Oncology - Science topic
Oncology is concerned with the diagnosis of any cancer in a person; cancer therapy; follow-up of cancer patients after successful treatment; palliative care of patients with terminal malignancies; ethical questions surrounding cancer care; as well as screening efforts of populations, or of the relatives of patients (in types of cancer that are thought to have a hereditary basis, such as breast cancer).
Questions related to Oncology
A patient with desminopathy (mutation Thr341Pro DES in a heterozygous state) with the progression of the disease has a decrease in taste and smell, immunosuppression, and an increase in IgA in the blood.
Oddly enough, but all this is characteristic of infections, including viral ones. For example, it is known that if the hepatitis C virus is not treated, then death will occur in 20 years.
In the identified case of late onset desminopathy, muscle weakness manifests itself at the age of 30, and death occurs 20 years after the onset of the disease.
Could the desmin mutation in myofibrillar myopathy be caused by an infection?
Perhaps the infection contributes to the progression of desminopathy?
All tumors have DNA mutations, and a predictive understanding of those mutations could inform clinical treatments. However, 40% of the mutations are variants of unknown significance (VUS). So the challenge is to objectively predict whether a VUS is pathogenic and supports the tumor or whether it is benign. We are working on this problem and would welcome feedback on our efforts (see doi: 10.3389/fmolb.2021.791792 ) and also alternative ideas and insight.
Updated Dec 26th 2021 as I know have some publications of relevance to Lenalidomide. Top of my list are  and  at the moment they are most recent publications I have found.
 BLOOD SPOTLIGHT| NOVEMBER 19, 2015
The novel mechanism of lenalidomide activity
Blood (2015) 126 (21): 2366–2369.
" Given lenalidomide’s mechanism of action, it is intriguing that IMiDs and proteasome inhibitors are synergistic in the treatment of multiple myeloma.(24) Recent evidence suggests that this synergy may result from the pharmacokinetic properties and dosing schedules of these drugs. Although treatment with proteasome inhibitors can block lenalidomide induced degradation of IKZF1 and IKZF3 in vitro,(14) this effect depends on both the order of administration and the dose. When the drugs are administered at the same time, lenalidomide-induced degradation occurs before the onset of proteasomal blockade. (25) " excerpt from  above.
First published: 13 February 2017
 Lenalidomide use in myelodysplastic syndromes: Insights into the biologic mechanisms and clinical applications
Maximilian Stahl MD,Amer M. Zeidan MBBS, MHS https://doi.org/10.1002/cncr.30585
" In this article, we review the recently recognized mechanisms of action of lenalidomide and discuss the most recent clinical data regarding its use in patients with both 5q− MDS as well as non-5q− MDS. " excerpt from  above.
Some additional references for background. Core Concept: Emerging science of chronotherapy offers big opportunities to optimize drug delivery https://lnkd.in/gpAz-28v
Optimizing circadian drug infusion schedules towards personalized cancer chronotherapy
Hill RJW, Innominato PF, Le´vi F, Ballesta A (2020) PLoS Comput Biol 16(1): e1007218. https://lnkd.in/gnCAAzk5 https://lnkd.in/g4sY-NDv
Temporal regulation of tumor growth in nocturnal mammals: In vivo studies and chemotherapeutical potential
The FASEB Journal. 2021;35:e21231.First published: 11 January 2021 https://lnkd.in/gm9mr6z
Paula M. Wagner,César G. Prucca,Fabiola N. Velazquez,Lucas G. Sosa Alderete,Beatriz L. Caputto,Mario E. Guido
Harnessing the predictive power of preclinical models for oncology drug development.
Honkala, A., Malhotra, S.V., Kummar, S. et al. Nat Rev Drug Discov (2021). https://lnkd.in/gYnT7VtF
Metabolic rewiring and epigenetic remodeling, which are closely linked and reciprocally regulate each other, are among the well-known cancer hallmarks. Studies have reported use of Onco-metabolites to metabolically reprogram the epigenetic of cancer. I was wondering what might be major limitations of such techniques?
