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Clinical Oncology - Science topic

Explore the latest questions and answers in Clinical Oncology, and find Clinical Oncology experts.
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Traditionally, we have performed surgery first, followed by chemotherapy for breast cancer. Neoadjuvant treatment was limited to patients with contraindications to surgery. However, according to the latest ASCO guidelines (1), only patients with T1aN0 and T1bN0 HER2-positive disease should not be routinely offered neoadjuvant therapy. Should we now reverse our therapeutic approach?
1. Korde, L. A., Somerfield, M. R., Carey, L. A., Crews, J. R., Denduluri, N., Hwang, E. S., Khan, S. A., Loibl, S., Morris, E. A., Perez, A., Regan, M. M., Spears, P. A., Sudheendra, P. K., Symmans, W. F., Yung, R. L., Harvey, B. E., & Hershman, D. L. (2021). Neoadjuvant chemotherapy, endocrine therapy, and targeted therapy for breast cancer: ASCO Guideline. Journal of clinical oncology : official journal of the American Society of Clinical Oncology, 39(13), 1485-1505. https://doi.org/10.1200/JCO.20.03399
Translated with www.DeepL.com/Translator (free version)
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Yes, neoadjuvant systemic therapy is now considered standard practice for following subsets of breast cancer patients:
1. Inflammatory breast cancer
2. cT4 disease
3. cN2 or cN3 disease
4. Operable breast cancer with triple negative or HER2 +ve molecular subtype with cT2/N+ or higher disease stage
5. Large primary tumor relative to breast size, or when cN+ likely to become cN0 with neoadjuvant systemic therapy to facilitate breast conservation
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Researching background on glioblastoma, I know that it has among the poorest survival rates of any malignancy. However, I have found few data or studies comparing survival rates from glioblastoma with other deadly cancers. Please let me know if you are aware of any.
Thanks,
David Neil
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The median overall survival of glioblastoma is around 10-12 months in population-based studies. This is actually an improvement from 4.9 months between 1984-1994. MGMT promoter methylation is a prognostic and treatment predictive marker with better outcomes and better response to temozolomide. Pancreatic adenocarcinoma has more treatment options available including biomarker based treatments, however GBM is continuing to be a hard nut to crack.
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How much literature is there on the use of this scoring system to assess the tumour's response to the neoadjuvant stage of therapy?
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Currently, treatment responses are assessed on the basis of measurement of tumor size before and after treatment with serial conventional radiography, such as chest X-ray, computed tomography (CT) or magnetic resonance imaging (MRI)
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Hi, I am a beginner in the field of cancer genomics. I am reading gene expression profiling papers in which researchers classify the cancer samples into two groups based on expression of group of genes. for example "High group" "Low group" and do survival analysis, then they associate these groups with other molecular and clinical parameters for example serum B2M levels, serum creatinine levels for 17p del, trisomy of 3. Some researchers classify the cancer samples into 10 groups. Now if I am proposing a cancer classification schemes and presenting a survival model based on 2 groups or 10 groups, How should I assess the predictive power of my proposed classification model and simultaneously how do i compare predictive power of mine with other survival models? Thanks you in advance.
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The survAUC R package provides a number of ways to compare models link: https://stats.stackexchange.com/questions/181634/how-to-compare-predictive-power-of-survival-models
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Please find attached the full medical file of our patient and all biological reseaults included.
We are seeking to explain how can she produce such levels of immunoglobulins with no B cells expression.
NB ! : * The patient ddidn't recieve any immunoglobulins injection.
* We made another dosage for immunoglobulins levels after 01 moth of the first one and we had the same resault ( high levels ).
Best regards
Msc, Abdelwahab
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First thing i would like to comment on it that you may change the clone of CD20, check CD19 as well if they are even few?
Secondary, The absence B cells might be the drug effect (Like: Rituximab or any alternative/traditional medicine).
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I am looking for some pointers on what medical imaging techniques that are capable of estimating total cell number in a tumor. Being able to estimate the difference between a tumor of a defined size presuming tumor 1. has half the mount of cells and tumor 2. of the same size with double the amount of cells would be a great start.
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Do you have the data? Why not train a model like Mask R-CNN on it and deploy in the wild.
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Has anyone have used TCGA analysis to get useful publications. If yes, would it be possible to get a copy of R code to use it as a road map for the procedure.
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Numerous nanoparticles have been designed and tested to great effect in animal models but the translation to clinical application and success has been very limited and disappointing in cancer treatment. Where and what is the barrier? Is there any breakthrough in near future?
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I think its important to keep in mind the properties of the tumor and incorporate direct targeting strategies to tumors. I think that biotechnological advances are paving the way for better clinical outcomes. Drug delivery systems need to be designed to mimic the in vivo environment and computer aided simulations are a growing resource for it.
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For any no-relapse cancer gene therapy, all cancer cells need to be transfected. Is it possible? Will repeated administration be able to reach all cancer cells? I know different serotypes viral vectors must be used for repeated administration to evade antibody response, but let's not focus on little details. I want to know if its fundamentally possible? Cancer cells have mutated antigens that viruses use to get in, so there can be resistance. Perhaps repeated non-viral transfection in-vivo? What do you think? If not, then why can't repeated transfection reach every cancer cell? It seems to me that due to minuscule size of vectors, spatial availability in-vivo isn't the issue. What do you think?
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Hi John Schloendorn , Thanks a lot for your reply. I might have phrased my question in a wrong manner. 100% transfection efficiency is impossible, let's say it is 20% efficient. Is it possible to still transfect all cancer cells in a patient with repeated administrations each with 20% efficiency, given that the treatment is selective and non-toxic? It seems like non-viral transfection is more stochastic, in a sense that it in principle can transfect any cell, it just happens that it doesn't, so with enough repeated administration it should be able in principle to transfect all cells, right? Thank you very much for your time. Your experience is invaluable on this matter. I am asking for a research proposal I have made, where this issues now stands out.
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I was posed a question by a hematopathologist in training this morning: Why are B-cell lymphomas more prevalent than T-cell Lymphomas?
My initial guess was perhaps there is increased tolerance training in T-cell populations, but it turned out she did not know either. Her best guess was that it is multifactorial in nature, i.e. genetics, viral infections (HTLV), and environmental factors.
