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Chemotherapy - Science topic

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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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Does anyone have any recommendations as to the best software to use to produces a Swimmer's plot for Oncology patients in a clinical study.
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I have used "swimplot" in R for a previous study, link and instructions here:
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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.
Best.
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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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Hello, I am stimulating CD4+ genes with doxorubicin to see effect on FV, but am having real trouble finding a good endogenous control gene for qPCR. I have tried GAPDH, PMM1, 18S and HPRT1. None of these seem very good at all, 18S shows some promise but the others are no good.
I can't seem to find any research on this particular cell stimulation, and based on what I have found I am thinking of trying B- actin or RPLP0 and maybe combine these with 18S...
I am desperate for any kind of advice here.
Best regards, Kaja
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Control genes are usually selected from β-actin, tubulin, GAPDH, Lamin B, PCNA, Na+/K+-ATPase, Histone H3, etc.
The following articles related to DOX-stimulated CD4+ may be helpful to you.
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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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I have looked on many different publication websites but I cannot seem to find any papers relating to the idea of having a two-stage release profile for a loaded hydrogel. Would it be feasible to create a gel loaded with an attractant protein towards the edges of the gel with a chemotherapeutic drug in the center to treat cancer post-resection? Thank you in advance.
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Dear Stephen Szpak, one way to do that is via "dual stimuli hydrogel". Also Gels having two LCSTs present dual thermoresponses. My Regards
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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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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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What is the best available treatment to get rid of (or limit the development of hepatocellular cancer in babies ( enfants about 1y)? Is the chemotherapy is dangerous for babies? Can a baby survive liver cancer if it is spread over many spots?
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Currently, I am working on an aggressive breast cancer cell line. I intend to restore and enhance the expression of tumor suppressor genes by siRNAs against the DNMT gene and induce apoptosis after treating the cells with siRNAs and subsequently exposed to a chemotherapy drug. I performed the MTT and Annexin V/PI apoptotic assays and I have got weird results.
In MTT assay the conc. of chemo drug with no siRNA was ranged from 100nM to 3200nM and the incubation time was 12 hours. In that experiment, the IC50 was 270nM. But, In cells treated with siRNA and the drug, even the highest conc. of the drug, i.e. 3200nM, did not induce cell death (the ODs were the same for each conc.). To clarify, I reverse transfected the cells with siRNA using RNAimax lipofectamine by Thermo fisher protocol (12 hours incubation time). subsequently, replaced the medium with the serially diluted conc. of the drug in RPMI containing FBS. after 12 hours of incubation, I have proceeded with MTT assay.
In the annexin V/PI experiment, I reverse transfected the cell only with the siRNA. the percentage of the cells in the Q4 quadrant was 90%!! As I understand, the siRNA against DNMT is supposed to induced apoptosis. but the results are showing a completely different outcome.
I have done the same procedure on CMML cells and the results were showing a considerable induction of apoptosis. the only difference was the transfection time, 19 hours against 12 hours.
Any ideas?
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Linna Green and no, I have not tested the transfection efficiency. Because of the sanctions against Iran, I am short in recourses in materials, including lipofectamine RNAimax. I thought if I perform my experiments by the general information in Thermo fisher protocol, maybe it is more efficient. But it seems I was wrong. Do you have any suggestions on how I could optimize the process by using low amounts of lipofectamine?
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Currently, I am looking for a solution to develop chemotherapeutic drug resistance in a primary cancer cell line. But after a quick look at the literature, it is indicated that the management of acquirement of drug resistance takes plenty of time, more than eight months! Is there any convenient method to subculture chemoresistant cell lines in a short time? Or any other suggestions rather than eight months interval with an increasing dose of chemotherapeutic agent?
Best regards.
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Dear researchers, thank you all for your contributions. Dear Mohana Krishna Gopisetty, the method you have suggested is time-efficient and problem-solving, I appreciated that. However, the cancer type we are working with is a little bit struggling. Our drug of interest is one of the members of the chemotherapy regimen which consists of other different drugs (we can say that it is given as a cocktail). Also, the relative survival rate of patients is low, diagnosis with specific drug chemoresistance takes time. (but we know that chemoresistance happens - under investigation)
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We want to analyze the expression of long non coding RNAs from human cancer tissues, so we want to understand if we should consider patients undergoing radiotherapy and chemotherapy.
