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Hematological Malignancies - Science topic

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Blood cancer is a very dangerous disease. Blood can circulate to all parts of the body. Blood cells are generated in the bone marrow. So I decided that I work on both blood and bone cancer and collectively hybrid cancer. I need data set of both of these types of blood cancer collectively or separately. I want to research the base of genes by the use of Artificial Neural Networks
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It is not the right choice. You need to work on blood cancer and bone cancer separately.
The bone is made up of compact bone, spongy bone, and bone marrow. Compact bone makes up the outer layer of the bone. Spongy bone is found mostly at the ends of bones and contains red marrow. Bone marrow is found in the center of most bones and is the soft, spongy tissue that has many blood vessels. There are two types of bone marrow: red and yellow. Red bone marrow contains blood stem cells that can become red blood cells, white blood cells, or platelets. Bone marrow makes nearly all the components of your blood responsible for creating billions of red blood cells daily, along with white blood cells and platelets. Bone marrow also stores fat that turns into energy as needed.
A blood cancer is a disease in which abnormal blood cells reproduce rapidly and begin interfering with the body’s usual operations. Cancers of this type originate in the bone marrow, where red blood cells, white blood cells, and platelets are produced. There are three primary blood cancers: leukemia, lymphoma, and myeloma.
You may refer to the article below for the genes related to hematologic malignancies.
On the other hand, bone cancer is an uncommon type of cancer that begins when cells in the bone start to grow out of control. The cause of most bone cancers is unknown. A small number of bone cancers have been linked to hereditary factors, while others are related to previous radiation exposure. Primary bone cancer is cancer that forms in cells of the bone. Some types of primary bone cancer are osteosarcoma, Ewing sarcoma, malignant fibrous histiocytoma, and chondrosarcoma. Secondary bone cancer is cancer that spreads to the bone from another part of the body (such as the prostate, breast, or lung).
You may refer to the article below which has summarized the whole genome and/or whole exome genomic studies and placing these findings in the context of genetic hallmarks of somatic mutations and mutational processes in human osteosarcoma.
In the following paper, the authors go on to enumerate the genetic and epigenetic defects identified in osteosarcoma.
Best.
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I want to base my research on some procedures of reducing the cost of the treatment of blood cancer. Discussing this with intellects will greatly appreciated
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There was a time bone marrow transplant, especially allogeneic, used to be very expensive compared the conventional chemotherapy. But those days are, regrettably, gone. Most of the recent anti-leukaemia/lymphoma/myeloma treatments ('targeted therapies') are so expensive that the BMT looks relatively cheap (especially autologous). If you really want to explore economical treatment options, you may have to either (1) use conventional drugs (most of them cost a fraction of the new ones) or (2) use drugs that are out of patent. Generic formulations are considerably cheaper.
Remember, not all the new 'wonder drugs' are not so wonderful as the drug companies claim. Some of them offer few months of response at a cost of tens of thousands of dollars.
Good luck
Siva
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This 15 years old guy presented with left scapular mass 3 years ago , labeled as ewing sarcmoma. He was treated with 14 cession of Ifosfamide- base chemotherapy as well as involved field radiation. However, he developed multiple bone metastasis so the protocol shifted to irrinotecane+vincristine and then gemcitabine+ decetaxel due to stable disease. Despite 4 courses of GemDox protocol his bone metastasis have remained unchanged. what do you advise next for this poor guy?
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More clinical data than those described here should be considered, but there are records of a low 5-year survival in patients with multiple therapy who do not respond to treatment. That is, it is an advanced disease that leaves the patient without conditions for surgery.
A treatment based on high-dose methotrexate alternated with ifosfamide is an option, but the odds are not favorable and you may fall into therapeutic obstinacy, therefore in some cases, a treatment that limits pain has been chosen, a treatment focused on palliative care and the proximity of care with the family.
