Questions related to Clinical Oncology
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
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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.
How much literature is there on the use of this scoring system to assess the tumour's response to the neoadjuvant stage of therapy?
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.
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 ).
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.
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.
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?
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?
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.
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!
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 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 ?
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!
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.
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?
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.
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).
What will be the best test in order to differentiate between Seminoma and Non Seminoma ?
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?
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.
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.
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?
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.
No conclusive evidence exists for the role of chemotherapy in the management of immature teratoma high grade involving the retroperitoneum.
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
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.
- 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?
- Are surrogate parameters sufficient evidence of additional benefit in view of the significant (additional) cost of combination therapies?
- 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)
- 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?
- 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?
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?
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?
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?
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.
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)
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.
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
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!
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.
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.
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?
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.
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?
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”.
I am looking for some databases to apply some techniques for the detection and classification of abnormalities in images of cytological tests.
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?
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?
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?
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.
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?
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.
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).
We are working on introducing the procedure in our hospital, your experiences will help us start successfully. Thank you all
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?
I am working on SIB technique planning. I have done dosimetry on Phantom but I am curious about acute and late effects.
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.
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?
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.
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.
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?
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.
A 10 year old boy has proptosis of the right eye.. Biopsy results reveal orbital lymphoblastic lymphoma. No brain or bone marrow involvement.
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!
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?
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 ?
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?
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
I want to design the experiment for cancer (except breast cancer, colon, prostate) treatment with anti tumor agent Hydroxycinnamaldehyde with molecular mechanisms or pathway.
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...