For example AI can automate processes in the initial interpretation of images and shift the clinical workflow of radiographic detection, management decisions. But what are the clinical challenges for its application?
#AI #cancer #clinical #oncology #biomedical
I'm doing a survey as part of an Audacious program (https://www.startupdunedin.nz/audacious), which essentially is a StartUp initiative at Otago University. I'm curious to understand what level of programming do biologists these days need during their day to day research.
For all the biologists out there here are some questions to start the discussion on this topic:
1) Have you done any programming till date? If so which language did you use and for what purpose?
2) How have to overcome programming limitations? For example, did you get the work done through bioinformaticians, or sought help from your programming friend, etc?
3) Have you used online biological databases for your research? If so, which one?
4) How much of artificial intelligence have you used in your research? Do you see AI potential in your current work?
If you have anything else to add, please feel free.
What do you think is the best programming language for cancer informatics for a beginner?
I have found some recommendations for Python, R, MySql, PHP, and Perl, yet as a novice in informatics I couldn't reach a clear conclusion.
I have obtained the mean for each of 10 domains for the CarGoQol scale as instructed. Then I calculated an Index score by summing the mean of of all 10 domains and dividing it by 10. The scoring procedure outlines I now need to linearly transform and standardize the domain and index scores on a scale of 0 to 100. How do I do that? Please help!
I have 3 group populations.
Group A has marked nuclear pleomorphism (change in nuclear shape and size), like 1 um, 4um, 2 um, 4um, 6um, 1um, 3um. etc
Group B has also nuclear pleomorphism but not as wide of change as group A
Group C the control group has consistent nuclear size of say 1um for example
I would like to use a stat test to evaluate
1. how significantly different are the groups based on rate of differences
Here are my ideas:
T test probably wont help
I can use clustering analysis
I can do regression analysis
Confidence intervals to show spread of values?
Would ANOVA work?
I just want to visualize and get a P value that these three groups can be different based on variance/change.
Goal is to establish diagnostic criteria based on nuclear size cut offs of either length, width, and circumference of nuclei.
end goal is like 1um - 4um = Grade 1 , 4 - 5um = Grade 2, >6 um = grade 3 and to correlate it to progression free survival.
I’m conducting a meta analysis for my dissertation and have issues running my data. It utilises median overall survival (months) and does not have usable controls. I’m counteracting that by using a second treatment method fir comparison. I’ve noticed some studies use historic controls, and form hazard ratios from them. Is it possible to treat the secondary treatment as a historic control and form hazard ratios across studies?
Otherwise single arm survival studies are awful to try and run analysis on. (Oncology is a pain).
Please find attached the full medical file of our patient and all biological reseaults included.
We are seeking to explain how can she produce such levels of immunoglobulins with no B cells expression.
NB ! : * The patient ddidn't recieve any immunoglobulins injection.
* We made another dosage for immunoglobulins levels after 01 moth of the first one and we had the same resault ( high levels ).
Possibily not an open access journal which does not add any publishing costs once being accepted. Thank you in advance
SV40 is not considered an oncogenic virus in this review:
Article Oncogenic viruses and cancer
Why is SV40 not considered an oncogenic virus when it produces the large T antigen, which is used to immortalize mammalian cell lines?
Additionally, SV40 proteins have been found in human tumors.
Could this lack of coverage possibly have something to do with the fact that the polio vaccine introduced SV40 into the human population in the late 1950’s? How many people are actually positive for SV40 proteins? How many of these people develop cancer? Why are SV40 proteins not tested for regularly, given that they are an indicator of cancer?
