Science topic

Drug Therapy - Science topic

The use of DRUGS to treat a DISEASE or its symptoms. One example is the use of ANTINEOPLASTIC AGENTS to treat CANCER.
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Dementia is a classical symptom of Alzheimer's disease, Can nootropic be the perfect candidate for the pharmacotherapy.
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Yes, Nootropics like citicoline and piracetam can be given because these drugs increase oxygen utilization in nerves so nerves can grow better.
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We are isolating human PBMCs (Ficoll-Paque) from fresh human blood samples and after 24hours we wish to treat the cells with a range of chemotherapy concentrations and perform a WST-1 (cell viability assay). As these cells are suspension cells, does anyone have a recommendation as to how to add the chemotherapy? I have read that you can add the desired concentration directly into the well, but we generally make up the treatments in fresh culture media and first remove the old media, rinse the cells and then add treatment.
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Hello Caria Fourie,
Unlike adherent cells, suspension cells may be treated within 6-8 hours after plating. You need not wait for 24 hours. You may add the chemotherapeutic drug directly into the wells containing the cell suspension in concentrated form such that the desired concentration is achieved.
Alternatively, if you have a microplate compatible centrifuge, you may centrifuge the plate at 2000rpm for 5 mins at 4°C, carefully pipette out the old media and add fresh media containing the chemotherapeutic drug. You need to be careful as there is a risk of losing cells by using this method.
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Basically aside the chemotherapy are there alternative methods to treat cancer and what are the current improvements on the method with relation to its previous states?
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Currently there are lots of approaches, but unfortunately the money seems to swing dramatically towards what's currently the most trendy approach. This results in the loss of funding for older approaches that are being refined with significant improvements. Unfortunately the people who make the decisions either aren't the brightest, or have large conflicts of interest and just fund their colleagues quid pro quo.
Here are two of our approaches that were abandoned when our lab was closed down due to lack of funding.
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The journal entitled Quality assurance of Antimicrobial Susceptibility Testing by Disc Diffusion by King, A., & Brown, D. F. (2001) stated that resistant organisms are necessary when testing particular resistance mechanisms. These mechanisms are said to be unstable and should be monitored carefully. How can we observe these organisms' resistance loss, which is essential for quality control procedures?
Reference: King, A., & Brown, D. F. (2001). Quality assurance of antimicrobial susceptibility testing by disc diffusion. The Journal of antimicrobial chemotherapy, 48 Suppl 1, 71–76. https://doi.org/10.1093/jac/48.suppl_1.71
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Work from stock lyophil with limited transfer - ala USP 51.
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Can you please suggest as soon as possible potential research topics on diabetic or cardia or nephrology pharmacotherapy , i need something retrospectively and drug related
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Belumosudil (KD025) is a specific inhibitor for ROCK2, which has been used for lung fibrosis and some other diseases. It may also be a potential drug in renal diseases.
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Dear colleagues..
We are trying to find the essential genes or proteins that promote chemotherapy resistant in cancer in order to identify them in our study. Does anyone can suggest some?
Thank you a head.
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I would suggest a few which you could include in your study.
Multidrug resistance of cancer cells during chemotherapy can be associated with a variety of mechanisms, including enhanced efflux of drugs, genetic factors (gene mutations, amplifications, and epigenetic alterations), growth factors, increased DNA repair capacity, and elevated metabolism of xenobiotics.
Transmembrane transporters responsible for the drug efflux are primarily from the ABC transporter superfamily. The human genome contains 48 ABC genes, and they are classified into seven subfamilies (ABCA-ABCG). Among them, ABCB1, ABCC1 and ABCG2 are highly involved in the acquisition of multidrug resistance to cancer chemotherapeutics.
Losing the tumor-suppressive activities by missense mutations in the TP53 gene, which are especially widespread in human cancers, reverses the protective role of the TP53 pathway by initiating chemoresistance, invasion, and metastasis. Loss of the TP53 activity in cancer cells allows continued replication no matter the type/level of DNA damage, which makes them resistant to genotoxic drugs.
Mutation in gene encoding enzymes involved in DNA damage response (DDR) such as ataxia telangiectasia (ATM), ATR, RAD50, and WRN can enhance the risk of cancer emergence and resistance. Single nucleotide polymorphisms in DNA repair-associated genes can also induce cancer drug resistance.
Focal adhesion kinase (FAK), a tyrosine kinase also referred as PTK2 (non-receptor protein tyrosine kinase) is a downstream protein of integrin and growth factor receptors signaling pathways. FAK induces NF-κB pathway mediated cytokine production in response to DNA damage. This phenomenon protects the cells from DNA damage and maintains chemo-resistance in the cells.
The cancer cells can cause drug resistance via providing multiple copies of the dihydrofolate reductase gene. The gene amplification increases the copy numbers of the oncogenes per cell to several hundred folds.
Transcription factors superfamily comprising DNA binding domain includes Forkhead box (FOX) proteins. FOX has been reported to regulate cellular machinery and various homeostatic processes. FOX factors control numerous physiological processes including cell division, cell death, cell invasion and migration as well as drug resistance. Deregulation of FOX proteins is commonly associated with cancer initiation, progression, and chemotherapeutic drug resistance in many human tumors.
For more, you would want to refer to the articles attached below.
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Any protocol or guidelines for inserting dental implants in patients receiving chemotherapy
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I think, It must be consultation for surgery to hematology&oncology doctors in order to need any profilaxy and evaluate defence cell mechasm..
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please explain the process
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You may get detailed information on google. Nevertheless, I came across this review article which is attached below. I suggest that you should go through it.
A key mechanism of action of many chemotherapies is the induction of DNA damage which leads to the activation of cell death pathways.
Conventional chemotherapies are divided into several classes based on their primary mechanism of action. They include:
1. Alkylating agents and platinum analogues, which induce inter- or intra- strand DNA crosslinks that destabilize DNA and cause DNA breakage,
2. Antimetabolites that inhibit the synthesis of DNA, RNA or their components,
3. Topoisomerase inhibitors that block the DNA unwinding enzymes, and
4. Microtubular poisons that act on tubulin, impeding the mitotic spindle and stalling cell division.
These drugs also have known secondary mechanisms of action, such as effects on mitochondrial biogenesis or the production of reactive oxygen species, which contributes to their cytotoxicity.
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Hi everyone,
I am working on HPSCs and response the chemotherapy. So far, I harvested BM cells from Balb/c mice and do the ex vivo study on them. But right now I want to to move forward to Human HPSCs. Is there any cell line that I can order and also culture for a long period of time?
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Here are a few commonly used human HSPC cell lines:
  1. KG-1: The KG-1 cell line is derived from a patient with acute myelogenous leukemia (AML) and retains characteristics of early myeloid progenitor cells. It can be cultured for long periods and is often used in drug sensitivity and differentiation studies.