Does anyone have any papers or book chapters for reference? I would love to be able to bring a more detailed and concise answer back to her. So far, I haven't found anything that answers the question on PubMed.
Thanks in advance.
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Development, activation and contraction is more tightly regulated in T cells v B cells. Particularly the latter, so you are less likely to see t cell lymphoma secondary to chronic immune stimulation for example malt lymphoma. Also, ebv. B cells express cd21 whereas t cells only transiently do so during thymus development. So ebv causes hl, bl, mzl, malt, and dlcbl in b cells but basically, only extranodal nk/t cell lypmphomas in the cells as I recall. 97% of adults are ebv seropositive.dlbcl is the most common lymphoma in the us, roughly 15% is eber+.
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  • What is the time taken for steady state to be established in adults for ( Mycophenolate mofetil ) ?
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Please bear in mind that there is a large interindividual variability in the bioavailability and therefore the plasma concentration of parent mycophenolate and active metabolite. The variation can b as large as 30%. You may consider checking the plasma concentration in critical cases.
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I am trying to assess delays in the management of female patients with breast cancer. I am particularly interested in three delay intervals, but can adapt according to the tools available:
1. Patient-level delay: First symptom to first consultation.
2. Doctor-level delay: Initial consultations with GP and investigation of cancer-related symptoms.
3. System-level delay: Referral to specialist, consultations, diagnosis, and initiation of treatment.
Please let me know if you have any suggestions. Many thanks in advance!
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Dear Usama,
I recently attended this conference, if you check the speakers list and their work to date you would find good references I think.
Check the paper attached.
Good luck!
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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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I wish to estimate the expression of two types of markers by immunohistochemistry in the biopsy specimens of a particular type of cancer, and correlate their expressions with clinical parameters and outcomes. For this type of cancer, we see approximately 400-500 patients every year at our centre, which is about 10% of all of our cancer patients.The crude rate of this cancer in India is also around 10%. The estimated prevalence of the two markers vary between 50-75% as per published studies. What should be my ideal sample size ?
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At least a few hundred to establish a reliable research. I think you have enough samples here.
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Why do Anticancer drugs kill a constant fraction of cells (Log-kill Hypothesis) rather than a constant number of cells ?
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Anticancer drugs follows log-kill Hypothesis I.e kills constant fraction of cells because of the specificity of the chemotherapy drugs to the cell cycle of the cancer. Example is use of Cytarabine in treatment of leukemia.
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Hi guys!
I am advancing in the empirical design of my next project about regimes of knowledge production on Adverse Drug Reactions (ADRs) and I would like to know if you have any suggestions of literature about this topic in STS, Medical Sociology of related fields.
I am interested in the perspective of the coproduction of biomedical evidence which emerges in the circuit of pathologization/diagnostic/medicalization/evaluation/new research agenda, specially addressed to the diffusion of immunotherapies and artificial antibodies in Oncology and Rheumatology.
Keep safe and cheers!
Renan
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Wow, Barry, Renan can now go wild.
Those are the most important references.
I recall the frustrations of a US doctor who penned that as:
Death by Prescription - Dr Ray D Strand
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I would like to have a better understanding of the medical, biological, physical and economical factors that are taken into account when deciding on what dose is delivered per fraction of radiotherapy for any given tumor.
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As a result of massive RT overdoses, several deaths and severe side effects resulted, but also some cases of unexpected good results or cure.
Why unexpected!? The knowledge that such results should be expected is available at least from 1990s.
The trial put all compensations to be paid by machine producer.
To me this is a great injustice! The financial burden must have been put mainly on the hospital and the medical physicists put in jail. After each maintenance the medical physicists must perform the appropriate QA and assure that the LA is in adequate condition to treat patients. On the other hand the phrase “the people driving the LA“ is puzzling, pointing probably towards the lack of medical physicist there. If this is so – the director of the hospital and the minister of health must have been put on trial as well. That’s my verdict :).
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Thank you
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This paper may be useful:
Experimental mammary carcinogenesis - Rat models.
Alvarado A, Faustino-Rocha AI, Colaço B, Oliveira PA.
Life Sci. 2017 Mar 15;173:116-134. doi: 10.1016/j.lfs.2017.02.004. Epub 2017 Feb 8. Review.
Best regards,
Daniela
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I woul like to submit a Review article in the Journal of Cancer Research and Clinical Oncology. Are there publication fees for this Journal?
Thank you in advance!!
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Thank you to everybody! Is it the same for Current Hematologic Malignancy Reports Journal?No publication fees?
Thank you
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Although cancer immunotherapy can be quite effective, it has a variety of drawbacks.
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Can Metformin use as a medicine for breast cancer?
What are the advantages and disadvantages of using Metformin in patients with breast cancer?
Is it possible to use Metformin for both diabetes mellitus and breast cancer?
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There is no known medication or therapeutic technique that is able to completely prevent malignancies, oral or otherwise. Anyone who claims that metformin completely prevents Breast cancer is either a misinformed medical lay person, or a quack practitioner.
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Hello everyone,
EGCG and sulforaphane are attributed intriguing pharmacological effect in a wide variety of fields. Recent research also investigates the synergistic effects of those two compounds (e.g.
Epigallocatechin gallate and sulforaphane combination treatment induce apoptosis in paclitaxel-resistant ovarian cancer cells through hTERT and Bcl-2 down-regulation (Chen et al. 2013)) with astonishing results compared to the isolated application of the compounds.
Although, there is one in vivo study in mice that investigated the combined effect (Nair et al. 2010, Regulation of Nrf2- and AP-1-mediated gene expression by epigallocatechin-3-gallate and sulforaphane in prostate of Nrf2-knockout or C57BL/6J mice and PC-3 AP-1 human prostate cancer cells), I doubt that these results can be simply transferred to humans, as I came across this study
Inhibitory effects of green tea and grape juice on the phenol sulfotransferase activity of mouse intestines and human colon carcinoma cell line, Caco-2. (Tamura, Matsui, 2000)
It occurs to me, that the co-administration of EGCG and sulforaphane might actually counteract what was intended. From what I understand, sulfotransferase responsible for the uptake of sulfones (like sulphorafane). Therefore, inhibiting that enzyme might prevent the uptake of sulphorafane at all.
Am I right with that conclusion or am I mistaken?
