New Fight Against Skin Cancer

            Alexander Boiko at the University of California Irvine has discovered a new way to fight against melanomas. Melanoma is the most lethal type of skin cancer and can also metastasize very easily. He did this by blocking CD47, which is a cell surface protein on melanin cells, since this will increase the amount the cells were phagocytosed by macrophages. The term phagocytosed is referred to in the paper as “eaten,” and macrophages are a part of the innate immune system and act as phagocytic cells. Another surface protein, CD271, was also found to be important when used with the CD47. CD271 was used in order to target the most aggressive melanoma cells selectively.

            In order for the CD47 to not be eliminated by the immune system, CD47 was overexpressed by metastatic melanomas. To have better results they decided that both proteins needed to be overexpressed in order to trick the immune system so that it could spread to other parts of the body. They found that by blocking of CD47 and targeting of CD271 metastases was stopped in human melanoma tumors that were put in mice. One thing to take note of is that there was major alteration of the microenvironment surrounding the tumors, which helped with the positive results.

            Before this could be done on humans, further research needs to be done in order to see if the combination of CD47 and CD271 can be safely used. But Boiko is hopeful that with the combination of this new therapy as well as other treatments emerging that positive outcomes in the fight against metastatic melanomas will arise.

http://www.cell.com/cell-reports/fulltext/S2211-1247(16)30890-7

Huntington’s Disease

            What exactly is Huntington’s disease? Huntington’s disease (HD) is an inherited neurological condition that affects both the brain and the nervous system. Some of the symptoms people with HD may exhibit are: involuntary muscle movements, slurred speech, depression and anxiety, emotional control issues, and difficultly with thought processes. Once the first symptoms begin normally people live 15 to 20 years with the disease slowly progressing. HD is caused by an inherited change in a huntingtin gene. The huntingtin gene is the gene that is associated with HD. Each parent passes on one of the two huntingtin gene copies they have to their child. If a person has a faulty huntingtin gene copy then they are either affected or pre-symptomatic. This person has a 50% chance that this faulty gene will be passed on to their child.

People can get pre-symptomatic genetic testing done in order to see if they have the faulty huntingtin gene. This means they will test to see how many CAG repeats are in their huntingtin gene. A blood sample is taken from the subject in order to inspect the DNA. The first step of the test is to do polymerase chain reaction (PCR) in order to isolate DNA and make copies. From the millions of copies made from PCR, the DNA fragments need to be separated by Gel Electrophoresis in order to analyze them.

In the huntingtin gene if there are less than 26 repeats of CAG triplet then that is considered the normal range and not faulty, and this person would not have HD. The same goes for the range 27-35 repeats. If a person has 36-39 CAG repeats it is very likely that the person will develop HD. However, it might develop at a later age with less severe conditions, or they might not develop HD at all. Yet if there are more than 40 CAG repeats that person will almost certainly develop HD.

As of right now there is no treatment or cure for HD, but research is ongoing in order to help manage the symptoms. Personally knowing a family that is affected by Huntington’s disease, I feel that more people should be made aware about HD and it’s affects. This is an important cause that people should know about.

http://web.stanford.edu/group/hopes/cgi-bin/hopes_test/molecular-biology-of-the-huntingtons-disease-genetic-test/

http://www.genetics.edu.au/Publications-and-Resources/PublicationsBrochuresandPamphlets/HUNTINGTON%20DISEASE%20AND%20GENETIC%20TESTING.pdf

Stem Cells to Help With Diabetes

Stem Cells to Help With Diabetes

            What exactly is insulin? Insulin is a hormone created from beta cells that is located in the pancreases that regulate the amount of glucose in blood. When there is not enough insulin in the body that is when a type of diabetes can come into affect. Insulin is what keeps a person’s sugar levels from either getting too high or too low.