Rodrigo Gómez Ayala
E. Borrego-Paredesa,∗, E. Prada-Chamorro et.al. (2017) Sarcoma de Ewing, análisis de supervivencia a los 6 años con terapia multidisciplinar. Revista española de cirugía ortopédica y traumatología, ISSN 1888-4415, Vol. 63, Nº. 2, 2019, págs. 86-94
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What are the best functional analyses to prove the pro tumor activity of human neutrophils after isolation from patients with hematological malignancies? We are considering assays to detect Arginase 1, ROS-production or performing co-cultures with autologous t-cells, but thus far have not found any common functional criteria for classification.
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I want to prove tumor-promoting activity of neutrophils as previously described in N2-polarized TANs. I found this area of research to be very heterogenous and yet without any common standards for functional assays- unlike in MDSC. So I was wondering whether somebody maybe had any suggestions or references.
Cheers
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I need to recent protocols for bone marrow and peripheral blood culture to perform chromosomal karyotyping analysis in each type of Hematologic malignancies, Can someone help me and send them to me?
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For the care of Prof.Mona
@Mona Ellaithi
Regards
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categorical value (not images)
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I have several publications on acute and chronic leukemias as well as on hematological diseases including hematological malignancies. You can read them at my profile
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Hello everyone! For doing a research I need a dataset including blood cell images of Leukemia (blood cancer) based on leukocytes. There's one dataset "ALL-IDB1" used by Dr. Fabio Scotti in his paper but unfortunately I couldn't get access. Kindly help or guide me if you have a suggestion, thanks!
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leukemia
I think the best reference in hematology malignancies professor Barbara.
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Hi colleagues;
my review subject is "A review on CAR T-Cells recent progresses in hematological malignancies and solid tumors".
my preference can be journals with good impact factor which do open access and take no charges for publications.
Thank you
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Well.. it will depend on the type and quality of your review. It has to be really good to publish in Blood, British Journal of Haematology, Haematologia, Blood Reviews and other high calibre journals. If I were you, I would first do a literature search (eg PubMed) and find out the journals that haven't published a review article on this subject recently.
Good luck
Siva
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I am about to isolate CD138+ plasma cells using a Miltenyi Biotec MACS kit from the PBMCs of healthy donors.
Although I know that circulating plasma cells are scarce in normal individuals, I need to isolate them to use as control for primary malignant plasma cells that I am working on.
So, I need to know if I can successfully isolate plasma cells from peripheral blood of healthy individuals and the possible yields.
Thank you in advance!
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In normal person detection of plasma cell as an reactive cell especially in infective or inflammatory process is possible
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Researches claimed that this blood is more efficient for medical use than blood collected from donors. Patients with rare blood types will benefit the most.
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The term "Artificial blood" is a misnomers and can't be prepared in laboratory. There is a limitation of stem cells culture in vitro and component in whole blood is much more complex.
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It seems to be very hard to locate the impact factor for The Journal Article, Efficacy and Safety of micafungin versus intravenous itraconazole as empirical anti fungal therapy for febrile neutropenic patients with hematological malignancies: a randomized, controlled, prospective, multi-center study.
Is there a specific source I could utilize to help me find this?
Thanks!
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As mentioned in the previous answers journals have impact factors and papers do not. This paper was published in a journal with an impact factor of 3.083.
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I would like to start with rare mutation detection with ddPCR and I have to deal with a problem of positive control. How can I prepare positive control with certain mutation when I am working with human blood cancer samples? I am looking for rare mutation but I dont have samples with that mutaion in every cell.. Thank you for your advice.
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Hi Monika,
Companies such as IDT can provide modified gene fragments. You can design a fragment with the rare mutation as the positive control, you can also have a WT fragment as a reference and mix these two at different concentrations, so you can test the LOD (limit of detection).
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I would specifically like to culture Type 3 Innate Lymphoid Cells
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Did you succeed to culture innate lymphoid cells in vitro ?
How did you do it and what culture medium did you use?
Thanks for you answer
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I was wondering why the skin colour turns black in dry gangrene ?
Arterial occlusion means there is no blood or minimal blood supply - thus why the skin turns black ?