Best regards,
Christian
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Hi dear Christian Neumann
i think the following paper can help you
best and kind regard
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I have been looking for information about this but I still can't find a reliable answer. I have contacted Cancer Treatment Centers of America, The National Cancer Institute, American Society of Clinical
Oncology as well as the US National Library of Medicine but still no exact answer.
Anyone with reliable answer and evidence will be mentioned in my project as source of information.
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There is a well documented radiation application by the dermatologist Leopold Freund in Vienna, Austria, who treated a 5 year old grl suffering from Naevus pigmentosus piliferus in 1897.
Source: Wiener Medizinische Wochenschrift: "Ein mit Röntgen-Strahlen behandelter Fall von Naevus pigmentosus piliferus" (in German).
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A hallmark of cancer cells is defects in the apoptotic cell death program. Apoptosis is a highly regulated cell suicide process that functions to remove unwanted cells. One means of inhibiting the apoptotic pathway in cancer cells is through up-regulation of the anti-apoptotic BCL-2 family members, including BCL-2, BCL-XL and MCL-1. To restore the ability of cells to undergo apoptosis, small molecules have been designed to inhibit these proteins (Nature Webcast).
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Yes. there is a technique names as BH3 profiling which predict the interplay between Bcl2 family members and response to drugs. Anthony Letai from HMS developed this technique.
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What will be the best test in order to differentiate between Seminoma and Non Seminoma ?
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You may look the levels of tumor markets, if with elevated alphaphetoprotein, it does have a nonseminoma component; however gold standard for the diagnosis is pathology specimen result, so a biopsy should be done.
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More than 2 years ago, Tomasetti and Vogelstein brought that question to prominence when they tried to sort out environmental versus inherited causes of cancer. They examined the extent to which stem cell divisions in healthy cells—and the random mutations, or “bad luck” that accumulate—drive cancer in different tissues.
Vogelstein and Tomasetti developed new test that successfully detected cancers 70 per cent of the time in trials. and they stated that ".. Our study lays the conceptual and practical foundation for a single, multi-analyte blood test for cancers of many types. We estimate the cost of the test to be less than $500, which is comparable or lower than other screening tests for single cancers, such as colonoscopy. The eight cancer types studied here account for 360,000 (60%) of the estimated cancer deaths in the U.S. in 2017 and their earlier detection could conceivably reduce deaths from these diseases. To actually establish the clinical utility of CancerSEEK and to demonstrate that it can save lives, prospective studies of all incident cancer types in a large population will be required. ..." now
It is not easy to understand how cancer became an easily detectable disease from bad luck?
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I am afraid that by the time blood test is positive - that is cancer cells are in the circulation - it may be too late. Nevertheless, it seems to be a step in the right direction
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I would like to understand the current landscape of patterns in the diagnosis/ treatment and outcome measure of current therapeutic interventions that are available in LMICs for cancer.
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Cancer pattern and outcomes in low-middle income greatly differs from that of high income countries. It will also vary between countries within the low-middle income groups. Mostly, cancers of the esophagus, stomach, mouth, lungs, and pharynx in men, and uterine cervix, breast, ovary, stomach, esophagus, and mouth in women are commonly seen in India. Next, is the stage at diagnosis. Most or around 80% of all cancer patients are diagnosed in advanced stages (Stage III and IV). Thus, the outcomes to conventional treatments are relatively poor in comparison. The late diagnosis results due to lack of specialized services in the rural or under develop areas, low level of cancer awareness , and virtual absence of population-based cancer screening contributes to the late diagnosis of cancer in low-middle income countries. In India for example, more than 70% of our population resides in rural areas, however, almost every cancer diagnostic and treatment centers are located either in urban or semi-urban regions. This also contributes to drop-out during the course of treatment leading to incomplete or sub-optimal treatment, and thus poor outcomes. There are many gaps that needs to be addressed in low-middle income countries to fight cancer, given its socio-economic impact in these countries. I hope this would be useful .
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I need the most common methods and procedures to screen a phytochemical having anticancer activity both in vivo (animal model) in vitro and in computational systems. 
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1 year old girl. She had nephroureterectomy for Wilms' tumor. She has stage 1 favorable histology. She is being treated with NWTS 5 EE protocol. Following the second dose actinomycin-d and vincistine (3rd week) uric acid levels raised 9 mg/dl. Uric acid level returned to normal levels with hydration and allopurinol. other laboratory levels were normal. In this case we can not consider tumor lysis. Which mechanism can raise the uric acid levels? Is there any expert opinion for this case?
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Hyperuricemia in this case might be due both to an increased cell lysis- of probably normal cells due to the chemotherapy the child gets along with a reduced excretory capacity of the remaining kidney. Renal function should be thoroughly assessed as well as possible involvement of the second kidney with another Wilms tumor- which might be the case for so young kids presenting with Wilms tumor before 1 year of age. 
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Fibromatosis is a benign but locally aggressive lesion. Several agents such as Tamoxifen, NSAID, Imatinib have been proposed in the management but none have a definitive role.
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You can try apatinib or  sorafenib or Traditional Chinese Medicine
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No conclusive evidence exists for the role of chemotherapy in the management of immature teratoma high grade involving the retroperitoneum.
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I am sure that chemotherapy can not play a definitive role in management. Surgery is absolutely necessary.
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Dear Reader,
Please find below the detailled description of my current research and a couple of specific questions. I am glad for any opinion/input that you have on the topic, so please don't feel forced to answer the entire set of questions!
Many thanks and best regards
Stephan Schmidbauer
Preface
Combination treatments are an ever-increasing presence in oncology. In terms of explicitly approved drug combinations, the question is how the (additive) prices of these combinations can be reconciled with the financial power of the public healthcare system. If a clear advantage to overall survival can be demonstrated in a head-to-head clinical trial, the combination in question will usually be reimbursed. Often, however, manufacturers will refer to historical comparisons, one-arm trials, surrogate endpoints or adapted pathways for approval in order to provide evidence of efficacy. Despite subsequent approval, this leaves a significant degree of uncertainty in relation to efficacy and safety of new combination drugs. On the other hand, results on efficacy and safety in comparisons of phase II and III trials are frequently revealed to be in direct contrast (up to 50% of combinations are eventually found to be ineffective and/or unsafe, cf. doi:10.1038/nbt.2786 pmid:24406927).