For any no-relapse cancer gene therapy, all cancer cells need to be transfected. Is it possible? Will repeated administration be able to reach all cancer cells? I know different serotypes viral vectors must be used for repeated administration to evade antibody response, but let's not focus on little details. I want to know if its fundamentally possible? Cancer cells have mutated antigens that viruses use to get in, so there can be resistance. Perhaps repeated non-viral transfection in-vivo? What do you think? If not, then why can't repeated transfection reach every cancer cell? It seems to me that due to minuscule size of vectors, spatial availability in-vivo isn't the issue. What do you think?
without allowing our study be reduced to just rubber stamping of other people's findings. How do we ensure critical rather a mere descriptive discourse ?
What are the tips to highlight the originality of the research project?
Global spotlight is on 2020 Nobel prizes which is slated to commence today, Monday October 5, 2020. Many researchers have been mentioned and nominated in various capacities for their discoveries such as;
1. American Mary-Claire King, who discovered the BRCA1 gene responsible for a hereditary form of breast cancer.
2. The duo of Emmanuelle Charpentier of France and Jennifer Doudna of the US, for their gene-editing technique, the CRISPR-Cas9 DNA snipping tool, a type of genetic “scissors” in cutting mutated gene, and for insertion of a corrected manipulated one.
3. Dennis Slamon, American oncologist for research on breast cancer and the drug treatment Herceptin.
4. Leroy Hood, US gene sequencing pioneer.
5. And host of others.
Not only limited to medicine, in any field, who do you have in mind for his/her discovery roles in the past few years?
A study by Peeters et al. (2017) suggests that sugar traps cancer in a 'vicious cycle' which make it more aggressive and harder to treat (1). On the question-and-answer site Quora, Ray Schilling, MD, concludes: "there is a connection between the consumption of sugar and starchy foods and various cancers in man. Animal experiments are useful in suggesting these connections, but many clinical trials including the Women’s Health Initiative have shown that these findings are also true in humans. It is insulin resistance due to sugar and starch overconsumption that is causing cancer" (2).
1. Peeters K, Van Leemputte F, Fischer B, Bonini BM, Quezada H, Tsytlonok M, Haesen D, Vanthienen W, Bernardes N, Gonzalez-Blas CB, Janssens V, Tompa P, Versées W, Thevelein JM. Fructose-1,6-bisphosphate couples glycolytic flux to activation of Ras. Nat Commun 2017; 8: 922. doi: 10.1038/s41467-017-01019-z. https://www.nature.com/articles/s41467-017-01019-z.pdf
2. Schilling R. Why isn't sugar portrayed as bad like cigarettes? https://www.quora.com/Why-isnt-sugar-portrayed-as-bad-like-cigarettes
I am investigating new therapeutic approaches to treat Glioblastoma. By testing my approach, I found that in one mouse model the data are promising. However, I am looking for validating my data. I would like to re-do the experiment using a different mouse model for the same disease.
I know that the best is to test the treatment approaches on two different mouse models (two independent experiments each) However, due to running out from the funding and time I must choose between two options.
Either using one mouse model (two independent experiments) or two mouse models (one independent experiment each).
Let me know what do you think?
Thanks a lot
COVID-19 has pull people apart from each other. Social distancing is the main way to prevent spreading of infection. Tele-medicine, once used for rural area remote healthcare model, is the emerging new way of practice under COVID-19.
Different specialties have different practicing needs, what difficulties do you encounter on applying tele-medicine under COVID-19 in your specialty? Will tele-medicine totally uproot the usual face-to-face room consultation of medical practitioners? And becoming the new service model?
What is your view?
Virtually Perfect? Telemedicine for Covid-19
Covid-19 and Health Care’s Digital Revolution
Telemedicine in the Era of COVID-19
The Journal of Allergy and Clinical Immunology: In Practice
Keep Calm and Log On: Telemedicine for COVID-19 Pandemic Response.