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Hi Lilian
No problem and Good Luck.
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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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post #for #concern #people #oncology #research #area
For metastatic pancreatic cancer apart from chemotherapy is there any other medical treatment (newly adopted) exists in India?
As you know in this stage the theoretical prognosis is very poor. Is there any other treatment by which we can treat the patient with best comfort?
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How about thalidomide, celecoxib and valproic acid?
Clinical Review Prevention and Treatment with Probiotics, Thalidomide, Celecoxib and Valproic Acid for Metastatic Pancreatic Duct Adenocarcinoma.
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I want to conduct a proliferation assay to test a chemotherapy combination on a cancer cell line. At first, I thought about the MTT assay. But now, all sources are saying that these do not measure proliferation.
If you had a hypothesis that some drugs decrease proliferation, how would you go on about it? what experiments/assays would you use?
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Hello, Aicha!
1. Probably the simplest analysis for proliferation is to sow the same number of cells, treat with drugs and after the same time count the number of cells (for example, in a Goryaev chamber or using an automatic cell counter). Then, in relation to the ratio of the grown cells to the initial number, the proliferation index in% can be estimated.
2. You can use antibodies to marers of proliferation Ki-67, PCNA and use flow cytometry or immunofluorescence.
3. MTT test can also be used. The viability of cancer cells will be proportional to their proliferation. If your drugs act on proliferation, then cell viability will also change.
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I have been working on Cancer chemotherapy and Drug resistant cancer cell lines. Presently, I have developed two drug resistant cell lines. However, I need more cell lines to check the drug resistant reversal activity of my compounds. I would be happy if anyone of you agree to provide me the resistant cell line or provide me the address from where I can get the resistant cell lines in India. I will duly acknowledge their support and provide the authorship as well. Thank you.
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You should make your own resistant lines. These are something not available in cell repositories or shared by other scientists. Of course this is a costly, time consuming and tricky process.
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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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a 35 year lady underwent ileofeacalnresection for presumed Lokeshs. Hpr showed adenocarcinoma 1/3 nodes positive, received 2 cycles chemotherapy and presented after 6 months with normal cea , ct scan and colonoscopy
tretament plan should be revision right hemicolectomy or close observation ?
recurrence after non Cme procedure can present later as well, what percentages of these recurrencecdo u think are salvageableb
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Thanks dr graymer
Complete mesocolic excision is recommended to improve dfs and local recurrence for right colon cancer
the older concept of adjuvant therapy for suboptimal clearance still holdstrue
but does adjuvant chemotherapy compensate for inadequate clearance or non cme
perecentage of salvageable recurrences after right colectomy uncertain and challenging with superior mesenteric vein involvement
would be interesting to see if any data available regards this
Joe Graymer
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I need some specific cancer tissue samples' slides for IHC which is resistant and sensitive to specific cancer drugs, especially for prostate, lung, and breast cancer. Is it possible to buy or collect from some organization? If anyone has the information of proper source as well as if anyone has some sample, I would like to request you all to help me with this issue.
Thanks in advance.
Regards,
Mamun
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Gürhan Abuhanoğlu Dear Professor, Thank you for your kind information. However, I do not need any cell line, I have so many cancer and normal cell lines. I am just searching for a cancer drug-resistant tissue array for the immuno-histochemistry experiment.
Regards,
Mamun
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I am interested in different treatment modalities that are used for men with breast cancers. I will also highly appreciate if you can share relevant research on this topic as well. Many thanks in advance!
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The breast cancer treatment is similar in both, female and male. And this treatment may change by the stage, molecular profile (the last TNM by the AJCC).
The options are medical treatment (chemotherapy, anti-hormones, anti-her2, inmunotherapy), surgical options are more limited, normally in the male the surgery is a radical mastectomy w/wo sentinel node Vs LAD, and the third option like treatment is the radiotherapy.
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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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Is chemotherapy the current solution to the pandemic, or is the vaccine safe and sound?
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Follow
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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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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.