A further case for consideration is the simultaneous administration (or sequential, if necessary) of drugs approved only as monotherapies; so-called “free combinations”. Aside from a pharmacological rationale, there is often no evidence to support such a regimen, yet the costs are additive.
  1. What data on efficacy, safety and (additional) benefit would you demand before reimbursing (as a payer) or prescribing (as a doctor) combination therapy instead of a monotherapy?
  2. Are surrogate parameters sufficient evidence of additional benefit in view of the significant (additional) cost of combination therapies?
  3. Do you differentiate between explicitly approved and “free” combinations when prescribing or reimbursing? (E.g. pertuzumab + trastuzumab vs. trastuzumab + anti-PD1; i.e. https://clinicaltrials.gov/ct2/show/NCT02129556?term=pembrolizumab+AND+breast&rank=1)
  4. How will you meet the financial challenges posed to your healthcare system by the foreseeable spread of combination drugs?
    • A:In your opinion, are the current combination drugs fairly priced?
    • B:Given that the value (to patient–relevant benefit) contributed by the individual partner of a drug combination  is normally unknown (i.e. it is unclear whether x months of drug 1 and y months of drug 2 contribute to i.e. Overall Survival ), how would you determine fair prices for the combination drugs?
  5. Do you view drugs reaching the market via accelerated approval processes more critically than drugs with full approval? If so, why? Do you reimburse/prescribe differently depending on the route to approval?
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Dear Stephan, this article, which I enclose, is not on the drug combinations in oncology. However, it addresses the issues of effectiveness, ethics and costs related to the introduction of new oncology drugs. I hope it will be useful to you.
Best regards, Maurizio
Cancer drugs, survival, and ethics
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Agressive angiomyxoma of the vulva commonly express estrogen and progesterone receptors. There are isolated reports of endocrine therapy used for downstaging these tumors for surgery or for management of recurrence. 
Do you have any experience of endocrine therapy for these tumors?
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Dear Dr Reza
i recommend to read this case report:
Aggressive Angiomyxoma of Vulva Which Grew with Pregnancy and Attained a Huge Size Rarely Seen in Literature
Vandana Sinha,corresponding author Kalpana S. Dave, Ronak P. Bhansali, and Ruchi S. Arora
Author information ► Article notes ► Copyright and License information ►
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Introduction
Aggressive Angiomyxoma (AA) of the pelvis and perineum was identified as a distinct clinicopathologic entity in 1983 [1] with less than 250 cases reported since then. The tumor usually arises in women of the reproductive age group with peak incidence in the fourth decade. Few cases of its occurrence outside the pelvis have been reported.
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Case Report
A 43-year-old female came to our OPD with complains of a growth over her private parts for the past 10 years and difficulty in walking for the past few days. She had delivered by Cesarean Section 9 months ago. The tumor increased gradually for 9 years, but grew suddenly during and after her pregnancy.
On examination, there was a huge mass arising from the left labia majora of about 55 × 45 × 45 cm with a broad pedicle (Fig. 1). The skin over the tumor was smooth, intact, and without any obvious nodularity. The right labia majora had multiple warts of 2–12 mm in size, also involving the peri-anal region.
Fig. 1
Fig. 1
Angiomyxoma of vulva arising from left labia majora with multiple warts on right labia majora
Pelvic examination was normal. There were no palpable lymph nodes. Biopsies from the large mass diagnosed angiomyxoma and biopsies from the warts diagnosed them as fibroepithelial polyps.
Her routine investigations, Pap Smear were normal. CT scan showed the presence of 53 × 43 × 46 cm sized heterogeneously enhancing soft tissue density lesion involving the left labia and perineum.
A wide excision of the tumor with adequate tumor-free margins and primary closure was done. There was no significant blood loss during the surgery. Histopathologic examination of the excised mass confirmed angiomyxoma, which was further confirmed by immunohistochemistry. The tumor was an infiltrating, diffuse, very low cellular spindle cell tumor with extensive myxoid areas and thick and thin blood vessels with foci of lymphocytes around the blood vessels. The base of the resection was free of tumor. She is symptom free for the past 8 months.
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Discussion
Aggressive Angiomyxomas are benign tumors. The term “aggressive” refers to the tumor’s locally infiltrative and recurrent nature, but with rare distant metastases [2].
In our case, AA showed the typical insidious growth pattern. Patients can present with an asymptomatic perineal nodule or a pelvic mass diagnosed on imaging studies. Our case also reflects the possible hormone dependence of this tumor as its growth was pregnancy related. Estrogen receptor positivity was also seen in the immunohistochemistry.
Pre-operative diagnosis helps in planning the extent of excision and patient counseling. However, the rarity of these neoplasms and a lack of typical features make it a difficult pre-operative diagnosis. They are misdiagnosed as labial, Bartholin’s, or Gartner’s Cyst and are diagnosed histologically after surgical excision.
Magnetic Resonance Imaging accurately detects the trans-levator spread and relation of the mass with the anal sphincter, urethra, bladder, and pelvic side-wall.
Tumor recurrences are high and can be seen even within 6 months from initial resection. There is no proven therapy for recurrences. Radiotherapy, selective angiographic embolism, hormone antagonists like tamoxifen, or GnRH analogs are also treatment options, but their role is still unclear.
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Conclusion
Angiomyxomas are rare tumors. Complete surgical excision is necessary to prevent recurrence. Patient counseling, individualization of each case, and long-term follow-up are essential.
Best wishes
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I want to find a high expression and low expression colorectal cell line to culture
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While there is this warning "Warn patients who are on immunosuppressant doses of corticosteroids to avoid exposure to chickenpox or measles and if they are exposed to consult their healthcare provider without delay. Inform patients of potential worsening of existing tuberculosis; fungal, bacterial, viral, or parasitic infections; or ocular herpes simplex " on the procpectus, I was not able to find any case report documenting an infection caused or got worse by the use of nasal steroids in immunocompromised patients. Would you prescribe them to a cancer patient who is on immunosuppressants, if she has severe nasal allergy or rhinosinusitis?
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Hi Omursen!
