Questions related to Drug Therapy
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.
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?
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
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
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.
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?
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.
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?
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)
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!
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?
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...
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
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.
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??
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
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?
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....)
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.
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
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?
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.
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?
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.
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
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?
There is a controversy about the use of preoperative therapy in upfront resectable pancreatic cancer. Also some researchers recommend the combination of chemo-radiotherapy.
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.
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!
How is the survival of children after Salvage with Chemotherapy in ALL with isolated early CNS relapse ? Is HSCT mandatory ? What are the options ?
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!
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.
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...
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!!!
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.
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 ...
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 ?
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?
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?
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.
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.
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?
Glucosylceramide synthase (GCS) performs ceramide glycosylation which is important for resistance to chemotherapy. Which cancer resistance cells express more GCS. Thanks