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Dear Qureshi , as you know skin epidermis has no blood supply and takes oxygen and nutrition from superficial papillary dermal plexus, so in dry gangrene epidermis get dry as no perfusion from dermis, here melanosomes that injected from melanocytes in keratinocytes get dry too which stain epidermis black.
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I recently submitted my research for publication on Comparative therapies in AML. Although a different blood cancer than CML, it was concluded that there were no differences seen between the therapies in prognosis of AML. I was wondering if similar results can be seen in CML. 
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 Based on our experience in the molecular monitoring of CML patients treated with 1st or 2nd generation TKI, the adherence to the treatment correlates with changes of bcr-abl transcript leves and in some instances we can predict whether a patient has stopped treatment by the increase pattern of transcripts level in sequential samples. 
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Hello!
How frequently a blood test (CBC count) should be done in people with various leukemia (ALL, AML, CLL, CML) at remission "to catch up a relapse"? How early in leukemia's manifestation/relapse the WBC anomalies appear?
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Very important practical questions. As to the question of frequency of testing, the answer would be 'depending on the blood counts'. If a patient's blood counts have recovered fully, there is no need to repeat them too frequently. The standard practice is to start repeating weekly and then fortnightly and then gradually reducing the frequency (two monthly, three monthly... and so on). The important thing is the stability of the counts- ie if there is a change in any of the cellular parameters, the frequency of testing should be increased.
The answer to your second question is 'extremely variable and unpredictable and will depend on several factors that are unique to each disease category( and any associated prognostic factor(s). Just to give you one example, a young patient with common ALL with no adverse prognostic markers may enjoy a long period of remission. On the other hand, an elderly patient with Philadelphia chromosome positive ALL, the situation will be different. So the bottom line is  'one cannot have a uniform policy for all disease categories in all the patients. Should be patient specific. Hope that makes sense. Best wishes.
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Pronotn& technology will be valuble for anmeia.
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HemaApp measures hemoglobin levels and screens for anemia non-invasively by illuminating the patient’s finger with a smartphone’s camera flash.
                                                                          OR
ToucHb is a completely non-invasive (no blood!), portable, instant and cost-effective (affordable!) hemoglobin screening device to diagnose and monitor anemia in rural areas in developing countries.
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What is Your experience with sticky platelet syndrome (SPS) ?
SPS, characterized by platelet hyperaggregability has been identified as cause of 21% cases of unexplained arterial and 13,2% of unexplained venous thrombosis.
Do You treat patients with aspirin in first line and clopidogrel as second line treatment, or do You preffer different approach?
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Dear Peter Kubisz, we do evaluate the patients for thrombophilia which also includes ruling out other causes of thromboses( factor 5 maiden, thrombomodulin gene mutation, Anticardiolipin ab, factor deficiencies etc)We do follow the protocol usually. 
However , in arterial thromboses ( after opening of the artery either surgically or thrombolysis) we use continuous infusion of heparin initially, followed by oral anticoagulants. If a patient does not respond to warfarin I shift to dabigatran / or other recent congeners. If I am not able to find the cause for arterial thromboses ,the patient has to be on life long anticoagulants and only on anti platelets for venous thromboses. However if there is recurrence of thromboses on anti platelets in the latter , we shift the pt to  oral anticoagulatants.
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There was a phase-2 trial by Roussel et.al in Blood 2010
[Bortezomib and high-dose melphalan as conditioning regimen before autologous stem cell transplantation in patients with de novo multiple myeloma: a phase 2 study of the Intergroupe Francophone du Myelome (IFM) ]
which showed CR was higher if velcade was added. But I couldn't find any data on long term outcomes. Is there any data on this? 
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Little evidence of added efficacy at this point.
Would be surprising that 1-2 Bortezomib doses would add efficacy over many previous doses pre-transplant + high-dose melphalan.
Randomized trial ongoing at IFM.
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Dear colleagues , what is your recommendation for a aml young male primary refractory despite salvage regimen with an full match donor.
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The regimen suggested by Dr. Romon is good providing you have access to amsacrine. If that is a problem, you can use CLAG-M regimen and take the patient to an allogeneic HSCT afterwards. I have seen good results with this regimen.