Literature search reveals that humoral responses were independent of inhaled corticosteroid use (even high-dose inhaled corticosteroid use) in one study of 294 patients with asthma  receiving influenza vaccine156 and another of 162 patients with chronic obstructive pulmonary disease taking inhaled steroids (87 patients), oral steroids (33), and no steroids (42). Corticosteroids alter immune function through direct effects on gene transcription and have broad effects on non-lymphoid and lymphoid cells.144 Corticosteroid use predisposes patients to infections, particularly with doses higher than 10 mg/day and cumulative doses higher than 700 mg.
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hi: when a patient With a Central venous cathether has a feber should cultures be done only when the cathether is red, etc or even if teh area surrounding the cathether looks normal?
I have always done the former: patient With a CVC + feber= culture.
can anyone Direct me to some evidence on what is correct?
Thanks!
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many thanks!
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A 84 year old woman with hypertension, 2 type diabetes mellitus and chronic renal failure (GFR 30-50 ml).
2005 NSTEMI: LAD and LCX PCI
2006 angina pectoris: distal RCA PCI. LAD and LCX stents no changes
2014 UA: RCA ISR. 1 BMS implantation. Other stents without ISR 
Echocardiographia all the time showed good systolic ejection fraction with good wall motions. 
In 2014 starts: in ECHO showed a non siginificant pericardial effusion. After coronarographia seen hematuria and anemia. 
An urological examination was negative for tumor, but an pelvis CT was done, whith some negative result.
2014.07 gastroscopia: duodenitis erosiva and chronic erosive gastritis was.
              colonoscopy: negative
2015.08.03-04 was admited with melena.  Gastroscopy and colonoscopy was not showed a point of bleeding. 3 U of blood was transfused.
An echo showed a significant pericardial effusion and a pericardiocentesis was performed. 1200 cc. straw-yellow liquid evacuated. And other day 100 cc.
2015.08.05-12 admited to hospital with anemia for blood transfusion. Colonoscopy was done again.  The source of bleeding was not found. A polyp of the  Bauchin valve was cut of.
The histology result of the colonoscopy sample not confirmed malignancy.
2016.01.05 Admited agin with huge pericardial effusion and symptoms of HF. 1500 cc straw-yellow liquid evacuated. A pleural effusion was this time and a diagnostic thoracocentesis was done.
The results from the pleural fluid showed a sigillocellulare cc. cells
The CA 125 was elevetad.  (95 the normla range upper limit is 35 at our lab)
Pericardial fluid: eosinophil cells, mesothel and lymphoid cells was seen.
An cardiac MR was done with negative result for a  autoimmune disease or primer cardiac malignancy.
An chest CT was done: negative for cc.
An abdominal and pelvis MR was done: at the point of obturator in both side an 6 mm diameter  lymphaticus nodus was detected. In the corpus of uterus an 8 mm myoma detected (T2)
Tuberculosis negative.
The hemoculture results is negative
2016.04.20 was admited with huge pericardial effusion. 1200 cc bloody liquid was evacuated. 
And now 2016.05.31. Again was admited with effort dyspnoe and not a very huge pericardial effusion.
The pericardial effusion sizes was 30-35 mm mostly left side and 25 mm from apex and right side.
The gastroentereologist, onkologist, gynecologist and urologyst do not know the reason of chronic pericardial effusion. Please help, what is the diagnostic option which can use to find the cause of pericardial effusion.
Thank you that you read and help.
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I think a partial pericardiectomy and biopsy will both help symptomatically and will probably give the diagnosis.  Malignancy should be high in the differential especially sonce the last effusion was bloody. You can also do a mammography and a thorough skin examination. Please let us know of the progress. 
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Hello;
We want to use NK cell for our hematologic oncology patients. I found some papers about it but couldnt be sure. If you could share your protocol or at least address me to a paper  please I would appreciate it..
I am looking for protocol for  NK isolation, NK expansion and NK quality control tests
Thank you
  B.S.
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Hi Berrin, Prof Cerwenka´s lab from DKFZ, Germany works extensively on NK cells. Please follow their papers. Miltenyi offers a human NK cell isolation kit and I know that their lab uses that. They use a triple cytokine cocktail for expansion. Please follow their lab papers for anything related to NK cells.
Sustained effector function of IL-12/15/18-preactivated NK cells against established tumors.
Ni J1, Miller M, Stojanovic A, Garbi N, Cerwenka A.
IL-12-producing monocytes and HLA-E control HCMV-driven NKG2C+ NK cell expansion.
Rölle A, Pollmann J, Ewen EM, Le VT, Halenius A, Hengel H, Cerwenka A.
Hope it helps. All the best!
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I have to perform intracarotid artery injection to build up a cancer brain metastasis model. Can anyone help me by providing a detailed mouse intracarotid artery injection procedure? Please include how to locate the common artery, how to steadily insert a needle? Do I need to close the incision on shealth and fat? Thanks in advance!
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Changting's response is very helpful. Thank you so much! I will try to contact you and talk more about this.
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I am looking for information regarding extravasation of chemotherapeutic agents from capillaries to tissues. If you could share your information, that would be very helpful.
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I do not know at all wether the attached article can be of help.
Best regards
Robert
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Can we diagnosis tumor subtypes such as lung cancer with EGFR mutant or EML4-ALK according to the special Metabolites. The Metabolites could be a good marker in prognosis ? I speculate that lung cancer with EGFR mutation or EML4-ALK have different Metabolic phenotype, which means that tumor with EGFR mutation primary addicted to glycolysis, whereas tumor with EML4-ALK addicted to glutamine metabolism.
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It has recently been reported that BRAF, KRAS oncogene mutant colorectal cancer cells highly depend on glycolysis as compared with other kinds of colon cancer cells.  BRAF, KRAS oncogene mutant colorectal cancer cells are known to exhibit resistance to EGFR inhibitors such as gefitinib. Therefore, vitamin C which consumes NADPH and GSH after uptake via GLUT1 shows therapeutic effect due to the imbalance of redox stress and impaired ATP synthesis. 
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Is it true that self breast exam is found to be not as sensitive as it was thought to be in detecting breast cancer? If so, is there any evidence available on the matter?
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Dear Ms. Alia .. this is very interesting thought since many people encourage ladies to do BSE without looking to the available evidence ..
Breast self-examination (BSE) has been compared with usual care (no screening activity) and has not been shown to reduce breast cancer mortality.