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Epigenetic therapy inhibits metastases by disrupting premetastatic niches
  • Zhihao Lu,
  • Jianling Zou,
  • […]
  • Malcolm V. Brock
Nature volume 579, pages284–290(2020
Abstract
Cancer recurrence after surgery remains an unresolved clinical problem1,2,3. Myeloid cells derived from bone marrow contribute to the formation of the premetastatic microenvironment, which is required for disseminating tumour cells to engraft distant sites4,5,6. There are currently no effective interventions that prevent the formation of the premetastatic microenvironment6,7. Here we show that, after surgical removal of primary lung, breast and oesophageal cancers, low-dose adjuvant epigenetic therapy disrupts the premetastatic microenvironment and inhibits both the formation and growth of lung metastases through its selective effect on myeloid-derived suppressor cells (MDSCs). In mouse models of pulmonary metastases, MDSCs are key factors in the formation of the premetastatic microenvironment after resection of primary tumours. Adjuvant epigenetic therapy that uses low-dose DNA methyltransferase and histone deacetylase inhibitors, 5-azacytidine and entinostat, disrupts the premetastatic niche by inhibiting the trafficking of MDSCs through the downregulation of CCR2 and CXCR2, and by promoting MDSC differentiation into a more-interstitial macrophage-like phenotype. A decreased accumulation of MDSCs in the premetastatic lung produces longer periods of disease-free survival and increased overall survival, compared with chemotherapy. Our data demonstrate that, even after removal of the primary tumour, MDSCs contribute to the development of premetastatic niches and settlement of residual tumour cells. A combination of low-dose adjuvant epigenetic modifiers that disrupts this premetastatic microenvironment and inhibits metastases may permit an adjuvant approach to cancer therapy.
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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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Can we consider photodynamic therapy of cancer (PDT) as an alternative method of conventinal cancer therapies like surgery, radiotherapy, chemotherapy ?? or it is just a complementary modality that can be combined with these therapies?
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Hello Issawi, PDT depends on how and where the cancer is too. If the patiente has a big tumor, probably the doctor will operate and PDT can be used as a complementary tecnique, but if cancer is on surface and not so deeper, PDT can be used as an alternative method.
I hope it has helped you.
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Dear Sir/Madam, I invited as a guest editor from high quality journals to handle special issues. If anyone can prepare a review similar to my review papers, particularly about a natural product in cancer prevention with focus on the structure activity relationship and mechanism of action, please kindly let me know to send an official letter. At this stage you should just send the title, authors and affiliation and abstract. Please kindly let me know as soon as you can. The suggested deadline for sending review is about 3 month. Best wishes, Suggeted topic: Genotoxicity of different agents and possble protection. Reducing side effects of radiotherapy and chomotherapy. Next generation of cancer therapy; Natural products. Natural products as novel therapeutic compounds. Radiation protection.
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What is names of the journals
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Some hospitals, that practice G-CSF-transfusion e.i. for patients with neutropenia due to leukemia and chemotherapy, apply G-CSF on the day of granulocyte-transfusion to support the effect of the transfusion. Some centers apply G-CSF everyday throughout the time of neutropenia.
I heard rumors, that high dose G-CSF in granulocyte-transfusion-recipients may cause immunotolleranceinduction and therefore would weaken the effect of the transfusion. However, I couldn’t find any paper or other publication working on that.
Thank you very much for your answer and help.
Kira Thies (PhD Student, Dresden, Germany)
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Hi there,
thank you for your answer and sorry it took me so long to reply. I heard of the mechanism you are describing and read some paper discussing their experiences about inducing immunotolerance to treat auto-immune diseases. I think that this might be a promising therapeutic option for patients who do not respond to established therapy. However, my question related to another group of patients. Patients with haemato- oncological diseases are prone to infectious complications during the time of neutropenia. Granulocytetransfusion (GTX) is practiced at some medical centers as ultima ratio therapy to save their lives. In my thesis I analyzed the overall survival of patients receiving GTX. On first sight it seemed as if patients receiving high doses of G-CSF tend to have a lower overall survival – that was when I thought of the immunotolerance induction caused by G-CSF. However, in a subgroup analysis results showed that patients, receiving high doses of G-CSF tend to suffer from more serious infectious complications than patients receiving lower doses of G-CSF and that this is more likely to explain the lower overall survival than the immunotolerance induction.
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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 working with pancreatic cancer cell lines PT45P1 and would like to know whether there is a better test rather than wound healing assay to assess the cellular proliferation after and before treating the cells with chemotherapy. Also, I am interested to investigate how my drug effect the cellular apoptosis.
