Doctors and scientist use blood every day for research. For examples, they use blood in studies to help make medication or to even find cures. Doctors also use their patients’ blood to preform test to see if they have some sort of an affection or life-threating virus that is causing their patients to be sick. Reasons why doctors use blood for their test or research is because the human blood or any organisms blood is very complex because it has all sorts of pathogens, leukocytes (white blood cells), erythrocytes (red blood cells), and plenty of more types of cells or antibodies. Although doctors already know tons of information about the human body, more research is done every day. A lot of the research is done with our blood. Now with all
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While in Coleman’s study, she found the presence of SRSF2, SF3B1, U2AF1, ZRSR2, EZH2, BCOR, or STAG2 mutations in her patients with AML (1). Out of the 82 genes Coleman targeted it was those seven genes that stood out in over 95 percent of all patients with both types of AML. While Harrison found mutation in chromosome 21 (iAMP21) and found out that it had a great link to all patients with ALL and affected primarily they B-cells (2). Before all patients were treated with COG which showed improvement but when ALL patients where treated for the iAMP21 mutation it showed better improvement but not much (2). Coleman realized that with the mutations she found could actually be something that can either better off the treatments for patients with AML or maybe even cure it (1), while Harrison seen that the new mutation in the chromosome works better with treating patients with ALL then doctors using translocation t(12;21)(p13;q22)/ETV6-RUNX1 for the prognosis of ALL (2). With both of their finding and them seeing that the new mutations work a lot better with treatment by focusing on them instead of what doctors use to do can have a huge impact to help leukemia …show more content…
Goel just did not do his study on any one but only on people who have had platelet transfusion for their leukemia. Also the people he is studying got arterial thrombosis or died from the transfusion (4). Goel is trying to figure out a better way for this transfusion or why is it when people get it for leukemia they either get arterial thrombosis or die. There has been reported 10,624 people put in hospital after the transfusion with TTP. There are all different types of thrombosis’s he looked at to see which where affected the most. There is thrombotic thrombocytopenic purpura (TTP), heparin-induced thrombocytopenia (HIT) and immune thrombocytopenic purpura (ITP) (4). Those different types of thrombosis had different effects on patients with platelet transfusion for leukemia. Some where worse then others. With TTP and HIT there was reported more arterial thrombosis and mortality, while there wasn’t “no associations were significant for ITP” (4). After transfusions most patients had ITP calculating at “66.6” percent (4).
Overall
With Yanez and Goel information, they are able to do future research and can find out why with the certain cells (neutrophils, monocytes and platelets) are a huge part dealing with leukemia patients.
While in Coleman’s study, she found the presence of SRSF2, SF3B1, U2AF1, ZRSR2, EZH2, BCOR, or STAG2 mutations in her patients with AML (1). Out of the 82 genes Coleman targeted it was those seven genes that stood out in over 95 percent of all patients with both types of AML. While Harrison found mutation in chromosome 21 (iAMP21) and found out that it had a great link to all patients with ALL and affected primarily they B-cells (2). Before all patients were treated with COG which showed improvement but when ALL patients where treated for the iAMP21 mutation it showed better improvement but not much (2). Coleman realized that with the mutations she found could actually be something that can either better off the treatments for patients with AML or maybe even cure it (1), while Harrison seen that the new mutation in the chromosome works better with treating patients with ALL then doctors using translocation t(12;21)(p13;q22)/ETV6-RUNX1 for the prognosis of ALL (2). With both of their finding and them seeing that the new mutations work a lot better with treatment by focusing on them instead of what doctors use to do can have a huge impact to help leukemia …show more content…
Goel just did not do his study on any one but only on people who have had platelet transfusion for their leukemia. Also the people he is studying got arterial thrombosis or died from the transfusion (4). Goel is trying to figure out a better way for this transfusion or why is it when people get it for leukemia they either get arterial thrombosis or die. There has been reported 10,624 people put in hospital after the transfusion with TTP. There are all different types of thrombosis’s he looked at to see which where affected the most. There is thrombotic thrombocytopenic purpura (TTP), heparin-induced thrombocytopenia (HIT) and immune thrombocytopenic purpura (ITP) (4). Those different types of thrombosis had different effects on patients with platelet transfusion for leukemia. Some where worse then others. With TTP and HIT there was reported more arterial thrombosis and mortality, while there wasn’t “no associations were significant for ITP” (4). After transfusions most patients had ITP calculating at “66.6” percent (4).
Overall
With Yanez and Goel information, they are able to do future research and can find out why with the certain cells (neutrophils, monocytes and platelets) are a huge part dealing with leukemia patients.