1st RCT study done in Russia " Results of a prospective randomized investigation [Russia (St.Petersburg)/WHO] to evaluate the significance of self-examination for the early detection of breast cancer ". (see the link)
2nd RCT study done in China " Randomized trial of breast self-examination in Shanghai: final results. (see the attached full text)
both studies showed no benefit of doing BSE compared to no screening and led to more breast biopsies and diagnosis of more benign breast lesions.
3rd link from NCI .. very helpful for more info about BSE & CBE 
Best Regards
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Squamous carcinoma of the cervix (2 x 0,8cm). 
Left ovary - micrometastasis, tube - N
Righ adnexa - N
LN - metastasis (right  1/5, left 0/5).
What will be the pTNM?
TNM-book doesn't clarified ovarian metastasis.
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If we use FIGO staging, it clearly states that any distant metastasis means stage IVB. SO, ovarian metastasis is IVB. 
If we use TNM, then of course M1
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Usually In the Heterotopic Xenograft studies, we are assessing the efficacy of NCE on the Tumor growth. I have the doubt on the effect of NCE on the normal tissue? Could anybody have an idea in this regard? 
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Dear Dinesh, 
If NCE means New Chemical Entities check this out: 
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In 1869, the resident physician at Melbourne hospital, Australia, Thomas Ashworth for the first time observed cells from a postmortem blood sample, from a patient who had about 30 subcutaneous tumors, that were morphologically identical with those of the cancer itself. This observation prompted him to suggest they “may tend to throw some light upon the mode of origin of multiple tumours existing in the same person”.
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You don't happen to have the publication available somewhere ... and a photo of Thomas Ashworth?
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I am looking for some databases to apply some techniques for the detection and classification of abnormalities in images of cytological tests.
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I am dealing with invertebrate tissues but my supervisor ifor bowen has a lot of papers about cancers you can search for i.d. bowen and also cathrin saraf
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What would be the best way of predicting VO2 max, uniformly, for cancer survivors, who have finished treatment at least a year prior to testing and who had a type of gynecological cancer?
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Dear Silvie,
maybe our study design (regarding a training program in lung cancer patients) is helpful in your context: http://linkinghub.elsevier.com/retrieve/pii/S155171441300195X
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I have already done ANOVA and two-WAy ANOVA. my sample size is not big (3*4). I was going to do linear fixed model but not sure whether assumptions are met.
I want to see that if there is any significant interaction in 2 different concentration of two drugs. if so, which concentration is significant. so what type of statistical test you would suggest?
Thanks 
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thanks for reply.
please take  a look at the following example:
we have  fixed concentrations of a variable( categorical). let's say, 0, 10 and 20 ug. and we have four different concentration of each variable, let's say, 0, 10,20 and 40 ug. in the latter, each group has a concentration(continuous). please take a look at the attachment file.
so now, I am wondering to know whether there is any significant combination between each different concentration (I mean drug interaction or combination).
please note that these measuring were repeated in three different days.
I want to know if each concentration  is significant per se or when they are combined.
Thanks,
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First congratulations for the excellent and promising article on 3-bromopyruvate. Can someone suggest a clinic in Germany or anywhere in Europe providing 3-bromopyruvate for treatment?
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We have C3H3BrO3 (3-bromo-2-oxo-propanoicaci;3-bromopyruvate) Molecular Weight 166.96
If U need - ask on ccmt@mail.ua
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Radiation oncology.
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Brainlab has worked well.
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Thoracic surgery.
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Yes. Seen a few patients. Usually need a combined surgical and adjuvant radiotherapy approach of treatment. 
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Alpha - fetoprotein is an alpha-globulin produced by embryonic hepatocytes and present in normal fetus and new born during the first days of life. But, in serum, high level is encountered in children with various neoplasia including emryonic carcinoma, vitelline tumor, teratoma and 2/3 of malignant epithelial hepatic neoplasia.
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Thanks! Dear Yoshida for your observation, but, have you any analysis of alpha fetoprotein in the evolution of any of those patients that developed tumor even above 70yrs? 
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Outpatient palliative care in oncology.
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Had my first experience of educating nurses on cancer palliative care. As cancer palliative care is a new concept for Sri Lankan nurses the module and the DVD on cancer palliative care we prepared  were appreciated by the nurses.
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With the sarcoma PNET, what would be suggestions for palliation after ˜Grier" protocol failure and temozolomide+irinotecan failure, in a metastatic young and fit patient?
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The most  active agents include vincristine, actinomycin D, high dose cyclophosphamide, doxorubicine, ifosfamide , topotecan and etoposide. The combinations of these drugs are effective in progressive and recurrent PNET
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I am currently using anti-bromodeoxyuridine (BrdU) antibody to detect BrdU. according to the manufacturer it detects the iodo analog as well, which I have seen to work. Since each of the analogs differ by one element....would this antibody detect the fluoro analog? has anyone done this before?
Thank you
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Thank you for your answer. I will be trying this during the week.
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We would like to give our mice a clinically relevant treatment of 5-Fluorouracil rather than the single 150mg/kg that seems to be more std with mice. However a conversion of a 5 day treatment for colon cancer in the clinic works out to giving the mice 132mg/kg per day for 5 days, which seems to me like it would be lethal. I am struggling to find access to literature on this (the paper below seems perfect but don't have access), does anyone have any information that could help us plan this experiment? Thank you. 
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Con'td: once you have set up the administration mode (and once again I strongly encourage you to choose the subcuntaneous continuous perfusion - beware, take the smalest osmotic pumps available (even if Alzet claims that bigger ones can fit into 25 g mice, it's just weird)), and next  just make a basic translation from human-to-mice dosing by considering that a normal 70 kg adult is about 1.73 m² (obviously this is quite variable, but this will give you the range) - depending on the mg/m² dosing  of the 5-FU regimen you are referring to in patients (quite variable as well, depending the protocol), then you can translate into mice eventually.  I have not made the calculations, but 132 mg/kg a day for 5 days by direct injection looks quite high indeed - having said that, switching to continuous infusion may improve the tolerance. Good luck!
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The data analysis of 1H- and 13C-NMR spectra of the tumor extracts demonstrated a significant increase in the concentration of the 2HG in IDH mutated tumors. On 13C-NMR spectra, 2HG signals were detected in the IDH1 mutated but not IDH wild type tumors. It is expected that 2HG may be actively being produced during the period of 13C-substrate infusion (e.g., [U-13C]-glucose). 