‘Healing at a distance’—telemedicine and COVID-19
Public Money & Management
The Role of Telehealth in Reducing the Mental Health Burden from COVID-19
Telemedicine and e-Health
Respiratory infections can be transmitted through droplets of different sizes: when the droplet particles are >5-10 μm in diameter they are referred to as respiratory droplets, and when then are <5μm in diameter, they are referred to as droplet nuclei. According to current evidence, COVID-19 virus is primarily transmitted between people through respiratory droplets and contact routes.2-7 In an analysis of 75,465 COVID-19 cases in China, airborne transmission was not reported.
Droplet transmission occurs when a person is in in close contact (within 1 m) with someone who has respiratory symptoms (e.g., coughing or sneezing) and is therefore at risk of having his/her mucosae (mouth and nose) or conjunctiva (eyes) exposed to potentially infective respiratory droplets. Transmission may also occur through fomites in the immediate environment around the infected person. Therefore, transmission of the COVID-19 virus can occur by direct contact with infected people and indirect contact with surfaces in the immediate environment or with objects used on the infected person (e.g., stethoscope or thermometer).
Airborne transmission is different from droplet transmission as it refers to the presence of microbes within droplet nuclei, which are generally considered to be particles <5μm in diameter, can remain in the air for long periods of time and be transmitted to others over distances greater than 1 m.
In the context of COVID-19, airborne transmission may be possible in specific circumstances and settings in which procedures or support treatments that generate aerosols are performed; i.e., endotracheal intubation, bronchoscopy, open suctioning, administration of nebulized treatment, manual ventilation before intubation, turning the patient to the prone position, disconnecting the patient from the ventilator, non-invasive positive-pressure ventilation, tracheostomy, and cardiopulmonary resuscitation.
There is some evidence that COVID-19 infection may lead to intestinal infection and be present in faeces. However, to date only one study has cultured the COVID-19 virus from a single stool specimen. There have been no reports of faecal−oral transmission of the COVID-19 virus to date.
A 60y/o woman with stage IV breast cancer (OSS, PER), ER / PR +, Her2 -, previous illnesses: HTN, devlops a recurrent ascites under the Treatment with letrozole + palbociclib, additionally to arterial hypotension, sleightly elevated creatinine 1.3 mg / ml, hyperkalemia up to 7 mmol / l, hyponatremia up to 118 mmol / l, compensated metabolic acidosis with BE of -7 und a hypoalbuminemia of 18 g / l. SIADH and hypocortisolism are excluded. What could be the cause for this clinical and laboratorypicture?
Oncology is a branch of medicine that deals with the prevention, diagnosis, and treatment of cancer. A medical professional who practices oncology is an oncologist. The name's etymological origin is the Greek word ὄγκος (óngkos), meaning 1. "burden, volume, mass" and 2. "barb", and the Greek word λόγος (logos), meaning "study".
Cancer survival has improved due to three main components: improved prevention efforts to reduce exposure to risk factors (e.g., tobacco smoking and alcohol consumption), improved screening of several cancers (allowing for earlier diagnosis), and improvements in treatment.
Metformin's anti-cancerous properties have been demonstrated in various cancer cells in vitro, such as lung, pancreatic, colon, ovarian, breast, prostate, renal cancer cells, melanoma, and even in acute lymphoblastic leukemia cells.
It was suggested that the tumoral microenvironment is associated with long-term outcome in primary and metastatic tumors.Metformin reduces inflammatory microenvironment Is regulated microenvironment with metformin reprogramme malignant cancer Cells toward a benign phenotype.
"In conclusion, high-dose intravenous ascorbate represents a promising and inexpensive anticancer therapeutic option that should be further explored in clinical trials. Given its low toxicity and low financial cost, ascorbate could become an important weapon in our arsenal against cancer, either acting as a single agent with predictive biomarkers or used in combination as an adjuvant therapy."
Targeting cancer vulnerabilities with high-dose vitamin C
Bryan Ngo, Justin M. Van Riper, Lewis C. Cantley & Jihye Yun
Nature Reviews Cancer volume 19, pages 271–282 (April 2019)
Invitation: Start a clinical trial.
