Questions related to Neoplasms
Are you aware of any publication on mucinous cystic neoplasm of pancreas where the serum estrogen levels where measured? I am aware that many express ovarian tissue (struma ovarii). I keep getting hits on estrogen and progesterone receptor expression but I want to know the estrogen levels. Thanks in advance
I'd like to determine microvessel dimensions in various tumor groups and am looking for an online database to draw pathology slides from.
I am trying to establish an ovarian cancer preclinical model through peritoneal injection into C57BL/6 mice.
The parental ID8 p53-/- cell line was modified through lentiviral infection in order to express OVA peptide and GFP-luciferase. We injected 5·10e^6 cells per mice.
In day 40 after injection we did not get any tumor in any of the mice.
Hi, I need to have a dataset including the expression level of a particular miRNA and a particular mRNA in tumor (digestive cancer :Colorectal+gastric)+ its matched normal tissu across samples provided by TCGA database .What exactly should I do? thanks
Hi. I am struggling with the mouse animal model. I found that the subcutaneous tumors are extremely uneven in my mode. I injected the same volume of tumor cells (human cell line) suspension s.c. in balb/c null mouse and the size of the tumor show uneven after 1-2weeks. This has a great impact on the following treatment. So, I wonder what is the best practice for subcutaneous tumor inoculation? Or, are there any ways to prevent uneven tumor growth?
Thanks a lot!
Hi has anyone had experiance of GL-261 not growing subcutaneously? I have inoculated 10e6 cells in C57BL/6J female mice and the tumors became palpable after a week cca but have subsequently disappeared except in few mice. The cell line is routinly used in the literature s.c in imunocompetent strains so I don't know what's the problem.
Hi, everyone, i am a fresher of tumor immunology.
Recently, i am preparing to study how pdl1 regulation in tumor cells will affect the function of t cells. and i have read a paper " miR-424(322) reverses chemoresistance via T-cell immune response activation by blocking the PD-L1 immune checkpoint. Nat Commun" . In this paper, author applied PBMC from healthy human with the anti-CD3, anti-CD28 and incubation of skov3 tumor lysates. Then, isolated CD8 T cells to co-culture with skov3 cells. i would like to apply this model, but i have a question, anti-CD3 and anti-CD28 has made CD8+ T cells activated, why do they need to add tumor lysates?
And, right now, i don't make sure whether i should apply antigen-specific CD8+T cells to coculture with tumor cells? other papers indicated that firstly isolated monocyte-derived DC and then make them matured with some cytokine stimulation and tumor lysates incubation. Then matured DC cocultured with CD8+ T cells to get the tumor-antigen specific T cells. These obtained CD8 T cells then cocultured with tumor cell lines. could you kindly give me some advice based on my research purpose?
Hello, i am searching for breast cancer elastography datasets, so that by using machine learning technique, sort out whether the given elastography of breast is benign or malignant.
However i cannot find the place to get enough number of elastography datas...
Would you let me know any?
I sincerely appreiciate it in advances!
There are rat strains that are more likely than others to spontanuously develop tumors. Are there litteratures covering this questions?
EBV-B cells have been using our lab to investigate the role of B cells in tumor micro environment. Recently, I have realized that EBV-B cells start to turn into black cluster in 2nd passage after culturing from stock. You can see the pictures of healthy EBV-B cells and black cluster.
Thank you in advance,
I'm observing a small tumor with confocal. I imaged the expression of a fluorescent protein, which is supposed to express everywhere. However, I can see some vague DAPI signals, where I can't observe the fluorescent protein. Is this normal? If so, wouldn't the images that I obtained for a single layer be always interfered with vicinity layers?
I want to know about the general mechanism of radiosensitizers.
how they locate tumor cells in the body?
how they differentiate between normal cells and tumor cells?
what basically happened when we take a radiosensitizer before the radiotherapy?
in children, is liver transplantation for large HCC confined to the liver allowed or contraindicated?
SLURP1 protein is known to be an anti-cancer protein. It can inhibit certain cancer cell lines at very low concentrations as observed in in vitro experiments. However, gene expression data on NCBI GEO database reveals SLURP1 expression is relatively high in tumors than normal tissues. Can anybody give an explanation for this phenomenon?