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According to Saka HK et al of Harvard Medical School, intrahepatic cholangiocarcinoma and subsets of neural, hematopoietic and bone tumors are characterized by frequent gain-of-function mutations in the isocitrate dehydrogenase 1 and 2 (IDH1 and IDH2) genes which acts through a novel mechanism of oncogenesis, producing high levels of the metabolite 2-HG, which interferes with the function of α-ketoglutarate-dependent enzymes that regulate diverse cellular processes including histone demethylation and DNA modification. Thus, a form of differentiation therapy is possible in clinical application to inhibit the mutant enzymes. And I think probably you are right in saying that clinically we can use the metabolite 2-HG to classify whether the tumors are IDH-mutant or wild-type which may have different tumor behaviors and tumor biology.
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Either it is acute or late effect.How it is prevent?
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Many highly effective agents , including anthracyclines and trastuzumab, are associated with well-described risks of short- and long-term cardiac events. As these agents are often used with curative intent, maximizing the benefits while reducing cardiac risks has become a priority in oncologic management, as well as monitoring for late-term toxicity.
Additionally, given the influx of novel biologic therapies designed to fulfill unmet medical needs, efforts are needed to promote strategies for risk detection and management to avoid dangerous toxicities which may impede development of and patient access to new agents.
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We are working on introducing the procedure in our hospital, your experiences will help us start successfully. Thank you all
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Dear Dr. Irfan,
Thank you so much for the information. We had some experience with the Diode laser in cordectomy for bilateral VC palsy too, and the results are encouraging; though we are yet to write about it. For the patient selection in the early laryngeal cancer, i quite agree with you because the outcome matters alot to both the patient, the surgeon and the system at large. My regards.
Dr. Kirfi, AM
Nigeria
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I have been researching endometrial carcinoma. Are there any distinctive markers that are used that will help classify sub groups?
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In fact it may be better to clarify your question: do you want to subclassify by any means (this is usually easily done by light microscope by pathologist) as  Dhiraj mentioned; or by molecular subsets?
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I understand the SOLE (Study Of Letrozole Extension) study is trying to answer some related questions, but has not yet reported. Is this true, or are there some nuggets leaking out?
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Thanks Konstantine, this is a very thorough and comprehensive review on extended hormonal therapy involving AIs, covering a lot of aspects on a subject that has not clearly answered yet. In my practice, the most common problem - and difficult to answer without solid data - is what to do with those patients who started initially with an AI and now reach 5 or (more difficult) 10 years (I use to extend AIs for more than 5 years if there are no complications). CM.
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Regards,
Jitendra
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Thanks Ravi Sir!
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I am working on SIB technique planning. I have done dosimetry on Phantom but I am curious about acute and late effects.
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yes
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I tried to use the few suggestion of peadiatrics dosing of RAI treatment in the ATA and EANM guidelines. I realised that there was a wide range of dosing after using those suggestion. Please help. Thank you. 
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Radioactive therapy with iodine 131 (131 I) is indicated to ablate residual normal thyroid and to treat functioning metastases in differentiated thyroid tumors. Because pediatric patients are few and the prognosis is generally excellent, 131I is usually recommended only for patients with extensive unresectable cervical nodal involvement, invasion of vital structures, or distant metastases.
From Rivkees SA1, Mazzaferri EL, Verburg FA, Reiners C, Luster M, Breuer CK, Dinauer CA, Udelsman R.
The treatment of differentiated thyroid cancer in children: emphasis on surgical approach and radioactive iodine therapy. Endocr Rev. 2011 Dec;32(6):798-826. doi: 10.1210/er.2011-0011. Epub 2011 Aug 31.
Ample evidence suggests that more extensive surgery is associated with lower rates of recurrence. Surgery is associated with clear and definable rates of complications that can be minimized when surgery is performed by high-volume thyroid surgeons. Evidence shows that, when properly applied, RAI is associated with lower recurrence rates. Evidence also shows that DTC is associated with an increase SPM risk, which reflects intrinsic factors related to having DTC itself. Evidence also suggests that relatively high doses of 131I may contribute to an increased risk of SPM. Thus, the proven benefit of 131I in preventing cancer recurrence and cancer-related deaths needs to be weighed against potential long-term risks.
Based on the constellation of the above information, the following recommendations are made for children with DTC (Figs. 5 and and66).
Fig. 5.Algorithm for the evaluation and treatment of DTC in children. US, Ultra
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Do you administer induction chemotherapy such as 7+3 for myeloid sarcoma in fit patients who can tolerate it? What is the best way to treat myeloid sarcoma?
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The decision for treatment does not depend on the chronologic patient age but on the biological age. At this monet I have a lady aged 71 years who is getting ready for allogeneic tranplant after 2nd. remission of AML. 
Radiation is another thing, there is no contraindication, but these are the ages with higher incidence of COPD and other pulmonary problems that are important risk factors for invasive fungal diseases...
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Tried
Cyclosporin, cyclophosphamide FCM , intolerant to methotrexate
considering cladiribine and alemtuzumab
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You can use G-CSF for the neutropenia; it might exacerbate the patient's joint problems; however, he could benefit from it, and you can combine it with extracorporeal photopheresis (ECP).
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Do you think it is safe and non-toxic?
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There is a good publication on Augmented Hyper-CVAD that combines Hyper-CVAD with Peg-Aps (and much more steroids than classical Hyper-CVAD). This is associated with toxicities (mainly sepsis/necrotising fascitis!). We at SQUH Oman usu the classical Hyper-CVAD augmented with Peg-Aps (2500 units/m2 I.V.) on Day 1 of A  part and Day 5 of B part and i think it is of major benefit based on previous studies assessing the addition of peg asp to a number of protocols. 
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What is the general opinion on the use of chemotherapeutic agents like fluoropyrimidine for treatment of non-tumoral stage (Adenoma) in a mouse model of colon carcinogenesis.
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our studies in Nude mice showed the ineffectiveness of this Protocol.
Action pyrimidine drugs had no effect on the cells (benign kladochnye line adenoma intestine, prostate and others) both in vitro and in vivo.
Protocols on request.
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A 45-year-old male patient had low-grade myxoida sarcoma in rt.lower leg (size: 7cm) and rt.ascending colon (pericolic lesion: 5.5cm) After complete resection both lesions, rt.lower leg lesions were treated adjuvant radiotherapy.