  2. K-562: Originally derived from a patient with chronic myeloid leukemia (CML), the K-562 cell line represents a myeloid precursor stage and can differentiate into erythroid and megakaryocytic lineages. It is commonly used to study drug response and differentiation processes.
  3. HEL: The HEL cell line is derived from a patient with erythroleukemia and represents a more differentiated stage of hematopoietic cells. It can be cultured for long periods and has been used to investigate drug sensitivity and erythroid differentiation.
  4. TF-1: The TF-1 cell line is derived from a patient with erythroleukemia and is often used as a model for early myeloid progenitor cells. It can be cultured long-term and has been utilized in drug sensitivity assays and differentiation studies.
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I work with 3D cell culture. So far I had always cultured the spheroids or organoids in 100% geltrex for my experiments. In the following experiments I would like to work with gemcitabine. However, I am not sure if the chemotherapeutic agent (gemcitabine) will pass through the Geltrex.
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I have not worked with this drug before, but being a small molecule, it should possess appropriate physicochemical properties to enhance its trafficking through the ECM and indeed, the organoid itself. But bear in mind that the drug has to overcome 2 barriers: the matrigel and the organoid. You make do a pilot trying different delivery systems e.g direct delivery via microinjection, nanobased delivery etc
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Is chemotherapy different between squamous cell lung carcinoma and lung adenocarcinoma?
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Lung squamous cell carcinoma and lung adenocarcinoma are the main subtypes of NSCLC. These subtypes, which start from different types of lung cells, are grouped together as NSCLC. Though lung adenocarcinoma and lung squamous cell carcinoma have drastically different biological signatures, yet they are often treated similarly and classified together as non-small cell lung cancer.
Increasing evidence suggests that lung adenocarcinoma and lung squamous cell carcinoma should be classified and treated as different cancers. Please refer to the paper I have attached below for your reference.
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Case reports on common post cancer chemotherapy complications
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@diwakar
Add your answer (type @ to mention people)
The most common complication is GIT upset, fatigue and anorexia with subsequent weight loss
While the mist serious is pancytopenia with immune suppression which puts the patient at high risk of fulminant infections .
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Dear colleagues,
Can you tell me what is the best chemotherapy method for BALB/c mice with colorectal cancer?
Thanks in advance
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Thank you Malcolm for your valuable answer! I helps.
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I am looking for the answer as to why Multidrug Resistance or MDR becomes an effect on some cancer patients undergoing chemotherapy despite not being exposed to some drugs used in the therapy.
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Maybe we do not understand the underlying mechanism of the genesis of "cancer" and because of that not the therapy... The world know spontaneous healing and nobody does research on this...
Maybe we have to look for new ways to regard the (re)actions of the body and the biological meaning wihtin. Just to allow us to do new research. Only the thinkung of new ways brought mankind further, the repetition of the thinking until today not. Modern cancer therapy found out many ways, but most cancer patients die after serveral years, especially the patients who are treatet much and have a long journey in the healing system. This circumstance should be the point of thinking new ways...
In every biological being the sensation/perception of the surrounding (context) determinates reactions of the whole organism. E-Motion is Energy in motion and leads to reactions in the body ant its organs.
For example: If a shep looses his lamb, the milk ducts reacts. Under a microscope we may find a so called "ductal mamma carcinoma". This reactions forms back if the shep is pregnant again.
If you treat mouses with cigarette-smoke the lung reacts with metarmophosis according to the fear of death, the air sacs proliferate as a ancient evolutional reaction of the fear of death. Like a cancer-patient who got the idea that he/she will die soon... If you treat hamsters in the same way nothing will happen, because hamsters have no fear of getting burned according to the hamsters lifestyle in contrast to the lifestyle of mouses. A mouse needs a high sensibility for smoke, a hamster not.
Humans have the brain and its main-funktion the prediction. This ability of the brain - to scan the context and create predictions - is in humans on a high level. Old patterns of our socialisation are mixed in our daily prediction-process and if context meets imprint we call that "Emotion". Our interpretation leads to reactions of the body.
If a woman is in huge worry about her child for serveral months it is very probable the she becoms a ductal mamma carcinoma. This carcinome build back if the worry is solved in reality (the child is cured, alive not harmed any more...).
If a man looses his son and heir (in his interpretation of the death of his son) it will be very probalble that this man becomes cancer of his testicle.
Those mechanisms are very good investigated but rarely told according to the conclusion that these relationships between feeling of the context and its inner (unaware) interpretation in our prediction engine (brain) leading to biological reactions is not lucrative!
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Can CRP be measured as a parameter of how well chemotherapy has progressed against a tumor
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Hello Sama Yaqoo
You may please refer to the article attached below for more information.
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We have lung cancer cell lines when we treated these cells with chemotherapy for 24h the gene expression level of cancer progression genes like (MMP9, CXCL8, EGF, TGFb, FGF2, CCL22, and more) were increased. What could be the reason of increasing expression level of these genes?
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Yes you could or you could compare treated (i.e. at IC50 dose) vs. untreated (mock treated).
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Can inflammatory markers be used to determine how effective chemotherapy is against tumors?
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Thank you very much for answering my question
I am currently working on solid tumors in children, and I thought of taking three types of tumors and measuring some inflammatory markers for them, so I wonder to myself whether this is true or should I work on one type and do the tests
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Traditionally, we have performed surgery first, followed by chemotherapy for breast cancer. Neoadjuvant treatment was limited to patients with contraindications to surgery. However, according to the latest ASCO guidelines (1), only patients with T1aN0 and T1bN0 HER2-positive disease should not be routinely offered neoadjuvant therapy. Should we now reverse our therapeutic approach?
1. Korde, L. A., Somerfield, M. R., Carey, L. A., Crews, J. R., Denduluri, N., Hwang, E. S., Khan, S. A., Loibl, S., Morris, E. A., Perez, A., Regan, M. M., Spears, P. A., Sudheendra, P. K., Symmans, W. F., Yung, R. L., Harvey, B. E., & Hershman, D. L. (2021). Neoadjuvant chemotherapy, endocrine therapy, and targeted therapy for breast cancer: ASCO Guideline. Journal of clinical oncology : official journal of the American Society of Clinical Oncology, 39(13), 1485-1505. https://doi.org/10.1200/JCO.20.03399
Translated with www.DeepL.com/Translator (free version)
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Yes, neoadjuvant systemic therapy is now considered standard practice for following subsets of breast cancer patients:
1. Inflammatory breast cancer
2. cT4 disease
3. cN2 or cN3 disease
4. Operable breast cancer with triple negative or HER2 +ve molecular subtype with cT2/N+ or higher disease stage
5. Large primary tumor relative to breast size, or when cN+ likely to become cN0 with neoadjuvant systemic therapy to facilitate breast conservation
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Having looked at the data showcase on the UK Biobank, I can find prevalence of cancer types according to gender etc, but I wonder if it were possible to see how many people were treated with a certain type of chemotherapy i.e taxanes/platinum-based etc?