Thank you in advance
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A BrdU incorporation assay, DiviTum, can be used in cell cultures, mouse and human sera/plasma. Dr Klaus Felix from Heidelberg have published results using DiviTum in pancreas PDAC:
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I injected two injections into rats via tail vein, irinotecan injection and an herbal extract injection-A (composed of Astragalus membranaceus extract, ginseng extract and oxymatrine). Group1 received only irinotecan; Group2 received a mixture of irinotecan and A; Group3 received A first, and irinotecan was injected 15 minutes later. The injection volume of each group and the concentration of irinotecan in each group were the same. The data demonstrated that at 5 minutes after injection, there was no difference in the plasma concentration of irinotecan between group 3 and group 1, while the plasma concentration of group 2 was increased about 5 times compared to group 1, and AUC was also significantly increased. I analyzed the concentration of irinotecan before and after mixing of the two injections in vitro, no difference. The change in pH after mixing also did not cause too much conversion of lactone and carboxylate forms of irinotecan (lactone forms still accounts for the majority). So why did the injection of a mixture of irinotecan and another drug increase the rat plasma concentration of irinotecan?
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Hello Yanfei, it is highly probable that your extract inhibited the metabolizing enzymes for irinotecan. Co-administration of certain agents either induces the metabolizing enzymes (leading to rapid clearance/elimination, decreased duration of action and perhaps therapeutic failure) or inhibits the said enzymes, leading to slow clearance/elimination, increased plasma concentration, increased duration of action and perhaps toxicity.
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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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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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What we know:
So, what percentage of physicians actually order KRAS genetic testing for their colon cancer patients? To be determined.
Is it cost effective? Turns out it's average.
"Results
Screening for both KRAS and BRAF mutations compared with the base strategy (of no anti-EGFR therapy) increases expected overall survival by 0.034 years at a cost of $22 033, yielding an incremental cost-effectiveness ratio of approximately $650 000 per additional year of life. Compared with anti-EGFR therapy without screening, adding KRAS testing saves approximately $7500 per patient; adding BRAF testing saves another $1023, with little reduction in expected survival.
Conclusions
Screening for KRAS and BFAF mutation improves the cost-effectiveness of anti-EGFR therapy, but the incremental cost effectiveness ratio remains above the generally accepted threshold for acceptable cost effectiveness ratio of $100 000/quality adjusted life year."
To Consider:
(1) What drugs might be more effective against colon cancer cells bearing the KRAS mutation?
(2) What drugs might be more cost effective against colon cancer cells bearing the KRAS mutation?
(3) Relating to cost effective treatment, how often do we prescribe drugs or assign treatment plans that are expensive $$$, decrease the length of the patient's life, and decrease the patient's quality of life? How can this be prevented? (E.g., recommending surgery procedures for aged colon cancer patients). How do we incentivize treatment that is most cost effective?
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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,
Roel
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I think the answer depends on what you intent to measure and what the details are. Chemotherapy can induce somatic DNA alterations and potentially predispose to acquired aberrant clonal expansions (https://www.nature.com/articles/gim2017196). Are you plannig to get blood samples for germline DNA testing? Hematologic malignancy testing? Cell free DNA?
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what is the effect of aloe vera on cancer cure , Is there any approved benefits from using aloe vera with chemotherapy in cancer 
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In chemotherapy trials and using time survived as the outcomes, do we define the magnitude of the effectiveness variable equal to the cycle length?
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See this Video you will understand
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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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I'm currently formulating my protocol for creating a resistant cell line against PDT. I'm planning to use a cancer cell line and expose the cells in several cycles of PDT. The cell line will be considered resistant if survival assay (MTT) will have 1.5 fold compared to the parental cells. My question is, how can I be able to test each cell generations with MTT assays if that cell generation itself must be subcultured to be exposed to PDT again. Could I make 2 plates in each generation cycle, one will be for MTT, the other one for PDT?
Thank you very much.
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J. Antes Yes, it is. You can have a try. Good luck.
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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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Has anyone experience in the effects of chemotherapy in non malignant splenomegaly. We have a patient with lymphoma and a non inflitrating spleen, which go on and off with chemotherapy. My doubt is if the spleen can be transiently reduced with chemo
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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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Would you please share your knowledge regarding inducing breast and colorectal cancers in mouse model chemically or through xenograft. Here we do not have access to genetic model?