There are currently 15 clinical trials. See details of those trials here: https://www.nature.com/articles/s41568-019-0135-7/tables/1
Intraductal papillary mucinous neoplasms (IPMNs) of the pancreas are being diagnosed with increasing frequency. IPMNs comprise a histologic group that ranges from adenoma to invasive carcinoma with different degrees of aggressiveness (borderline tumor). Actually, it is not known whether all IPMNs have this malignant potential or what is the best treatment of IPMNs. The'identify the right time of surgical treatment or follow-up is the great dilemma .
Hi everyone! I need your advice.
I have been working with Truven MarketScan® Commercial Claims and Encounters Database and the Medicare Supplemental and Coordination of Benefits (COB) Database in the past, and most recently with the SEER-Medicare data.
The oncology medicines I am working with are either injectable ( antibodies or targeted treatment) or chemo ( I guess it can be both orally taken or given infusion in an out-patient setting). I want to pull out all the claim information about the medicines. Should I just use J-code to pull them out from the in-patient (part A in Medicare) and out-patient (part B in Medicare) database? These medicines also show up as NDC# in the pharmacy database ( Medicare part D). Should I include the pharmacy claims in my analysis? All the medicines are reimbursed by Part B in Medicare. I don't understand why they show up in the pharmacy claims (part D). The patients wouldn't go to a pharmacy to pick up an oncology drug right?
Thank you so much for your advice!
Their is need to understand the safety and efficacy of exercise therapy on cancer treatment–induced cardiovascular toxicity and tumor progression and metastasis in oncology practice, this can be achieved by having a fundamental knowledge of exercise prescription, dosing and personalization with regards to cancer treatment and according to global best practices.
I want to know whether tumor cells share their information by time passing. I were wondering if anybody could answer my question and introduce some good resources in this regard?
I once had a colleague in a university, he was a professor of postgrad studies. About three years ago he suffered a bladder cancer, see for example: http://www.cancer.org/cancer/bladdercancer/. Then he took a surgery abroad, but it seemed that the cancer was spreading. So he decided to take herbal remedies besides taking chemotherapy.
I am not sure what happened then, except the fact that two years ago he passed away. I dont know exactly if his condition worsened because of cancer grew or not. But this story makes me ask about the safety and effectiveness of herbal remedies. Some people think that herbal remedies have better credibility over other alternative medicines.
So do you agree that herbal remedies are safe for cancer treatment? Do you have experience. Thank you.
For a background on herbal use for cancer, see for instance: http://www.cancerresearchuk.org/cancer-help/about-cancer/treatment/complementary-alternative/about/harm/the-safety-of-herbal-products-and-medicines
I am looking at tumor cells + surrounding immune cells and their expression of IL-6 in B-cell derived cancer. In some samples I can recognize comet-like plasma cells, and their cytoplasm is very clearly stained for the IL-6 antibody. Can plasma cells express IL-6, and if not, what might (in theory) activate the expression of this gene?
Mack et al studied subtypes of three ependymoma(same histopathology) brain tumors and found that one subtype carries an intrachromosomal translocation that creates a new tumor-driving gene, another lacks tumor-driving mutations but has aberrant epigenetic modifications, and a third shows neither gene mutations nor epigenetic aberrations. There were three genotype but one cancer phenotype. Similarly Martincorena and colleagues found thousands of mutations in cancer-relevant genes, including cancer-driver genes, in normal eyelid epidermis .(multiple cancer genotypes but no cancer phenotype).
In disparate classes of biological systems, there are more genotypes than phenotypes. Where sufficient information exists to enumerate these phenotypes, there are exponentially more genotypes than phenotypes, as a function of the number of system parts. This means that any one phenotype typically has many genotypes that form it.
In a brief, cancer is the decision of the cell to choose the innovative/adaptive phenotype and understanding the genotype does not mean understanding cancer.