Does anyone know if this data is available, I don't want to apply and spend months looking if it's not!
Thank you al!
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Hi Stephanie Pearson, I also looked for information on chemotherapy treatment in the UK Biobank. But the web shared in the response did not work. Do you figure out this question? Could you please share it with me? Thanks!
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I have two chemotherapy drug (A and B), at baseline, after first cycle, second cycle and third cycle, I want to compare between two drugs after each cycle and and which drug associated with more adverse events with time at the end of third cycle and after each cycle?
Some safety data is continuous such as liver enzyme, and some is categorical such as grade of some adverse events.
I think for continuous data repeated measure ANOVA can help but what about categorical variables?
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It is dependent from data: parametric or nonparametric.
When we have parametric data, to be used: paired t test, unpaired t test, Pearson test, ANOVA.
Nonparametric tests are: Wilcoxon test, Mann-Whitney test, Spearman test, Kruskall Wallis tests.
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We want to know if one protein can be used as a breast cancer biomarker or not. So we'll have to compare normal and patients, and our question is whether we can get samples from patients who received chemotherapy before?
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thank you for answring my quesion dear Dr Erum Zafar
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I am trying to find the best way to assess viability for an in vitro experiment in which the cells are treated with chemotherapy.
After treatment, even in very high chemotherapy concentrations, I see only 30-40% of cell are DAPI+ cells by flow cytometry (DAPI concentration for the staining is 200 nM). In contrast, a viability kit (titer glow by Promega) shows more than 80% decrease in viability compared to untreated cells with the same chemotherapy concentrations.
Do you have any logical explanation for the difference, and more importantly, what assay should I trust?
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I believe it may have something to do with DAPI concentration. In your shoes, I would trust Trypan blue kit more.
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I wanted to know how to decide the treatment time for clonogenic assay with chemo drugs. Would you choose the time when cell death is first noticed with the respective drug treatment or is there a standard treatment time that is used for the assay in general?
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Ruby,
At first, calculate IC50 of that particular drug for your cell line. Then you can treat different concentration of that drug for 8-14days.
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A 4 year old known case of ALL after starting chemotherapy ,few months later start to have abdominal dissension and bloating with attacks of diarrhea and abdominal pain ,many investigations done include stool Cs ,fecal CP ,reducing substances and hematological Ix with celiac screen all were negative ..upper endoscopy done and biopsy revealed subtotal to total villous atrophy...
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Thanks Dear Dr for your suggestion ,I visit the website and read their guidelines which mainly about mucositis of GIT tract ,in this case endoscopy reveal no evidence of inflammation or ulcers ,biopsies where of villous atrophy ,most properly due to chemotherapy ..unfortunately trial of treatment were not so successful
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Can chemotherapy give you cancer?
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Dear Asaad Hamid Ismail thank you for your interesting and important technical question. Yes, certain kinds of cancer have been related to chemotherapy (and also radiotherapy). For more information about this, please have a look at the following useful article entitled:
Second Cancers Related to Treatment
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I was trying to do meta-analysis on RevMan5 to compare the likelihood of toxicities among two groups of chemotherapy regimens. The problem is that the total number of toxicity events is higher than the number of patients in each group. subsequently risk ratio could not be calculated. I added a multiplier to the total number so the denominator will be higher than the nominator . The risk ratio still the same after this. However , I am not sure it is correct statistically in the meta-analysis point of view and how can we tackle this problem.
I wonder if there is any reference I can refer to
Many thanks
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Hi Ahmed,
I think that you chose the wrong effect size. It seems to me that the most appropriate effect size is a count and not a risk. I thinkt that you can transform the count data to a rate ratio which can be pooled using Revman. The Cochrane manual offers some guidance on this: https://handbook-5-1.cochrane.org/chapter_9/9_4_8_meta_analysis_of_counts_and_rates.htm
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Chemotherapy for breast cancer costs the UK economy more than £248 million annually, including ‘out-of-pocket’ personal costs of more than £1,000 per patient – according to new research from the University of East Anglia.
Key findings: - The total cost of breast cancer chemotherapy in the UK economy is over £248 million.
- Societal productivity losses of £141.4 million - including £3.2 million lost to premature mortality, and £133.7 million lost to short-term (£28.7 m) and long-term (105m) work absence. Further costs include £3.4m associated with mortality losses from secondary malignancies due to adjuvant chemotherapy and £1.1m in lost productivity arises from informal care provision.
- £1.1 million in lost productivity arises from informal care provision.
- Out-of-pocket patient costs for chemotherapy total £4.2million, or an annual average of £1,100 per patient. In addition, costs for the emotional wellbeing of carers could be as much as £82 million. Emotional wellbeing reflects how much additional income would be required to offset a wellbeing loss.
‘Societal costs of chemotherapy in the UK: an incidence-based cost-of-illness model for early breast cancer’ is published in the journal BMJ Open on January 5, 2021.
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Yes, we added as many cost as we could given the data available.
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Hello researchers.,
I am trying to find a simple mathematical model for getting the Tumor size variation during chemotherapy treatments. All most all of the models have been trained with the mice models. What are the simple mathematical models available to show the tumor size variation which can be also validated with the real clinical data?
Thanks so much in advance..!!!
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I am afraid that you cannot replace diagnostic imaging with a mathematical model. At least that is the situation in real life patients.
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Dear
What is the effect of chemotherapy on zinc levels ?
and what are the mechanisms implicated ?
best regards
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White cell counts drop after chemotherapy
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Decision making regarding use of antibacterial prophylaxis involves weighing measures of efficacy against potential negative consequences.
Measures of efficacy of prophylaxis include reductions in fever, bacteremia, sepsis, infection-related mortality, and overall mortality.
Potential negative consequences of prophylaxis include Clostridioides difficile infection, invasive fungal disease, drug toxicities, and antibiotic resistance.
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I confused about the %?
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In our manuscript, we describe the main schemes that caused neutropenia in our population.
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Hello,
I was wondering the following;
I add a chemotherapy agent to cell culture media to make a solution. I store the solution in a 4°C fridge. I use the solution to treat cell cultures, with the goal in mind to measure the cytotoxicity of the chemotherapy agent added to the culture media.
Can the effects of the chemotherapy agent be diminished over time, when the agent is put into solution with culture media?
Please let me know what you think.
Thank you in advance.