Thank You,
Amal.
If I report a breast imaging exam (MRI, US or Mx) which not shows any malignant findings in a biopsy-proven breast cancer, which BIRADS score do you use?
Can a 3D mammary epithelial cell culture model be established using Matrigel since it is a tumor matrix? Or should we use collagen matrix to create a true model of the epithelium?
I'm conducting a retrospective study on diagnostic accuracy in detecting thyroid malignancy for 2 different ultrasound scoring systems. The same cohort will be scored based on both scoring systems and their pathological report reviewed to determine the malignancy pick up rates. When do I do the calculation for power of study - Is it before or after? And what test should I be using?
Hello,
I have developped 4 markers to detect microsatellite instability in a cancer type using digital PCR.
I would like to determine the discriminatory power of each marker, meaning the cut-off (mutant allelic frequency) to classify a tumor as microsatellite instable (MSI) or microsatellite stable (MSS). For each marker, I performed ROC analysis using 7 MSI tumors and 20 MSS tumors but I was wondering if ROC is the right analysis for this purpose. Could you help please ?
Best,
Khadidja
I have a question about T-cell recall assays. We vaccinated mice and wanted to see if there was a T-cell response against our tumor cells. There was no tumor challenge. We pulsed DCs from naive cells and then cocultured these DCs with the T-cells. But we also seeded the tumor cells and cocultured the T-cells with them. Could anyone shed light on why we would do both of these?
My guess is that the pulsed DCs activate naive T cells and can show that you have tumor specific T cells but they were not activated by the vaccination. But if you do it with the whole tumor cells and there is a response, it means the T cells were already activated by the vaccination. Is this correct?
Hi,
I want to stain brain sections of mice which have been xenografts with tumor and treated with a new anti cancer agent. Can some please share the protocol with me including tips and does and dont's for the staining. I would also appreciate cat# for antibodies and any other critical reagent.
Hi everyone!
I analyzed 20 tissue samples of oral leukoplakia (OL - an oral potentially malignant disease) through untargeted metabolomics to compare the metabolic profile of those OL who had malignant transformation (5) and those who did not (15). I know that the small sample size is one important limitation of the study, but OL is a rare disease and I have to deal with it.
Well, when I use my complete dataset (around 4k compounds) to perform multivariate analysis such as PLS-DA, my model is overfitted, exhibiting a negative q2. However, when I use the 72 compounds considered statistically significant by the univariate methods (hypothesis tests) as the input data, my q2 rises to 0.6. The improvement also occurs when I use this small dataset to build the heatmap that clearly distinguishes the malignant transformed from the non-transformed OL. Interestingly most of the compounds classified on the PLS-DA VIP list are the same, both using my whole data and using the 72 discriminant features as the input.
I recently presented my thesis to a metabolomics specialist and she told me that my analysis is curious and that she cannot tell me whether it is right or wrong.
Would anyone here help me with this question?
Thanks!
Magnetic nanoparticles are present in the center of the tumor and are the source of heat. Which is heated using an external magnetic field. Assuming that the tumor is spherical in shape.
Recently, I am exploring the potential function of one gene in cancer. Since the TCGA datasets as well as some other clinical data show that this gene is up-regulated in cancer and especially in basal-like subtype. I tried to knockdown it by shRNA and the result show the depletion of this gene accelerate the proliferation, migration and invasion rate of cancer cells. I also tested the over-expression in cancer cells and the result show the over-expression impaired the proliferation rate. This observations is also consistent with some previous report which reported it as tumor suppressor. Although I found that expression of this gene maintain the basal-like feature of breast cancer. The results is still confused me.
My question is whether you know some similar works or papers.
- We are working on a tumor microenvironment project in a mouse model of a cancer. We have generated tumors that develop at multiple anatomic sites and we want to identify the differences in tumor stromal cell changes at scRNA depth. We are obviously running scRNA seq on tumors, but would you recommend using databased control tissue (there is databased scRNA seq for each of the anatomic sites), or would you independently do your own control tissue and eliminate all batch effects?