1. Mack, S. C., Witt, H., Piro, R. M., Gu, L., Zuyderduyn, S., Stütz, A. M., et al. (2014). Epigenomic alterations define lethal CIMP-positive ependymomas of infancy. Nature 506, 445–450.
2. Martincorena, I., Roshan, A., Gerstung, M., Ellis, P., Van Loo, P., McLaren, S., et al. (2015). High burden and pervasive positive selection of somatic mutations in normal human skin. Science 348, 880–886.
We are looking for a patient monitering camera that is not degraded by radiation interactions. We need extended zoom capabibilitees so we can also do our HDR positioning QA in the morning. The current cameras we use last for about 2 years before they get radiation damage and become spoted.
JMML is well known for its non responsiveness to existing treatment options including HSCT, which has only shown to be the only curative option to provide for these patients. Even with HSCT prognosis is not so good. Does any centre in India have experience with HSCT in JMML ? Is there a specific recommendation/ guideline as to who all needs HSCT and whom to palliate ?
We are brainstorming about research involving the fields of genetics and oncology. We were wondering if chemotherapy could interfere with the results of the DNA isolation and Genetic results. Would it be possible to get blood samples during chemotherapy or is it best to do this between chemotherapy sessions?
Thanks in advance,
Is there any study with significant scientific value proving that sunscreen can directly or indirectly cause skin cancer?
I do believe that they protect the skin from the UVA and UVB thus reducing the risk of cancer.
Oxybenzone is being mentioned as a sunscreen chemical with high risk of causing cancer. Retinyl Palmitate is mentioned to be increasing the speed of development of malignant cells. However, after analysis of the ingredients of several sunscreen creams and lotions (Nivea, Garnier Ambre Solaire and Eucerin Sun Protection) I didn't find any of these compounds.
I am working with a PDCL cancer cells and I want to transfect GFP in the cells. I am using lipofectamine 2000 and I incubated it with the cells for 6 hour and seems to be good but after 6 hours they start to show some death due to Lipofectamine toxicity.
So I only incubated cells with the Lipofactamine and the vectors for 6 hours and then changed the medium to the normal medium that I am using for the cells.
I used in this experiment 10.000 cells and they showed some positive cells after 72 hour however they all died when I tranfered them to a larger T25 Flask,
Any suggestions ?
In our routine clinical practice, we are trying to kill mosquitoes (cancer cells) to cure cancer. sometimes we are using smart medications ( molecular-targeted therapies-it is look like, targeting the wings of mosquitoes ), I think that we must dry the swamp to cure cancer(fix the corrupted microenvironment)
I was planning to simulate hypoxia chemically in cancer cells using dimethyloxalylglycine (DMOG), desferrioxamine (DFO), ciclopirox olamine (CPX) or cobalt chloride (CoCl2), due to lack of a hypoxia chamber. However, I was also wondering if the results obtained from this form of hypoxia induction comparable to hypoxic simulation in a chamber, but I only found one article for this proof related to mesenchymal stem cells:
I have yet to find an article noting a difference between the two in cancer cells. Has anyone tried both cases and noticed a significant difference, or are they comparable? Similarly, does the agent type also affects results? I can't find any article comparing the effect of each agent in cancer cells as well. Thanks!
In reviewing methodology of a manuscript, I found out that CA125 levels in ovarian cyst fluids were measured using an ELISA kit. In the kit manual, it says that this kit is used for measuring CA125 in serum or plasma. Is this CA125 measurement valid?
- Would it help to linearize the plasmid before transfecting the suspension cells using Lipofectamine 2000 or 3000?
- Does it make a difference if the DNA is added in TE buffer or H2O (to OptiMEM)?
- Could I also use RNA for Lipofectamine transfection using the exact same protocol?