Cladribine (2-CdA) 5 mg/m2/d iv over 2 hrs d1-5
Cytarabine (Ara-C) 2 g/m2/d iv over 4 hrs starting 2 hrs after cladribine d1-5
Mitoxantrone (Novantrone) 10 mg/m2/d iv d1-3
Filgrastim (Neupogen) 300 mcg sc d0-5 
Wierzbowska A et al. Cladribine combined with high doses of arabinoside cytosine, mitoxantrone, and G-CSF (CLAG-M) is a highly effective salvage regimen in patients with refractory and relapsed acute myeloid leukemia of the poor risk: a final report of the Polish Adult Leukemia Group. Eur J Haematol 2008; 80:115
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How I can evaluate patients whom at high risk to get leukemia, , I'm asking about lab technique by which I can expect if patients at risk to be leukemic?
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You are welcome and best of luck.
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I have a patient with relapsed t-ALL after allogeneic hematopietic stem cell transplantation (AHSCT). She had received hyper-CVAD, Nelarabine, ICE and PEG-Asparaginase before we performed AHSCT for her. She presented with axillary and inguinal lymphadenopathy about day +45 after AHSCT, and lymph node core biopsy showed t-ALL. I have started an accelerated tapering of her Prograf, and I would like to administer chemotherapy before giving donor lymphocyte infusion (DLI) to her.
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Was the transplant performed in CR? If not, I'm afraid your (her) case is quite bad. Even if you performed the transplant in CR, the prognosis is terrible. 
The experience of a second allo after early relapse is usually bad, unless your patient is very young and very fit and you perforded a RIC transplant. You can add toxicity witout actually doing anything of consequence.
I tink you have done the best you can. As the comment above points out, the best would be to try new drugs that aren't too agressive. Clofarabine or even gemcitabine i associtation with other drugs  could be of help. If you achieve some kind of remission, then you can plan other things.
Besides, I'd inform the patient of her ominous situation. 
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Please let me know of methods & protocols required for the isolation of pure individual subsets of lymphocytes like B,T,NK & Plasma Cells from lymphocytes of blood. Isolation of Lymphocytes from blood is easy but how to further isolate its subtypes. Please suggest some protocols for that. Thank You.
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Sorry for writing this, but there is enough literature out there that gives you ideas. Just google cell separation.
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During anticancer chemotherapy, which usually involves DNA alkylating or intercalating agents, the patients become at higher risk of infection due to reduction of the WBC count, and damage to physical barrier. So, it is likely for the patient to easily get infected, specially in leukemia. Why the DNA acting antineoplastic drugs don't protect him from bacterial and fungal infection, why they don't act on the DNA of these microbes as they act on human cells.
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Several antineoplastic agents do have antimicrobial effect. See for instance this article below. That the drugs lack clinical significance as antimicrobials can have many explanations the most obvious being that at the time of highest infection risk the drugs have already been excreted,
J Clin Pathol. 1993 Dec; 46(12): 1124–1125.
PMCID: PMC501725
Antimicrobial activity of cytotoxic drugs may influence isolation of bacteria and fungi from blood cultures.
V Peiris and B A Oppenheim
Abstract
The potential antimicrobial activity of cyclophosphamide, vincristine, and adriamycin against Gram positive and negative bacteria and Candida albicans was examined. The time taken for different microbial inocula to turn a simulated blood culture positive in the presence of different concentrations of these drugs was measured. Doxorubicin retarded the growth of Staphylococcus aureus, Staphylococcus epidermidis, and Streptococcus sanguis in a concentration dependent manner. Cyclophosphamide and vincristine showed minimal antimicrobial activity. Escherichia coli and Pseudomonas aeruginosa were unaffected by any of the drugs. An inoculum dependent effect was seen with some combinations of microbial inocula and cytotoxic drug concentrations.
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Hematological reference values, is the measurement of majority normal individuals. 
In medical labs, we consider that as a (reference) value to measure the abnormality.