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PET-CT is great if readily available. Screening for pulmonal filiae is also paramount, since it is the most likely location for metastasis.
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In such cases, one questions himself about his ability of early recognition of melanoma, which is of great importance in the right on time removing of the nevus (or melanoma).
In your opinion, is it more a question of ignorance (you do not see, because you do not know) or could it be attributable to the nature of the tumor that can appear so suddenly and abruptly?
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Sir,
True nodular melanomas NEVER arise in a nevus. They always arise de novo, which means they are nodular from the very beginning. This is the definition of nodular melanoma. However, vertical growth phase in already present superfitial spreading melanoma (SSM) is usually mistaken for nodular melanoma. Vertical growth phase looks like a nodule, but it is NOT a nodular melanoma since it has its horizontal phase of SSM.
 Chances to miss melanoma and to allow to develop into vertical growth phase are zero if regularly followed-up with dermatoscopy.
Of course,
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NGS is a recent “big bang” in clinical genetics. I am curious to know how many of you are routinely used NGS in clinical setting (not for research only) – especially in cancer patients.
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We recently started using targeted panels and exome sequencing in the clinical practice mostly for targeted therapies in lung and colon cancer as well as melanoma. It is a rapidly changing field that is destined to grow especially as price continue to drop.  The real benefit will be as we are able to gather more exome or whole genome data on cancer genomes.  We will be better able to determine tumour heterogeneity and evaluate reasons for treatment failure.  Eventually this will be a front end analysis that will be more important than histopathology and radiology.
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A 10 year old boy has proptosis of the right eye.. Biopsy results reveal orbital lymphoblastic lymphoma. No brain or bone marrow involvement.
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You have to treat your patient as acute lymphoblastic leukemia with extranodal involvement.
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Dear colleagues,
I need some reliable information on treatment patterns in prostate cancer patients with regard to the two questions mentioned below.
Thank you for your help and all the best!
Sabine
1. Are patients in your country/region/center treated with hormonal treatment (LHRH) when they have rising PSA despite no metastasis on imaging?
2. Is adjuvant treatment after surgery or radiotherapy done and if yes, how long?
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a recent study presented at ASCO showed there was no benefit in early ADT for PSA relapse,until the occurence of clinical metastatic disease
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Would you combine imatinib with TKIs or mTORI?
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Dear Anna
I think there is no clear guidelines for the treatment of concurrent RCC and CML.  The determination of the CML status as primary or secondary is important.
I think after nephrectomy the determination of suspected getetic mutation is important before begining Sunitinib, sorafenib or Beva.
The combination of two target therapies is effective , but what is mandatory to register the genetic mutation during treatment.
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Leukapheresis is used in hyperleukocytosis condition in AML, CML, & ALLs to reduce WBC count mechanically. Can anybody explain or suggest reading materials clinical protocols and its procedure in clinical settings ?
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Here are the 2013 guidelines from the American Society for Apheresis. It is well researched and provides recommendations based on published literature with stratification of published literature by strength. http://italkid.org/Guidelines%20on%20the%20Use%20of%20Therapeutic%20Apheresis%20in.pdf
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In my center, an academic hospital in Spain, and an ESMO Designated Center of Integrated Oncology and Palliative Care, we are outlining a new protocol for Early Palliative Care intervention in advanced cancer patients. Does anyone have a protocol that is working well in university hospitals?
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Some of you may be interested in the free online resources available through the 'Palliative Care Curriculum for Undergraduates (PCC4U)' project.  PCC4U promotes the inclusion of palliative care education as an integral part of all medical, nursing, and allied health undergraduate and entry to practice training, and ongoing professional development.  Free learning modules (with video vignettes) are available on the following topics: Principles, Communication, Assessment, Optimisation, Multidisciplinary Care, Aboriginal Populations, Caring for Children and Culture-Centred Care.  Also available is a simulation scenario - instructional materials to support the implementation of a palliative care high fidelity simulated learning activity for health care students using an advanced patient simulator (you need a mannequin, associated software and clinical laboratory set up etc).  Visit:  www.pcc4u.org .
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Dear all,
I have been reading a review article published on Nature Review Clinical Oncology in 2013. In the paper entitled "Mutational landscape of HCC", I noticed that TTN was labeled as a gene frequently mutated in HCC in Table 1 but I couldn't find reference for it in the article and PubMed. Does anyone know where the citation is? I have emailed both authors months ago, but no responses.
Especially, I would love to know TTN mutation' roles in chromosome segregation.
Villanueva, A. & Llovet, J. M. Nat. Rev. Clin. Oncol. 11, 73–74 (2014); published online 7 January 2014; doi:10.1038/nrclinonc.2013.243
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@Pawel: Thanks for reply! Yes, I am aware of the titanic TTN and MutSigCV paper. Some papers even excludes TTN mutations right before any analysis. But, there are many muscular disorders resulted from TTN mutations. It is not entirely impossible that TTN mutations are not significant. Also, the review paper showed that the mutated rate of TTN in HCC is about 4 -10%. It conflicts with the idea that somatic mutations of TTN is frequently seen. I mean, the assumption of MutSigCV's paper is indeed charming. I love it. But, it doesn't mean that mutated TTN has no chance to contribute  in tumorigenesis. It is indeed very difficult to validate mutations on TTN because of its size. It is indeed that TTN is low abundant and may not have detectable expression levels (RNA and protein). Then, where did the citation of the review paper comes from? By the way, IntOGen considers somatic mutations in TTN as "driver mutation" in lung and bronchus cancer data from TCGA.
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I'm working on a book about ozone therapy and would like to hear any opinions on this topic.
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Thank you very much for your replies. If "prevailing scientific evidence does not support claims" but practitioners of alternative medicine believe ozone has therapeutic benefits, should more extensive research be funded?
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I want to design the experiment for cancer (except breast cancer, colon, prostate) treatment with anti tumor agent Hydroxycinnamaldehyde with molecular mechanisms or pathway.
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if so, I think you may do a microarray experiment first. Then you will find which pathway could change significantly. The drug may influence the modification of those pathway members, such as phosphorylation and acetylation.
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I've read "The Emperor of all Maladies" - having that scope covered as a training slide set for newcomers to the field would be really nice...
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