Questions related to Chemotherapy
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.
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?
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
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.
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!
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?
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?
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?
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...
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?
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.
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?
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.
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?
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?
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.
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.
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
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.
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!
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..!!!
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.
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??
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.
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.
As we knew that, chemotherapy drugs produces many side effects so is it possible to prevent them effectively in patients with cancer treatment
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?
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.
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)
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
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?
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.
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??
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
What we know:
- We know that ~35-45% of colorectal cancer cells bear the KRAS mutation.
- We know that certain chemotherapy drugs are NOT effective in treating colorectal cancer cells bearing K-ras mutations (cetuximab (Erbitux) and panitumumab (Vectibix)).
- We know that most experts agree KRAS testing is important in determining chemotherapy treatment.
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.
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.
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."
(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?
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,
In chemotherapy trials and using time survived as the outcomes, do we define the magnitude of the effectiveness variable equal to the cycle length?
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.
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
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.
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
There is a controversy about the use of preoperative therapy in upfront resectable pancreatic cancer. Also some researchers recommend the combination of chemo-radiotherapy.
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?
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?
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.
How is the survival of children after Salvage with Chemotherapy in ALL with isolated early CNS relapse ? Is HSCT mandatory ? What are the options ?
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.
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...
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.
Go J. Yoshida MD, PhD.
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
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.
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?
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?
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?
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?
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.
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:
- 5-fluorouracil (5-FU)
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.
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.
Glucosylceramide synthase (GCS) performs ceramide glycosylation which is important for resistance to chemotherapy. Which cancer resistance cells express more GCS. Thanks