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We run xenografts commercially, and you can find some examples of chemical treatment on breast cancer models (http://altogenlabs.com/xenograft-models/breast-cancer-xenograft/) and those of colon cancer ones (http://altogenlabs.com/xenograft-models/colon-cancer-xenograft/). These models are mainly necessary to confirm in vitro results on cells in preparation for human clinical trials.
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I'm looking for the %injection dose of doxorubicin that accumulates in a human tumor. The %injected dose/kg for humans (in clinical trials) would also be extremely helpful!
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Thanks! The type of tumor matters less, I'm trying to make a comparison between the accumulation of free chemotherapy vs. nanoparticle-encapsulated chemotherapy.
For some reason, the data for nanoparticles is easy to find, but free drug is very hard!
I just need a range of %ID/kg (ID-injected dose) in humans, for free chemotherapy.
Unfortunatley the clinical trial links didn't have any results...
Thanks so much for your help!
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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?
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I am not a doctor, but I have spoken with countless individuals who have survived cancer through natural means (diet, colonics and supplements) to boost their immune systems and detoxify their bodies. I have had a natural health store for more than twenty-five years and have read many books and articles as well as heard testimonials on this process.
What is ironic is that now the "breakthrough" method of cancer treatment that is touted by the medical establishment is the use of the individual's own immune system. Of course they say that the immune system must be "enhanced" by their drugs in order to work. They call it CAR-T cell therapy and they will provide it for one-half million dollars with the disclaimer that the boosted immune system might attack other organs. (TIME Mag. 12/25/2017).
Here's an idea - let people keep their one-half million dollars and use a small portion of it to buy organic vegetables and supplements, and maybe pay a practitioner to monitor their progress. Their naturally tuned-up immune systems will love all of their organs rather than attack them.
How gullible do we have to be to believe that we should pay the medical community one-half million dollars to use our own system that is in place naturally?
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Since there are long term treatments for some diseases or many type of cancers not knowing how to be treated, im wondering how brain activity can ever control the disease.
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Positivity (positive attitude) leads to the hope of improving the disease and in my opinion it really accelerate the speed of recovery from a disease.
For curing cancer pranayam (breathing practices) and meditation are really beneficial.
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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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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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I wonder whether or not high-dose administration of cyclophosphamide causes arrhythmia as well as other cardiopulmonary disorders such as congestive heart failure and pulmonary hypertension.
I am appreciated if you would give some comments.
Thank you in advance.
Sincerely yours.
Go J. Yoshida MD, PhD.
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Hi Go,, high dose of cyclophosmamide rarely can cause Myocarditis and heart failure. Cardiac side effect are common with doxorubicin but high dose cyclophosmamide can rarely also cause Myocarditis and heart failure. lt is usually occur within 10days of chemotherapy and does not occur because of cumulative effect. Cardiac side effect are because of Endothelial damage and leakage of fibrin and fluids in interstitium. Histopathology usually reveals acute pericarditis and haemmorragic Myocarditis which may be fatal. Congestive heart failure is the common manifestation and arrhythmia is rare. Following link might help you ..thanks
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We have reported several years ago the 5-year-old male patient with Li-Fraumeni syndrome with osteosarcoma and atypical type of hepatic cancer. Intriguingly, the cancer stem cell marker CD44 variant was ectopically induced after chemotherapy probably due to the selective pressure of excessive reactive oxygen species (ROS) provoked by chemotherapy.
I am appreciated if you would give me some feedback or comment on the following article.
Li-Fraumeni syndrome with simultaneous osteosarcoma and liver cancer: Increased expression of a CD44 variant isoform after chemotherapy
BMC Cancer2012;12:444
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I am appreciated for your kind comment.
It has been shown that CD44 variant 8-10 (CD44v), produced by the alternative splicing machinery regulated by ESRP1 protein, contributes to the attenuation of high level of redox stress in the tumor microenvironment.
My colleagues and I have demonstrated that CD44v interacts with and stabilizes the protein xCT at the cell membrane. This latter protein, together with CD98 heavy chain, forms an antiporter known as system Xc(−) that exchanges intracellular glutamate for extracellular cystine. Cysteine as well as glycine and glutamate are essential substrates for synthesis of GSH. CD44v8–10 thus promotes GSH synthesis by increasing the import of cystine and thereby increasing the intracellular concentration of cysteine. The elimination of ROS by GSH inhibits the activation of p38 MAPK signaling and thereby prevents ROS-induced senescence, apoptosis, or differentiation of cancer cells. The CD44v8–10–xCT–GSH axis thus protects CSCs from redox stress.