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I confirm the indications given by Dr. Campos-Vega. I suggest you to evaluate if your treatment could be stored at ultra-low temperature conditions (-68 ºC and below) using a proper solvent. Most treatments stored at these conditions are usually dissolved in DMSO, HBSS, PBS, or similar reagents but not the media itself since glucose and other components can form crystals and precipitate. It is always better to prepare fresh new treatments every day or evaluate several responses to your refrigerated solutions.
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In this era of great medical advancement, how far the customised cancer therapy is helping? Like for instance.. In the treatment of Hodgkin's lymphoma.. Although monoclonal antibodies are used, oncologists still suggest conventional chemotherapy like vinblastin, bleomycin etc.. But these are really painful for a cancer patient. Can't this conventional chemo be avoided at least in cases where customised treatment is available??
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Chemotherapy is still very much necessary in the treatment of cancer. The use of monoclonal antibodies can be added to potentiates its effect, though can't be given as a form of monotherapy.
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Th prolong TB treatment has been attributed to the presence of dormant subpopulation. To me, this implies compounds that can reactivate the dormant form could make could adjuvants in TB chemotherapy.
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As we knew that, chemotherapy drugs produces many side effects so is it possible to prevent them effectively in patients with cancer treatment
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The commonest side effects are
Nausea, Vomiting: Steps: 1. Eat small frequent meals. 2. Strong fragrance cooking may be avoided. Ondensetron and Apripitane are very effective & useful drugs
Lower immunity/ Low WBC count: 1. Take adequate rest, dont exert! 2. GMCSF/ GCSF are useful to bring back wbc count in normal limits.
Constipation: 1. Drink adequate water. 2. Have good amount of fibres / add esabgul. 3. Cremafin syrup.
Diarrhoea: 1. Avoid uncooked food. Have fresh, home cooked food. 2. Hydration, slat replacement and occasional use of antibiotics may be required. 3. Severe case with septicaemia; admission in hospital with IV fluid and salt replacement and IV antibiotics are often needed. Blood culture may help.
Hair Loss: Cooling of scalp may help. result are not predictable. Tolerance is also a big issue.
Repeated IV punctures/ Pain/ thrombosis of peripheral veins: Chemo Port insertion is great help!
Depression: Good counselling and prior information usually helps. Good friends and strong family support helps greatly. Meditation and light Yoga is also useful. Sometimes meeting cancer survivor helps to restore confidence.
Dr. Tarang Patel. Consultant Breast & Cancer Surgeon. CIMS Hospital, Ahmedabad, India
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Assume there is a patient with oral tongue SCC (pT3N1) underwent surgery (R0) and postop con. ChemoRT with weekly cisplatin. One month after completion a reccurence emerges in the radiated field. You want to start palliative chemo. Do you consider this patient as resistant to Cisplatin and choose other non-cis drugs? or Add something to Cis?
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Dear Reza, I appreciate for your kind attention and especially for bringing this dilemma up.
According to the published literature, the response rate for cisplatin-naïve head and neck carcinoma is approximately 50%. However, this rate is much lower in recurrent cases. There are a number of mechanisms that induce Cisplatin resistance in head and neck carcinoma (e.g. membrane transporters for cisplatin uptake or efflux, such as CRT1 and ABC transporter MRP2; DNA repair proteins, such as ERCC1 and TP53; apoptosis associated proteins including BCL-2, caspases, or MAPKs) (1). Moreover, Chang et al. showed alternate enzymatic pathway for Cisplatin resistance in head and neck carcinoma. They depict AKR1C1 induce Cisplatin resistance through activation of STAT1/3 (2).
Therefore, as is evident, due to enzymatic processes involved in Cisplatin- resistance, Cisplatin in second-line is expected to have clinical activity.
1. Galluzzi L, Senovilla L, Vitale I, Michels J, Martins I, Kepp O, Castedo M, Kroemer G. Molecular mechanisms of cisplatin resistance. Oncogene. 2012;31:1869–83.
2. Chang WM, Chang YC, Yang YC, Lin SK, Chang PM, Hsiao M. AKR1C1 controls cisplatin-resistance in head and neck squamous cell carcinoma through cross-talk with the STAT1/3 signaling pathway. Journal of Experimental & Clinical Cancer Research. 2019 Dec;38(1):245.
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I'm working on a report that suggests an alternative device for patients with lung cancer.
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Of possible interest in your design is that we performed inhalation paclitaxel chemotherapy in dogs with pulmonary metastases as a preclinical trial, and our facility stopped performing it, as there was occasional leakage from the device, and the potential for handler/administration exposure was too great. Scavenging could be a major drawback.
Other facilities continued regardless and the preclinical work is published (although they did not mention the potential for exposure). Clin Cancer Res. 1999 Sep;5(9):2653-9.
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I'm working on a report about alternative devices for patients with lung cancer.
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Add this article
Zarogoulidis P, Chatzaki E, Porpodis K, Domvri K, Hohenforst-Schmidt W, Goldberg EP, Karamanos N, Zarogoulidis K. Inhaled chemotherapy in lung cancer: future concept of nanomedicine. International journal of nanomedicine. 2012;7:1551.
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I am looking at expression of SASP factors in cells +/- chemotherapy treatment.
Some factors are not expressed at all in the control cells, but are expressed highly in the same cell type following chemotherapy treatment.
How can I quantify the expression of these markers when they fail to amplify at all in the control group?
( using Taqman probes >40 cycles....)
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Did you check by sequencing the PCR-product? Becasue I work in microbiology and I don't know if in your experiment the gene is more high in the control group than the other and if this gene is normal expressed in the controlo group. The problem is possible inside the mix reaction or in the quality/quantity of cDNA that you analysed.
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We are doing a study analyzing the expression of certain genes and correlating that with response to chemotherapy. So far I have been manually going through every dataset on the NCBI website and teasing out which ones have "therapy response" or any variation of that as a variable. Is there a more efficient way to do this? Like a query to filter out highthroughput/microarray data that also contains therapy response/pathologic complete response/etc. Any help would be greatly appreciated. Thanks.
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Hi Norman,
if you used the filters in GEO profiles and found nothing maybe you could go an other way. try in the pubmed query and see in found papers which one has data deposited in GEO...
fred
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Reduce the toxic effects of chemotherapy and radiation
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A 46 year old lady, had a left breast carcinoma 13 years ago- underwent left breast conservative therapy ( wide local excision + axillary dissection + whole breast radiotherapy), followed by tamoxifen (only completed 3 years and defaulted treatment).
Now presenting with recurrence at left breast and multiple right axillary node metastasis (both confirmed invasive carcinoma by core needle biopsy) , however right breast is normal.
Mammogram- multicentric left breast lesions, right breast normal
CT scan- no other distant metastasis except contralatetal axillary mets.
ER/PR positive
HER2 negative
Left breast tumor resectable and she's a good surgical candidate
What are our options?