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The production of health-associated reference values and the subsequent estimation of the reference interval for a given analyte must be carried out in accordance with a well-defined protocol. This involves following a sequence of operations as outlined here. This outline should be applied when establishing
reference values for a new analyte, for a different group of individuals, or for a new analytical method with improved analytical sensitivity and specificity for a previously measured analyte:
(1) Establish a list of analytical interferences and sources of biological variability from medical and scientific literature (in the case of a totally new analyte, the literature may not be helpful, which necessitates a new laboratory investigation of these matters).
(2) Establish selection (or exclusion) and partition criteria and an appropriate questionnaire designed to reveal these criteria in the potential reference individuals.
(3) Execute an appropriate written consent form for participation in the reference interval study and have the reference individual complete the questionnaire.
Even though performing a reference interval study is not—strictly speaking research, questionnaires, consent forms, and even the nature of the exercise may need to be reviewed by the institution’s Internal Review Board or Human Subjects Committee. Laboratories are urged to familiarize themselves with their local policies.
(4) Categorize the potential reference individuals based on the questionnaire findings and results of other appropriate health assessments.
(5) Exclude individuals from the reference sample group based on the exclusion criteria or other assessments indicating a lack of good health.
(6) Decide on an appropriate number of reference individuals in consideration of desired confidence limits.
(7) Prepare, properly and consistently, the selected persons for specimen collection for the measurement of a given analyte consistent with the routine practice for patients.
(8) Collect and handle the biological specimens properly and in a manner consistent with the routine practice for patient specimens.
(9) Collect the reference values by analyzing the specimens according to the respective analytical methodology under well-defined conditions and consistent with the routine practice for patient specimens.
(10) Inspect the reference value data and prepare a histogram to evaluate the distribution of data.
(11) Identify possible data errors and/or outliers.
(12) Analyze the reference values, ie, select a method of estimation and estimate reference limits and the reference interval (include partitioning into subclasses for separate reference intervals, if appropriate).
(13) Document all of the previously mentioned steps and procedures.
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Is anyone aware of similar papers or data discussing an increased risk of hematologic malignancies and radiation exposure among interventional radiologists, cardiologists, neuro interventionlists, electrophysiologists, vascular surgeons, or other health care professionals with frequent exposure to radiation in the angiography suite?
Also is anyone aware of any current or pending litigation regarding this possible increased risk, especially in light of recent evidence of premature cataract formation in Interventional cardiologists and Interventional radiologists as well as the rapid transition from a self employed or group physician model to an employee model /integrated health care system /vertical integration?
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there are lots of relevant data--possible the best summary can be found by reviewing the classic teaching text by Eric Hall from Coilumbia--"Radiobiology for the Radiologist". You could then do a quickie lit search by combining "..Radiologist  with Cancer..." on a Google search platform or equivalent.
Roger M. Macklis, MD
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and what is the difference between Tigecycline and other Tetracycline?
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Have alook at: Use of tigecycline for the treatment of prolonged bacteremia due to a multiresistant VIM-1 and SHV-12 beta--lactamase-producing Klebsiella pneumoniae epidemic clone.
Cobo J, Morosini MI, Pintado V, Tato M, Samaranch N, Baquero F, Cantón R.
Diagn Microbiol Infect Dis. 2008 Mar; 60(3):319-22. Epub 2007 Nov 9
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Do you think it is safe and non-toxic?
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There is a good publication on Augmented Hyper-CVAD that combines Hyper-CVAD with Peg-Aps (and much more steroids than classical Hyper-CVAD). This is associated with toxicities (mainly sepsis/necrotising fascitis!). We at SQUH Oman usu the classical Hyper-CVAD augmented with Peg-Aps (2500 units/m2 I.V.) on Day 1 of A  part and Day 5 of B part and i think it is of major benefit based on previous studies assessing the addition of peg asp to a number of protocols. 
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Your answer indicates that SCF might be involved
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Please let me know the simplest method for best results.