Ref.
* Inversed relationship between CD44 variant and c-Myc due to oxidative stress-induced canonical Wnt activation.
Biochem Biophys Res Commun. 2014 Jan 10;443(2):622-7.
* Alternative splicing of CD44 mRNA by ESRP1 enhances lung colonization of metastatic cancer cell.
Nat Commun. 2012 Jun 6;3:883.
* Therapeutic strategies targeting cancer stem cells. (Review)
Cancer Sci. 2016 Jan;107(1):5-11.
Sincerely yours
Go J. Yoshida MD, PhD.
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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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I’m studying genetic polymorphism of metastasis suppressor genes in breast cancer patients. Can I include those patients who recieved prior chemotherapy or radiotherapy in my study? Or they should be excluded?
How can chemotherapy affect the results of the study?
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The more chemotherapy you give to a patient more heterogeneity you will find in the tumor. This is because chemotherapy works as the "unnatural" selection process. Which is darwinian selection of the more resistant clones to chemotherapy.
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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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I have a similar article showed the serum level of that tumor marker change from (mean+-SD) 316+-564 (median 136) to 809+-1526 (median 143) after neoadjuvant chemotherapy. Now I want to assess the changes in serum level of a tumor marker after neoadjuvant chemotherapy in another study. How can I determine the sample size? What do I need more? What is the formula?
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You should use the "calculadora amostral", available online. Put your data in blanks and you will have a idea about your "n".After you have some results of your new experiments (pilot model), put your data again and check if the "n" is enough
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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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Aspergillosis
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Hi Dr Tomas
I mean a patient with aspergillosis and he needs transplantation.
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Hi all,
I'm currently working on my Honours thesis was wondering if anyone has any literature or data in regards to combining the following chemotherapeutic drugs with Wnt inhibitors, preferably in colon/colorectal cancer (but other cancers are ok).
The panel of drugs I'm working on are:
Chemotherapeutic Drugs
- 5-fluorouracil (5-FU)
- irinotecan
- oxaliplatin
Wnt Inhibitors
- ICG001
- NSC668036
- PNU74654
- XAV939
Much thanks,
Thomas
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I think the following information helps you:
Tankyrase 1 inhibitior XAV939 increases chemosensitivity in colon cancer cell lines via inhibition of the Wnt signaling pathway as was written by Professor Xueyun Zhong (gdqylkp@163.com gdqylkp@163.com). Hans Clevers writes about the consequences of Wnt deregulation in colorectal cancer (clevers@niob.knaw.nl clevers@niob.knaw.nl)
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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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In the development of a Co-registration method to compare two 3D MRI exams (before and post chemotherapy treatment for one patient using the same MRI modality) ==>you can see the problematic on the image uploaded enclose<==. The results show a correct alignment at the visual level. However, this is surely not enough. The first thing I have to think about is to validate the findings by comparing the anatomical points of interest (Landmarks). Are there any more practical propositions?
I thank the community in advance.
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Probably the most reliable and clinically most relevant way of verifying registration results is to ask experts to identify the same landmark points in both the fixed and moving image and then compute the distance between the fixed and transformed moving points.
Similarly, you can segment relevant structures in both the fixed and moving image and compare the fixed segments with transformed moving segments. Hausdorff distance (mean, 95th percentile) is a good metric, tells you how well the surfaces of the segments are matched. Some people use Dice Similarity Coefficient for segment comparison, which is a very poor metric, as its value is highly dependent on shape of segments (but it's very easy to compute, probably that's why many people still report that in papers instead of Hausdorff distance).
Both point and segment based evaluation can be performed in 3D Slicer (http://www.slicer.org - free, open-source medical image visualization and analysis software).
For segment-based evaluation, install SlicerRT extension and use Segment Comparison module (it can compute both Hausdorff and Dice metrics).
For point-based evaluation, you create two markup fiducial lists, apply the computed transform to the moving list, harden the transform, and compute distances in Python - or save transformed point positions to file and compute distances in Excel, R, etc.
If you have any questions, post it to http://discourse.slicer.org, you typically get expert help within a few hours.
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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.