which then was able to depict the overlap between the genes of the vaccination and the genes of the CREB1 activated and bound to. Their discoveries with the molecular mechanisms and pathways that can be seen with the interactions between the CREB1 target genes, the ALVAC immunity (the vaccines that were given to the correspondents of the study) and HIV-1 induced immunity could help create a new transition state to a better vaccination and a vaccination for HIV-1. This information continues to lay the foundation necessary for immunologists to utilize test trails to create specific medications or target specific pathways to induce a response to then aid people in their disease transgression.
The final mechanism the authors proposed utilizes, cGAS, cGAMP and the activation of T cells, B cells and VREB1. Further research into cytokines and their affect on this pathway can help express the missing link to formulate and generate a better therapeutic approach to HIV-1.
Source: https://www.nature.com/articles/s41590-021-01018-9