A) Neoadjuvant chemotherapy followed by surgery(left mastectomy) and hormonal therapy
B) Salvage left mastectomy and right axillary dissection followed by adjuvant chemotherapy and hormonal therapy
C) Bilateral mastectomy and right axillary dissection followed by adjuvant chemotherapy and hormonal therapy
D) Salvage left mastectomy followed by adjuvant chemotherapy and hormonal therapy
E) Other options??
Thank you
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I forgot to say that current studies of neo-adjuvant therapy evaluating aromatase inhibitors + CDK4/6 inhibitors look very promising...!!!
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How do you Control and manage your mood swings without drug therapy ?
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Exercise, yoga, and meditation are the best ways for the control and management of mood swings.
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I came across many cancer patients with black veins due to chemotherapy, and when I tried to grade them according to CTCAE, I couldn't find any terms related to black veins in that dictionary. If anybody knows, please share your valuable comments in this regard. Thank you
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Surender,
Here's a quote I found: •Serpentine hyperpigmentation: Some chemotherapy drugs (fluorouracil, vinorelbine, and some combination regimens) given intravenously (IV) can cause a darkening of the venous pathways up the arm. This darkening over the veins will eventually fade. ◦The cause of these skin reactions is currently unknown, but may involve direct toxicity, stimulation of melanocytes (cells in skin responsible for skin color), and postinflammatory changes. Although skin reactions may occasionally be permanent,in most cases, discoloration will gradually resolve after chemotherapy is stopped.
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Watching Valeria Sarmiento's The Black Book (a French period drama), I was surprised when a character who seemed to be an obvious case of 'consumption', actually recovered! Typically in such period dramas, people die (eg: Fantine in Les Miserables, Francis and Linton both pop their clogs due to TB in Wuthering Heights, Helen Burns in Jane Eyre etc...).
It occured to me that I didn't actually have any idea what proportion of active TB cases actually go into remission without chemotherapy, and what the correlates of recovery might be in these cases?
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Hi Matthew. In the first RCT of streptomycin vs bed rest (1948), about 1/3 of the patients recovered spontaneously in the bed rest arm.
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the articles are:
Safety and feasibility of home-based chemotherapy by Larsen FO, Christiansen AB, e.a. Danish medical journal 2018, May; 65(5) pii: A5482
A randomised crossover trial of chemotherapy in the home: patient preferences and cost analysis by King MT; Hall JP, Harnett PR.
Medical journal of Australia, 2001; Mar 19; 174(6) 312; author reply 312-3.
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Thanks!
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Midlle age female with bilateral liver mets from an obstructive sigmoid tumor (CEA = 55,7) who underwent an emergency laparoscopic retosigmoidectomy with primary anastomosis. She presented a good recovery without intercurrences. Histological analysis showed a moderate grade adenocarcinoma T3N0M1. The hepatic lesions were localized in the following positions: A) Left lobe : 1) segments IVA+B central lesion very near or invading left hylum (5,6 cm) and 2) segment II (superficial - 2,0 cm) - B) Right lobe : 1) segment VI (4,4 cm), 2) segment VII/ posterior VIII at end of right hepatic vein (3 cm). She underwent FOLFOX and bevacizumab treatment with stable disease. Since the left lesion was very close to the hepatic hylum mainly left side and the resection would be very difficult, we have purposed FOLFIRI treatment to the downsizing these lesions. After this second scheme she presented partial response with decrease of the lesions major lesions (3,4 CM). Then, the lesions have became resectable without major vascular resection. The question is: Is it worthiwhile to consider a single procedure by means of the open via? A left hepatectomy with a enlarged posterior right sectioniectomy to the posterior portion of segment VIII at same time (FLR was calculated near 55 % for these procedures) ? Or Should we resect them by means of two-stage Lap approach? Would it be safest to resect them in two-stage laparoscopic procedure such as : 1) First - enlarged posterior right sectioniectomy to the posterior segment VIII and intraoperative portal ligation or even postoperative portal embolization (left portal vein) followed chemotherapy and finally 2) straightforward laparoscopic left hepatectomy?
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Always is a better decision to do the total procedure in one-stage if it is possible
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The War on Cancer refers to the effort to find a cure for cancer by increased research to improve the understanding of cancer biology and the development of more effective cancer treatments, such as targeted drug therapies.. The signing of the National Cancer Act of 1971 by United States president Richard Nixon is generally viewed as the beginning of this effort, though it was not described as a "war" in the legislation itself.
War stated as “a state of usually open and declared armed hostile conflict between states or nations” in Merriam-Webster dictionary. War indicated attack of foreign army.
On the other hand meaning of rebel is opposing or taking arms against a government or ruler. Something has to cause rebellion. There are complaints. These complaints have usually been ignored over so long a period of time that people have become impatient with the slow pace of change; they begin to feel that conditions are unbearable. These complaints are most important causes of rebellion.
I think that cancer cells are rebels (cells live in bad conditions) and they try to live .
We must change our philosophy. We must accept cancer cells as rebels not enemy and we must try to correct bad environment to calm rebels.
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War against cancers will continue just as long as the war against human poverty will never end. I think war against cancers is part of nature motivation for humans to increase their knowledge about themselves as a vast collection of tiny biosystems.
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I am looking for a database which provides information on the change in the expression of protein before and after chemotherapy. Any information in this regard would be appreciated.
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Thank you all. I really appreciate your efforts for helping me. I did find the provided links informative but not to the extent I was looking for.
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squamous cell carcinoma can be treated with surgical excision , radiotherapy and chemotherapy
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In fact oral sq.c. carcenoma is chemoresistans and radiosensetive, so no role for chemotherapy in oral sq. C.c.,its used for palliative therapy
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what is the minmum count to perform paired sample gene expression assay
if my cases have pre and post reading
eg I have 4 cases with low expression
and 6 cases of high expression
baseline and post chemotherapy results , other cases didnt achieve CR.
can I perform paired samples statistics
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For paired sample analysis you need two values per sample, pre and post treatment. If you lack one of the values for a sample you cannot analyze it by that method since it would not be paired to begin with.
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primary brain tumor -such as glioma, astrocytomas- treatment is often surgery when possible, and glucocorticoids.
radiotherapy (and sometimes chemotherapy) is used for brain metastasis, why isn't also used in primary tumor?
are there specific indications for radiotherapy in primary brain tumor?
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There are specific indications for surgery, radiotherapy and chemotherapy for both primary and secondary brain tumors. Histopathology, location, extent of resection, age, and multiple other variables play a role in decision-making for neurosurgeons and oncologists. Multiple guidelines help specialists, however, each patient is a different world.
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I have a patient that is a dog with Subcutaneous (hypedermal) Hemangiosarcoma.