            In Type 1 diabetes beta cells are destroyed by the body’s immune system. For the most common form, Type 2 diabetes, the beta cells are not able to produce enough insulin in order to keep a person’s sugar levels where they need to be. One theory that has been mentioned to help control both types of diabetes is to use stem cells to create properly working beta cells. In order to create this type of cell pluripotent stem cells need to be used. Pluripotent stem cells are cells that have been genetically reprogramed in order to replicate that of embryonic stem cells. Dr. Douglas Melton has been striving to do just this.

            After more than 150 combinations of 70 compounds, Melton was finally able to figure out a system of 5 different growth methods and 11 factors that when added over weeks time produced cells that represented and functioned as beta cells. When these cells were exposed to glucose, insulin was secreted inside of healthy mice. The next step was to try these cells inside of mice with diabetes, whose glucose levels were greatly reduced when the cells were added. The next step is to now get ready for clinical trials on humans. I am very anxious to see what results this study produces in the future. With an aunt who has battled with diabetes from childhood, I am curious to see how this advancement could potentially help her. Other research that Dr. Melton has conducted on the study of diabetes can be seen below.

https://www.nih.gov/news-events/nih-research-matters/developing-insulin-producing-cells-treat-diabetes

https://www.nih.gov/news-events/nih-research-matters/hormone-may-help-treat-diabetes

The Life and Work of Francis Crick

            Most people know Francis Crick as one half of the famous Watson and Crick duo who discovered the double helix structure of DNA, but there is more to him than that. Francis Harry Compton Crick was born in Northampton, England on June 8^th, 1916 to Harry and Annie Elizabeth Crick. He earned a Bachelor of Science degree from the University College London in physics in 1937. Ironically WWII, which was the war that destroyed his PhD research, was the same war he ended up researching how to design magnetic and acoustic mines for the Admiralty Research Laboratory. After the war Crick wanted to go back to school and get his degree in a completely different subject, biology.

           

            In 1949 Crick started studying and researching at the Cavendish Laboratory in Cambridge where he met his future research partner James Watson in 1951. While doing his groundbreaking research with Watson on the unknown structure of DNA Crick was also working on his PhD, which he earned in 1954 from the University of Cambridge.

            Watson and Crick were able to determine that the DNA structure is a double helix by using X-ray diffraction studies of DNA, and announced this discovery on February 28^th 1953. Their hypothesis was that new identical strands could be formed from the splitting of the two sides of the double helix. This discovery led to the understanding of both replication of genes and chromosomes. If it had not been for previous DNA research, Watson and Crick’s discovery would not have been possible. Attached below is a link in order to find out more about the research that was used by Watson and Crick. In 1962 Crick was a co-winner of the Nobel Prize in Physiology or Medicine along with James Watson and Maurice Wilkins for their discovery of the double helix shape of DNA.

            Watson and Crick enlisted the help of Maurice Wilkins, who was colleagues with Rosalind Franklin. Franklin actually had a huge role in Watson and Crick’s discovery, but was not very well known for her help until after she passed away. She had written papers that were unpublished about the structure of DNA, and also took the famous Photo 51, which was her X-ray diffraction image of DNA. The reason Wilkins earned the Nobel Prize rather than Franklin was he provided the research that Franklin had to Watson and Crick without her knowledge.

            After his major discovery Crick went on to do quite a bit more research. Another important discovery he made was his explanation of “central dogma”. Central dogma is the flow of genetic information from DNA to RNA in order to make a protein. Also posted below is a link to learn more about central dogma. Another project he worked on was with a British chemist named Leslie Orgel where they figured out a process called directed panspermia.

Throughout his career Crick published many books and won numerous awards for his research. On July 28^th, 2004 Francis Crick died in La Jolla, California at the age of 88. Francis Crick was a major influence in the molecular biology field and paved the way for today’s DNA research.

http://www.nature.com/scitable/topicpage/discovery-of-dna-structure-and-function-watson-397

http://www.yourgenome.org/facts/what-is-the-central-dogma