- Also, would you do an admixture of cells from multiple mice (as a way to even out individual difference in cell composition) or just use a single mouse (we want to be somewhat cost effective, while still doing good science, especially when we are talking about scRNA seq)?
We have been orthotopic study to analyze the in vivo anti-cancer efficacy (brain, liver).
As you know, its study should do H&E staining to distinguish tumor from sectioned sample.
although we manually annotate the area and extract its intensity, I think, there seems like a automatic program to calculate a ratio of area (tumor / entire section).
Or Do you know some efficient and rapid way to calculate a ratio.
Hepatocellular carcinoma is one of the deadly malignancies. It usually occurs in cirrhotic patients.
TCIA - REMBRANDT consist of 130 cases with 3 categories of tumor such as glioblastoma, astrocytomas, and oligodendrogliomas. How to identify the images are belong to the 3 different categories?? how can I keep a separate folder to have these 3 tumor classes to use it on CNN.
I work on gastric cancer. I want to separate the top layer of tumor cells from the lower layers.
Hello everyone,
I am interested in expression of miRNA in different AML cell lines (such as HL-60, OCI-AML2, ... and also the myeloproliferative neoplasm cell line SET-2) which I will investigate with RT-qPCR. It is highly recommended to use endogenous controls for the experiments but I could not find literature for all of the cell lines. I thought about using Broad Institute Cancer Cell Line Encyclopedia (CCLE) to look for stably expressed miRNA.
Do you have any suggestions how I should proceed? Investigating endogenous controls can take a lot of effort like shown for T-Cell ALL (10.3390/ijms19102858) but I am looking for controls to use in just a few cell lines (less than 10).
I did Immunofluorescence staining of DAPI using the lung tumor tissue frozen section which contains part of the normal site, but I find it hard to figure out why the DAPI staining (or other antibodies) intensity was weaker compared to the normal sites under the same condition. I repeated it more than once, I don't know what's wrong with it.
We are in concern of CSF flowcytometry to detect lymphoid malignancies, Please could you give some of experience toward standardization
We injected different densities of GL 261 cells (1, 2, 5 or 10x106 cells) in 100 µL PBS or 100 µl 50%PBS/50%matrigel in the flank of 8-week female C57BL/6J. A few days after the injections we observed, on some mice, non measurable tumors. But in the end, we did not manage to obtain any tumor. Do you have some advice to obtain subcutaneous GL261 tumors.
I am interested in cancer treatment. Especially in Boron-neutron capture therapy(BNCT).
And my questions are as follow:
1) When the boron-10 compound will reach the malignant cell? Does it depend on the carrier?
2) How much time should be left from the injection of the boron-10 compound until the irradiation?
Out of T98G, U87MG, U118MG, A172, U251MG cell lines, which line is more preferred or considerable in GBM tumors? Can anyone provide subcultured cells with an excellent passage number?
Thank you
We used WB to analysis tumor sample from Hepa1-6 transplanted to C57BL6J mouse flank. In drug treatment group, we observed reduced p62 level and accumulation of LC3B-I.
We assumed that reduced p62 level indicates that autophagy is stimulated. However, accumulation of LC3B-I is the marker of autophagy inhibition. We feel confused to draw a conclusion.
How to explain these results? Can we do some more experiments to analyze autophagic flux?
Recently, we have injected s.c. B16F10 tumor cells in BL/6 mice. At around 12-15th day some animals showed ulcerations in tumors , with a big hole in the middle (it looks like a volcano). We have also observed this problem in MC38 and EG7 tumors. This did not happen to us so often until now. Any suggestion or personal experience that helps us to resolve this issue will be really appreciated. Thanks in advance.
I am looking for tools/methods for somatic variant calling for unpaired samples. The somatic variant calling through GATK best practices is specifically for tumor/normal paired samples. My study entails somatic variant analysis studying complex disorders, thus I have unpaired samples. I found following options:
Samtools, ISOWN, Mutect (only tumor mode) and SomVarIUS .
I would like to compile as many options as i could and choose the best suitable for my study.
Kindly suggest further options and any opinions and suggestions are welcome.