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Dogs with subcutaneous hemangiosarcoma are more likely to have small, localized stage 1 disease than dogs with hemangiosarcomas in other sites; therefore subcutaneous hemangiosarcoma usually carries a much better overall prognosis than visceral hemangiosarcoma and has the potential to be cured by surgery alone. On the other hand, when it is large, and particularly when it is intermediate to high grade, subcutaneous hemangiosarcoma may be more likely to recur or metastasize.
One study reported on 71 dogs with subcutaneous and intramuscular hemangiosarcoma, and found the overall survival time averaged 6 months, with 25% of dogs living a year after surgery. They found that tumour size was important; dogs with tumours <4 cm, between 4 and 6 cm and > 6 cm in diameter had survival times of 12 months, 7 months and 4 months respectively after complete surgical excision. Dogs that had clinical signs (lameness was most common) or had anemia at diagnosis lived an average of 3 months (compared with 7.5 months if neither), and those with complete surgical margins lived an average of 13 months compared with 4 months if margins were incomplete. Predictably those with metastases lived an average of less than 4 months.
In another study that proposed a histologic grading system for dogs with hemangiosarcomas; tumour grade (and specifically nuclear pleomorphism and mitotic index) appeared to predict survival time for these dogs that were treated with surgery and doxorubicin. (Grading is best done on a large, excisional specimen, rather than incisional sampling).
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There is a controversy about the use of preoperative therapy in upfront resectable pancreatic cancer. Also some researchers recommend the combination of chemo-radiotherapy.
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Adjuvant chemotherapy gemcitabine based is the most usual option
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Actually I have two problem, First: I am using a chemotherapy drug on LNCap cell line(prostate cancer), and I expect to get a dose dependent result, meaning a decrease in cell viability by increasing drug concentration. But I see my highest concentration has the same viability with the lowest concentration. Why is it like this?
Second: I have done the test for several times, and each time the answer is different.
I have optimized every thing which could be effective.
Thanks for your helps.
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your protocol is trued
i think your aliquot have problem it is not sufficient for your work
do you used the multichannel in your divide?
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I'm interested to hear about other's experiences in A549 xenografting and if there are any issues that come up. Do the cells form tumors efficiently? Are there issues with mouse survival, and what mice should be used? Would the xenograft be suitable for the evaluation of lung cancer drugs/therapies?
Helpful tips would be greatly appreciated!
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A549 xenografts depend on the end goals of your study; when we do A549 xenografts we usually want to have a tumor form, which is why our injection dose contains the cells in matrigel (http://altogenlabs.com/xenograft-models/lung-cancer-xenograft/a549-xenograft-model/). The timing and functionality are exactly what Anastasiya described them to be - a few weeks for growth and another few weeks for the treatment regiment.
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How is the survival of children after Salvage with Chemotherapy in ALL with isolated early CNS relapse ? Is HSCT mandatory ? What are the options ?
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You may be interested in the psychological reactions children with ALL exhibit:
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How is the prevalent dose of 5FU in chemotherapy?
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In general, it can be said that 5-FU has been applied in various chemotherapy regimens in a variety of malignacies, such as bolus doses in 5-day regimens 400-425mg/m<2> in colorectal cancer, that is of no current use, single bolus doses 500-600mg/m<2> in CMF or CAF in breast cancer, regimens that are rather of no utility today, high-dose continuous infusion schedules 500-1000mg/m<2> x 4-5 days in head & neck carcinomas (with CDDP) or stomach cancer (DCF regimen), low-dose continuous ampulatory infusion via portable pump, such as in ECF in advanced gastric cancer (replaced currently by oral Capecitabine; ECX) or colorectal cancer during early 90's, in the De Gramont schedule as a 46-hr infusion after Leucovorin (LV) (mFOLFOX or FOLFIRI regimens in the treatment of colorectal cancer), and at 2600mg/m<2> as 24-hr infusion after LV and Docetaxel (FLOT regimen) in advanced gastric cancer...!!!
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Gain-of-functional mutant p53 exhibits a longer half-life period as compared with wild-type p53, which is why the significant accumulation of the mutant p53 in cancer cells is recognized in many kinds of malignant neoplasms.
As compared with CEA and CA19-9, anti-p53 antibody (IgG subtype) can be detected in the very early stage of esophageal, colon, breast, prostate carcinomas etc.
Given that pseudo-positive ratio of anti-p53 antibody is less than 5% in the healthy population, the detection of anti-mutant p53 IgG antibody holds much promising.
I would like to know your opinion on this useful marker.
Thank you in advance!
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I would like to add that anti-p53 antibodies have been reported in other human diseases (other than cancers) such as auto-inflammatory and autoimmune diseases. Therefore, reducing its clinical usefulness.
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I am going to treat the myocardial infarction rats with spironolactone for 8 weeks/56 days. As you know, there are several ways to administer this drug, such as oral (gavage and mixed in rat chow), intraperitoneal and subcutaneous injection. We currently cannot mix it with rat chow.
Which technique do you think is more prior?
How to make the solution of it? Can we make the solution with physiological serum?
Your advice and suggestions will be much appreciated and welcomed.
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Hello!
I'm working on a project that would allow me to monitor efficieny of chemotherapy (cisplatin) minutes after an intake. So here's my question: how much time does it take to release ctDNA to bloodstream from the moment cancer cell would absorb the cytostatic? So by this question I mean: how long does cancer cell "need" to lose membrane's integrity after contact with chemo? Or maybe you know some researches, in which efficiency of chemotherapy was monitored right after the cytostatic was given into the bloodstream?
Thanks in advance for your help.
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Here is a reference, may be it helps you: Kim MK, Kyong-Ah Y, Myung WS, et al. KRAS mutation in cell-free DNA was correlated with treatment response to gemcitabine/cisplatin chemotherapy in patients with pancreatic cancer. Poster presentation at: AACR Annual Meeting 2016; April 16-20, 2016; New Orleans, LA.
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According to articles before CAR T Cell infusion patients with WBC more than 10^9/Lit will get a lymphodepleting chemotherapy, some patients will receive a bridge chemotherapy between their enrollment and lymphodepleting chemo.
What is this bridge chemotherapy? do all patients get it? what type of chemo medicine is it prescribed? do all patients get MTX or MAb or...
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Bridge chemotherapy is chemotherapy given in the time between leukapheresis and infusion of CAR T cells. This period is required for the manufacture the CAR T cells, which may take months due to the limited proc=duction capacity. In the mean time, the tumour of the patient may progress and requires treatment. This is the bridge chemotherapy.
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Kindly provide any real examples
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In the present scenario, immunotherapy is used along with chemotherapy upfront in adult ALL by addition of Rituximab to chemotherapy in CD20 + adult ALL. Blinotumomab is used as single agent in relapsed refractory ALL in adults and children.
At this stage, we don't have evidence to say if immunotherapy can be used alone in upfront setting in paediatric patients. Hopefully clinical trials will be able to answer this question in future.