We are using lipofectamine for transfecting synthetic miRNA mimics for the miRNA functional analyses and miRNA target site validation experiments that we are developing with human cancer cell lines. However I would like to know if in your experience those experiments work as well with jet-PEY or similar reagents, which seems to be more cost effective. Thank you, Inma
According to a 2004 report by Morgan, Ward, and Barton: "The contribution of cytotoxic chemotherapy to 5-year survival in adult malignancies. ... survival in adults was estimated to be 2.3% in Australia and 2.1% in the USA." See http://www.ncbi.nlm.nih.gov/pubmed/15630849, or https://www.burtongoldberg.com/home/burtongoldberg/contribution-of-chemotherapy-to-five-year-survival-rate-morgan.pdf
Although such conditions may vary for different types of cancer, it is commonly held that 80% of oncologists will not take chemotherapy if they suffer from cancer themselves.
Another possible approach is perhaps herbal chemotherapy, which according to another report may yield an 85% success rate. See http://breastcancerconqueror.com/85-success-rate-with-herbal-chemo/
So why is the success rate of chemotherapy very low? And is it possible to improve that?
EGCG and sulforaphane are attributed intriguing pharmacological effect in a wide variety of fields. Recent research also investigates the synergistic effects of those two compounds (e.g.
Epigallocatechin gallate and sulforaphane combination treatment induce apoptosis in paclitaxel-resistant ovarian cancer cells through hTERT and Bcl-2 down-regulation (Chen et al. 2013)) with astonishing results compared to the isolated application of the compounds.
Although, there is one in vivo study in mice that investigated the combined effect (Nair et al. 2010, Regulation of Nrf2- and AP-1-mediated gene expression by epigallocatechin-3-gallate and sulforaphane in prostate of Nrf2-knockout or C57BL/6J mice and PC-3 AP-1 human prostate cancer cells), I doubt that these results can be simply transferred to humans, as I came across this study
Inhibitory effects of green tea and grape juice on the phenol sulfotransferase activity of mouse intestines and human colon carcinoma cell line, Caco-2. (Tamura, Matsui, 2000)
It occurs to me, that the co-administration of EGCG and sulforaphane might actually counteract what was intended. From what I understand, sulfotransferase responsible for the uptake of sulfones (like sulphorafane). Therefore, inhibiting that enzyme might prevent the uptake of sulphorafane at all.
Am I right with that conclusion or am I mistaken?
I know how to calculate the MU time but not sure how to get the cumulative dose. I have gone through the Radiation Physics book by Faiz. However no clear cut approach is shown for getting the cumulative dose? So my question is 1) Is there any approach by which cumulative dose can be calculated? or it is prescribed by the radiologist? 2) Do we need to optimize the dose distribution for telecobalt therapy?
According to Kuhn, a paradigm change in science, that means an epistemological change, requests the agreement of the scientific community, like it is arrived with the institution of quantum physics. In medicine a new paradigm of Medical Science has been proposed and applied in Medical Education in 1998 at the Milan School of Medicine , with the introduction of Person Centered Clinical Method and after the presentation of the new person centered interactionist and teleological health paradigm in 2005 ,presented at WHO (by invitation) in 2011 along with Person Centered Medicine, Medical Education change the paradigm change has been formalized on 13-14-15 October in Milan along with the presentation of “La Charte Mondiale de la Santé-the World Health Charter”.