There are various points of view some of them reported the ratio of early/late apoptosis as killed tumor cells by CTLs. Others reported the sum of early and late. However, we know CTLs kill tumor cells through lysing so it seems PI positive should be considered as the killed cells. What is your idea?
Greetings, everyone! I am a student and have question about radiotherapy planning. Where can I find recommendations and/or instructions for beam arrangements of different tumor localisations? For example "box" for rectum and prostate, and tangencial fields for mammal.
Thank you so much and have a good day!
I want to make single cell suspension from mice ovarian tumor for FACS sorting. For that I will be using 10x triple enzyme stock solution (collagenase 10mg/ml, hyaluronidase 1mg/ml, DNase 200mg/ml or 20U/ml) prepared in DPBS . I am little confused regarding the concentration of DNase? Can anyone suggest if I am using the right conc. of DNase ? Should I use calcium free DPBS or HBSS-Ca2+ solution for incubating tumor pieces?
I tried to do a study about calculate the sensitivity and specificity of fine needle aspiration cytology (FNAC) in a type of cancer.
After I have collected all the data, I noticed that some results are indefinite (means the results are there but from the results, we couldn't identify whether it's malignant or benign tumor. )
I'm thinking whether should I exclude the inconclusive results from all the calculations (means consider the inconclusive result as false positive for sensitivity and false negative for specificity).
This is my first study so I am kinda' lost. Anyway, thank you in advance for your help.
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.
I don't understand it. Sellar tumors in the 2016 version of the WHO-classification of primary brain tumors contain craniopharyngeoma and several tumors originating from the posterior pituitary (pituicytoma, granular cell tumor...) but the pituitary adenoma is nowhere to be found. How come? What's the reason?
I'm fairly new to cancer research and there's a host of articles on Sunitinib being administered via oral gavage in mice models but I'm unable to find any information on studies that have explored directly injecting tumors with Sunitinib. Just curious.
Chemotherapy for breast cancer costs the UK economy more than £248 million annually, including ‘out-of-pocket’ personal costs of more than £1,000 per patient – according to new research from the University of East Anglia.
Key findings:
- The total cost of breast cancer chemotherapy in the UK economy is over £248 million.
- Societal productivity losses of £141.4 million - including £3.2 million lost to premature mortality, and £133.7 million lost to short-term (£28.7 m) and long-term (105m) work absence. Further costs include £3.4m associated with mortality losses from secondary malignancies due to adjuvant chemotherapy and £1.1m in lost productivity arises from informal care provision.
- £1.1 million in lost productivity arises from informal care provision.
- Out-of-pocket patient costs for chemotherapy total £4.2million, or an annual average of £1,100 per patient.
In addition, costs for the emotional wellbeing of carers could be as much as £82 million. Emotional wellbeing reflects how much additional income would be required to offset a wellbeing loss.
‘Societal costs of chemotherapy in the UK: an incidence-based cost-of-illness model for early breast cancer’ is published in the journal BMJ Open on January 5, 2021.
Which any type of tumors most commonly found in broiler chickens carcasses in processing plant ?
The tumor cells are from a variety of cell lines from ATCC .
I stored tumors in RNAlater. However, I want to use these tumors for making protein lysates for cytokine expression analysis.
Hello,
I am curious as to if anyone has any expertise or information about setting up a subcutaneous human xenograft model for a CD19 bearing tumor and human CAR experimental system. I looked up many different references using either the NALM6 or Raji cell lines at varying log differences in cells injected with and without matrigel. We piloted a tumor growth study using the range of cells published (10^4-10^6) without Matrigel and did not get any tumor growth in the time frame (21 days) of the published reports. Any tricks or hints on sublcones for the NALM6 and/or Raji cells would be helpful. The pilot was performed with the NALM6 CRL-3273 from ATCC. Thanks.
Dear all,
I'd like to introduce a tumor in such geometry, how I can do that?
Dear colleagues,
I would appreciate your advice on the following issue.
Let's say, first I had investigated expression of Prot1 and Prot2 in tumor tissue, it's association with relevant clinical data (stage, histotype, prognosis, outcome, etc).
Then, I studied expression of Prot3 and Prot4 again in tumor tissue.