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oncologists and kickbacks on chemo
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Sorry Ladislaus but besides the salary and in spite of regulations, kickbacks are there all the time...and mainly from big pharma.
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Any feedback, ideas, suggestions
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Interesting question and looking forward to read answers
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Recently, researchers have been looking for a optimum combination of chemicals to boost up the anticancer potential of certain chemical compounds. May be to overcome the resistance to of some drugs like cisplatin, 5FU etc. I am curious to know the updates regarding this type of research outcomes. Thank you!!!
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A totally agree with Dr. Tomas Koltai. We also perform synergistic experiments of several different classes of compounds, such as Hsp90 inhibitors or pH modulators combined with well known anticancer drugs. If compound itself is not relatively very toxic and it could enhance the activity of anticancer drugs, it is generally considered as a rational way to improve the treatment, and sometimes it could help to prevent from resistance to chemotherapy.
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The aim of this study is to gain insight into the experience of cancer patients with short term fasting during chemotherapy, as well as experiences and observations of relevant medical professionals involved in this approach.
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Very interesting project! And thank you Aftab Ahmad for sharing your article.
Unfortunately, I might have a subject at hand who just recently have been diagnosed with metastases. Previously succesful treated for breast cancer. Nonetheless, it would be interesting to propose fasting during her (likely) chemotherapy in order to have an efficient treatment with limited side effects. Any protocols on fasting and age limitations? Subject is 76yrs old.
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The most common way that conventional doctors look for the first signs of breast cancer in women is to identify lumps in the breast. They most often do this with mammogram x-rays. This offer physicians a basic road map for navigating the terrain of breast tissue, which they believe allows them to pinpoint any lumps, masses, or other warning signs of breast cancer that might point to a malignancy.
But mammograms can be a potential cause of cancer due to the ionizing radiation they send into breast tissue. They also aren’t accurate 100 percent of the time, despite what you may have been told. Lumps and masses in breast tissue can be either benign (harmless) or malignant (cancerous), and mammograms don’t differentiate between the two. This often leads to false diagnoses and unnecessary treatments with chemotherapy and radiation
is there any information about Is there any information about the diagnosis or early signs of this disease? share with me ...
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  • retraction, or inward turning of the nipple
  • enlargement of one breast
  • dimpling of the breast surface
  • an existing lump that gets bigger
  • an “orange peel” texture to the skin
  • vaginal pain
  • unintentional weight loss
  • enlarged lymph nodes in the armpit
  • visible veins on the breast
Having one or more of these symptoms doesn’t necessarily mean you have breast cancer. Nipple discharge, for example, can also be caused by an infection. See your doctor for a complete evaluation if you experience any of these signs and symptoms.
FIND A DOCTORCost of a mammogram near you
Where you live might affect how much you’ll pay for a screening mammogram. Explore the range of costs for screening mammograms in your region using the cost research tool below, powered by our partner Amino. Click on the cities to see nearby doctors. You can also start a new doctor search and book an appointment for free using this tool.
SIGNS IN MENMen and breast cancer
Breast cancer isn’t typically associated with men. However, male breast cancer can occur in rare instances at any age, although it’s more common in older men. Many people don’t realizethat men have breast tissue too, and those cells can undergo cancerous changes. Because male breast cells are much less developed than women’s breast cells, breast cancer in men isn’t as common.
The most common symptom of breast cancer in men is a lump in the breast tissue.
Other than a lump, symptoms of breast cancer in men include:
  • thickening of the breast tissue
  • nipple discharge
  • redness or scaling of the nipple
  • a nipple that retracts or turns inward
  • unexplained redness, swelling, skin irritation, itchiness, or rash on the breast
Most men don’t regularly check their breast tissue for signs of lumps, so male breast cancer is often diagnosed much later.
EXAMSBreast exams
When you visit your doctor with concerns about breast pain, tenderness, or a lump, there are common tests they might perform.
Physical examination
Your doctor will examine your breasts and the skin on your breasts, as well as check for nipple problems and discharge. They may also feel your breasts and armpits to look for lumps.
Medical history
Your doctor will ask you questions about your health history, including any medications you might be taking, as well as the medical history of immediate family members. Because breast cancer can sometimes be related to your genes, it’s important to tell your doctor about any family history of breast cancer. Your doctor will also ask you about your symptoms, including when you first noticed them.
Mammogram
Your doctor may request a mammogram, which is an X-ray of the breast, to help distinguish between a benign and malignant mass.
Ultrasound
Ultrasonic sound waves can be used to produce an image of breast tissue.
MRI
Your doctor may suggest an MRI scan in conjunction with other tests. This is another noninvasive imaging test used to examine breast tissue.
Biopsy
This involves removing a small amount of breast tissue to be used for testing.
Read on to learn more about breast cancer tests.
TYPESTypes of breast cancer
There are two categories that reflect the nature of breast cancer:
  • Noninvasive (in situ) cancer is cancer that hasn’t spread from the original tissue. This is referred to as stage 0.
  • Invasive (infiltrating) cancer is cancer that has spread to surrounding tissues. These are categorized as stages 1, 2, 3, or 4.
The tissue affected determines the type of cancer:
  • Ductal carcinoma is a cancer that forms in the lining of the milk ducts. This is the most common type of breast cancer.
  • Lobular carcinoma is cancer in the lobules of the breast. The lobules are where milk is produced.
  • Sarcoma is cancer in the breast’s connective tissue. This is a rare type of breast cancer.
GROWTHGenes and hormones affect cancer growth
Geneticists are starting to learn how genes affect the growth of cancer and have even identified one: the HER2 gene. This gene fuels growth of breast cancer cells. Medications can help shut this gene down.
Like genes, hormones may also speed up the growth of some types of breast cancers that have hormone receptors.
  • If a cancer is estrogen receptor-positive, it responds to estrogen.
  • If a cancer is progesterone receptor-positive, it responds to progesterone.
  • If a cancer is hormone receptor-negative, it has no hormone receptors.
TREATMENTSTreatments for breast cancer
Depending on the type and stage of cancer, treatments can vary. However, there are some common practices doctors and specialists use to combat breast cancer:
  • A lumpectomy is when your doctor removes the tumor while leaving your breast intact.
  • A mastectomy is when your doctor surgically removes all of your breast tissue including the tumor and connecting tissue.
  • Chemotherapy is the most common cancer treatment, and it involves the use of anticancer drugs. These drugs interfere with cells’ ability to reproduce.
  • Radiation uses X-rays to treat cancer directly.
  • Hormone and targeted therapy can be used when either genes or hormones play a part in the cancer’s growth.
RECURRENCESigns of recurrence
Despite initial treatment and success, breast cancer can sometimes come back. This is called recurrence, which happens when a small number of cells escape the initial treatment.