The person-centered paradigm change of Medicine,Health, Medical Education and research corresponds to re-birth of clinics like a discipline addressed to discover the individuality of the patient in a disease and not the opposite, reducing him/her to an abstract theory. To date it is impossible because the same basic sciences , neurobiology, physiology, psycho-neuro- immune-endocrinology (PNEI) , already at experimental level, evidenced the end of a mechanistic , deterministic paradigm in Medical Science and the birth o f a person centered one (Person Centered Medicine) , that discriminates biological reactions, whose variability is determined by the person’s existential choices (life style and quality) from biological constants , responsible of biological life, according the Relativity Theory of Biological Reactions (1996)
I invite you to read the e-book “ Medical Science and Health Paradigm Change” and to give your “YES or NOT” about this paradigm change determinant for the destiny of Medicine , Medical Science and Medical Education, reformulating in a new way the epistemological principles of medicine, clinical method and clinical supervision
You can download the e-book from Research Gate:
And , if you agree ,to fulfill the agreement form or download it from www.healthparadigmchange.it sending it to firstname.lastname@example.org
And to read some other info on Person Centered Medicine on www.unambro.it
Would 2 biosimilars, that have separately demonstrated interchangeability with the reference product, through adequate clinical designs (phase III trials with 2 arms, and at least three changes in the switching arm, as proposed by the FDA draft), be also interchangeable with each other?
The venom contains MP1 molecule.
MP1 molecule and lipid membrane.
The potential of MP1 molecule as cancer drug.
The potential applications of single cell genomics include biomarker discovery, clinical trials, therapy selection, and disease monitoring.
What is the importance of single-cell biology to understand how clonal diversity in cancer impacts response, resistance, and relapse?
How single-cell DNA analysis overcomes the limitations of bulk sequencing to understand clonal architecture and mutation co-occurrence which impacts hematological malignancies?
I have been looking for information about this but I still can't find a reliable answer. I have contacted Cancer Treatment Centers of America, The National Cancer Institute, American Society of Clinical
Oncology as well as the US National Library of Medicine but still no exact answer.
Anyone with reliable answer and evidence will be mentioned in my project as source of information.
Theoretically, the Quorum Sensing (QS) mechanism may be disrupted by any condition which prevents a faithful "count" of SC neighbors. This can be either due to reduced sensitivity of the SC itself, e.g., shortage of adequate receptors for environmental signals, or due to reduced "clarity" in the environment, concealing extracellular signals from the SC. The result in both cases is weakened ability to sense the "true" number of SCs in the micro-environment and, as a consequence, incessant proliferation and elusion of normal homeostatic tissue control. These two properties can be integrated into one parameter, the magnitude of intercellular communication sensed by a SC, which is expected to be the critical determinant of the tissue's steady-state production of end cells.
Agur Z, Kogan Y, Levi L, et al. Disruption of a Quorum Sensing mechanism triggers tumorigenesis: a simple discrete model corroborated by experiments in mammary cancer stem cells. Biology Direct. 2010;5:20. doi:10.1186/1745-6150-5-20.
Reviewers have often questioned whether peer review is a thankless job or a duty to the academic community for the lack of adequate recognition or compensation for their contribution.
Publons, which was launched in the year 2013, currently has over 28, 931 reviewers.
NGS data provides information on variant allele frequency which is to be used for calculating copies of total cf-DNA, variant copies of cf-DNA per ml.
I have used the method described in
Annals of Oncology 27: 862–867, 2016
Detection of ubiquitous and heterogeneous mutations in cell-free DNA from patients with early-stage non-small-cell lung cancer
authors in this paper, based on the assumption that there are 3.3 pg DNA per haploid copy of genome, have calculated the total cf-DNA, variant copies of cf-DNA per ml.
Is there any other method available for calculating copies of ct-DNA?
I would like to understand the current landscape of patterns in the diagnosis/ treatment and outcome measure of current therapeutic interventions that are available in LMICs for cancer.
First, I'm using Ficoll Histopaque centrifugation to obtain mononuclear cells. Then, I'm doing RBC lysis. I observe a drastic loss of CD138+ cells after that (as checked using FACS and two separate validated CD138 antibodies). E.g. a sample that contains 18% plasmocytes, has practically no plasmocytes left after Histopaque isolation.
I want to use MACS CD138+ Microbeads but they fail since the Histpaque-isolated cells are devoid of plasmocytes.
Does anyone have such problems? What would you recommend? I've read about autoMACS Pro being good for such cases, but I don't have access to this device.