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thalassemia can be classified into alpha and beta in Middle East is more prevalent  the first step is to take red cell indices .if MCV is below normal proceed to Hb electrophoresis if HbA2 more than 3.6 percent 
the person is carrier and should be careful if he got marrie
carrier female beca
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I am testing translocation of protein from the cytoplasm to the nucleus, I've got a lot of background nuclear fluorescence despite that I used 0.3M glycine in the blocking buffer.
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Decrease your secondary concentration by half and increase your wash times 30%. Also consider using a high quality anti-fade - it seems kind of backwards to add something to increase your fluorescence but my experience is that it seems to just increase the integrity of target signals and lower background. Be sure your using fresh PFA and your sells are not contaminated too. If there's myco on the slide is bleaches out everything and actually causes background in other (non-myco) areas to increase.
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Concerning (mono-)clonal B-cell lymphocytosis with a lymphoma fenotype: from a research perspective, would it not be necessary to perform a bone marrow biopsy in order to exclude lymphoplasmacytic lymphoma? The MYD88 L265P mutation is closely related but does not exclude all cases of LPL.
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Performing a bone marrow biopsy will be very important to detemine the grade of infiltration as well as to evaluate the presence of reticulin fibrosis. If you have cytopenias in peripheral blood it will also provide you information about red cells, leukocytes and platelets precursors.
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Erythrocyte microRNA in MDS?
Does anyone know or is there any study which microRNAs might occur as overexpresed in erythrocyte in some supgroup of myelodysplastic syndrome?
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Dear Ondrej
Please see this reference
Leukemia. 2012 Jan;26(1):13-22. doi: 10.1038/leu.2011.221. Epub 2011 Aug 19.
Deregulation of microRNAs in myelodysplastic syndrome.
Rhyasen GW1, Starczynowski DT.
Author information
Abstract
Myelodysplastic syndromes (MDSs) consist of a family of hematopoietic stem cell (HSC) disorders characterized by ineffective differentiation of hematopoietic progenitors, bone marrow dysplasia, genetic instability and a propensity to develop acute myeloid leukemia. The development of MDS is poorly understood and therefore, effective treatment options are limited. Recent progress has been made in identifying altered signaling pathways and understanding the HSC defects, which are thought to contribute to the pathogenesis of MDS. Several of these findings have implicated aberrant expression and function of microRNAs (miRNAs). Unique miRNA expression patterns have been identified in MDS patients and modeled in mice to recapitulate features of MDS. Here, we review miRNA expression profiles identified in MDS patients, and describe the association of miRNA expression with MDS subtypes and disease outcome, clinical implications of miRNAs in MDS and deregulation of miRNAs in mouse model systems of MDS.
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Normally MTT assay is used for evaluating the anticancer activity of synthesize compounds. How much MTT is reliable?
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The MTT assay measures the ability of cells to reduce the tetrazolium dye, MTT, to its insoluble formazan, resulting in a purple color. Since this requires a functioning mitochondria, the MTT effectively measures the metabolic activity of live cells. It is quick, cheap, easy to perform and relatively reliable. This is why it is used for drug screening.
However, there are some caveats. First, you must ensure that you are measuring activity at the most active part of the cells growth phase, which means you should do a growth curve optimization for your cells prior to doing any drug screening. Also, this is an absorbance-based assay which means it is not very sensitive at picking out minor changes. And, most importantly, it measures metabolic activity, not necessarily viability. Some cells can be perfectly viable but not necessarily with a lot of metabolic activity. So it is always important to validate your results using something that directly measures cell apoptosis and/or necrosis.
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List of N-Ras mutant cells....
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If you use the download function you get all the data and can import them into Excel. e.g. File:CosmicCellLineProject_v65_280513.tsv.gz
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The standard of care is Cytarabine + Daunorubicin
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AML de novo is different from AML from previous hematologic disease ie. MDS, PV, TE or myelofibrosis, secondary post chemo or RT for other malignancies, or in elderly when response can go from 70-80% down to 20 to 30%. Identification or personalized approach can show good prognosis in Inversion 16 chromosome, t(7;21), or molecular markers like NPM1 or CeBPa with normal cytogenetics. Multiple complex chromosome of FLT3ITD mutations identify bad ones.