Symptoms of a recurrence in the same place as the first breast cancer are very similar to symptoms of the first breast cancer. They include:
  • a new breast lump
  • changes to the nipple
  • redness or swelling of the breast
  • a new thickening near the mastectomy scar
If breast cancer comes back regionally, it means that the cancer has returned to the lymph nodes or close by the original cancer but not exactly the same place. The symptoms may be slightly different.
Symptoms of a regional recurrence may include:
  • lumps in your lymph nodes or near the collarbone
  • chest pain
  • pain or loss of sensation in your arm or shoulder
  • swelling in your arm on the same side as the original breast cancer
If you’ve had a mastectomy or other surgery related to breast cancer, you might get lumps or bumps caused by scar tissue in the reconstructed breast. This isn’t cancer, but you should let your doctor know about them so they can be monitored.
As with any cancer, early detection and treatment are major factors in determining the outcome. Breast cancer is easily treated and usually curable when detected in the earliest of stages.
The American Cancer Society says the five-year survival rate for breast cancer that is stage 0 to stage 2 is more than 90 percent. The five-year survival rate for stage 3 cancer is more than 70 percent.
Breast cancer is the most common cancer in women, according to the World Health Organization. Whether you’re concerned about breast pain or tenderness, it’s important to stay informed on risk factors and warning signs of breast cancer.
The best way to fight breast cancer is early detection, whether that includes self-examinations, annual breast exams at your doctor’s office, or regular mammograms. If you’re worried that your breast pain or tenderness could be something serious, make an appointment with your doctor today. If you find a lump in your breast (even if your most recent mammogram was normal), see your doctor.
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Adjuvant therapy for rectal caner stage II and III after radical TME surgery without preoperative chemoradiotherapy - Observation, Standard De Gramont, FOLFOX ,FOLFIRI, CAPOX, FOLFOXIRI - is there strong evidence to support one over another regiment in term of overall survival (OS) . And what is your opinion ?
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thamkyou
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A 65-year-old man with ductal adenocarcinoma in the head of the pancreas was operated elsewhere (laparotomy and biliary diversiobn) and he was considered inoperable. He was discharged and he came to see me for a second opinion. 6th postoperative day now. Analysis of CT scan was totally resectable. What to do next? Rush to the OR and perform a Whipple procedure or send him to neoadjuvant chemotherapy?
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Usually
1.the tumor size is not a key factor:
2. Artery involvement is a real key point:
3. Adhesions after by-pass surgery are not so heavy if there were no attepts to mobilize the tumor.
If the vein is involved, i think neoajuvant will be the best option
Best
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RT or chemotherapy can liberate huge amount of tumor antigens. Simultaneously these therapies damage immune system. Can this imbalance lead to anergy and tolerance of tumor antigens? How stable is this tolerance?
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Dear Mr. Chukwurah,
do you have a reference to support your statement?
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The number of people who diagnosed as cancerous patient is increasing every year. By increasing in cancerous population, the number of researchers and research group that working on cancer treatment is increased.
One of the famous method in cancer treatment is chemotherapy. But, it seems that this method didn't have considerable advancement in cancer treatment during the past decade and needs serious revolution in it.
What is your opinion about it, comparing to other cancer treatment method?
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We are not going to see the end of classical chemotherapy drugs any time soon.
Newer methods like direct targeting of proteins implicated in cancer, does not mean that usual chemotherapeutics are outdated.
Probably we shall see the old drugs used along with direct targeting and immunological targeting.
A deeper knowledge of chemoresistance may improve in the next future the outcome of classical treatments.
Better bioavailability will also be an important factor in order to deliver better results.
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Hello everyone, I would like to ask about radiotherapy and chemotherapy resistant in tumor hypoxia.
why tumor hypoxia resist radiotherapy and chemotherapy in patients who have a malignant tumor.
thank you
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For radiotherapy to work, oxygen is needed as most of the damaging effects on the DNA level of the cell/tumorcell is due to the production of reactive oxygen species. So less oxygen, less damage/efficiency.
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I thought that more differentiated cells (like epithelial cells as compared to stem cells) are more resistant to cytotoxicity?
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Well - we know that they indeed seem to be resistant. And there is a lot of people currently trying to find out why exactly :)
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Aspergillosis
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Hi Dr Tomas
I mean a patient with aspergillosis and he needs transplantation.
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There seems to be a notion among some oncologists that chemo/immuno therapy for late Stage I lung cancer has less than 6% prospects of effect. While clinical straregies seem absurd to me when based on clinical statistics-- so crude!-- heterogenicity of tumor cells at that stage seems a critical issue. Can anyone expand on this question, as opposed to the crude stats-type oncology? Thank you all in advance for any molecular perspective important to such considerations.
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Hello
We have no clinical evidence of its utility in patients in Latin America. In our hospital we are characterizing the expression of the PD-L1 and we are using it in second line, this due to state regulation.
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Any examples of pharmacotherapy used currently? 
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In addiction is the mesolimbic pathway, also called reward pathway, as a dopaminergic pathway in the brain, involved
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I have isolated a pure compound from a medicinal plant and now want to check its activity in mice models. In this case, what samples should I to take into account from the following?:
1. crude extract of medicinal plant
2. partially purified extract(s) of medicinal plant
3. Pure (HPLC purity more than 98%) compund
I have seen some research articles which use both, crude extract and pure compounds for such animal studies. Is it needed to test for crude or partially purified extracts? If yes, what is rationale for it? Are there any references available which justify the testing of crude or partially purified extracts? 
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I agree with Nisha.  It depends on your research questions/objectives.  What are your hypotheses that should be tested, particularly in your research?
If you test all of them, you may get relevant information about antagonstic, additive, or synergistic effect of the different plant secondary metabolites compared with the activity of the purified compound. As suggested by Nisha, you can check using in vitro methods prior to in vivo study in animal models.
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Glucosylceramide synthase (GCS) performs ceramide glycosylation which is important for resistance to chemotherapy. Which cancer resistance cells express more GCS. Thanks
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Hi Kartik. We have preliminary data showing that glioblastoma cells are rendered susceptible to chemotherapeutic drugs after alterations in the lipid metabolism, including the in GCS. There are some published research related to this. E.g.:
 Yeh,S., Wang,P., Lou,Y., Khoo,K., Hsiao,M. and Hsu,T. (2016) Glycolipid GD3 and GD3 synthase are key drivers for glioblastoma stem cells and tumorigenicity. 10.1073/pnas.1604721113.
 Lee,E.C., Lee,Y.S., Park,N., So,K.S., Chun,Y. and Kim,M.Y. (2011) Ceramide Induces Apoptosis and Growth Arrest of Human Glioblastoma Cells by Inhibiting Akt Signaling Pathways. 19, 21–26.