However the patients are not the same, although the all have same cancer type, but overall study groups barely slightly overlap.
My question is what might be a good approach to summarise previous work and analyze those proteins altogether (I mean without performing additional experiments). I thought of using some ML classification/regression but haven't gone too far.
Hi all,
I used tumor dissociation kit(Miltenyi Biotec) to first isolate cells from tumors. Then I washed cells twice with PBS, and cultured the cells in complete RPMI (5%FBS, and pen strep). However, 2 days later, I found my cell culture is totally contaminated by bacteria. Frustrated.
How to make primary cell line from tumors without contamination? Thanks!!
Our lab is trying to establish a BT-474 xenograft model. We have not been able to get the tumors to grow past 50-100mm3. We inject 1x107 cells in a 50:50 matrigel suspension. We used nude mice (5 weeks old) that have been implanted with estradiol tablets (90-day; 0.36mg). After 5 weeks the tumors have stopped growing and some are shrinking. Does anyone have experience with this model and can offer any advice? Should we go up on the estradiol dose? We used 0.36mg to avoid toxicity. Thank you!
I am looking for CT images of different Cancer cell like ( Brain- Head&Neck - Liver- Lung and Prostate ) with contoured area that shows me where is the tumor exactly.
I need to Download Dicom files which I know Where to find them but the important thing to be with previously known and determined exact place of the Tumor which I could not find them so I could use it later in the simulation in the master thesis.
I use many websites but the problem that I could not find where is the tumor in the CT images
I use the following websites but they do not have contouring around the tumor:
The only website I have found with contoured area with CTV and PTV is:
3- https://econtour.org but the problem that I could not download them as a DICOM files.
Any help is appreciated and Thanks in Advance
I have a protocol from Himes J Neuro-Onc 2020 using GBM EVs on peripheral blood monocytes. The endpoint is converting monocytes (CD14+ HDA-DR high) to MDSC (CD14+ HLA-DR low) with tumor derived EVs, and using these cells for functional studies. These cells are cultured w/o FBS, I am new in this field and wonder if not using FBS is routine in the field.
Thanks
Dominique
Hi, is there any dataset about occupational skin diseases (especially skin cancers) that contains skin lesions images (simple or dermoscopic or histologic) ,integrated with clinical data and occupational history (e.g. to see if they have had occupations with carcinogenic exposures particularly UV)
I want to use it to make a research on the contributions of these exposures in the development of skin cancers and the possibility of early detection of the malignancy of these lesions by data mining and image processing considering occupational exposure as an important parameter
any suggestion is appreciated
I am working on tumor induction in experimental rats and needed 1,2-Dimethylhydrazine to induced tumor in the lab. animals. Please I need help from anyone who can render help.
I am interested in identifying all relevant case reports or case series related to a very rare complication of neoplasms. I am currently searching PubMed and CINAHL for this purpose, but I am interested in expanding my search to other databases which are either specific to or which have a large number of indexed case reports or case series. Do you have any suggestions? Many thanks in advance!
I'm looking at doing a transwell migration assay with tumor conditioned media for RAW264.7 cells, but the literature has a pretty wide variety of pore sizes used for this specific cell line. Does anyone have recommendations on what's worked for them? Thanks!
I am trying to extract intact nuclei from OCT-frozen tumor tissue samples. Does anybody have a protocol for doing so? I need as many intact nuclei as possible for performing ATAC-seq on them.
What is the best way to quantify tumor cell death (cell lines) after incubating with CAR-T cells?
Thanks.
Hyperspectral medical imaging, hyperspectral image for cancer/tumor detection
with my matlab code as following
classNames = ["background","tumor"];
pixelLabelID = [0 1];
pxds = pixelLabelDatastore(im ,classNames,pixelLabelID, ...
'FileExtensions','.nii','ReadFcn',volReader);
Error using pixelLabelDatastore>parseInputs (line 202)
'FileExtensions' is not a recognized parameter. For a list of valid name-value pair arguments,
see the documentation for this function.
Error in pixelLabelDatastore (line 151)
[location, classes, values,params] = parseInputs(varargin{:});
Error in SEp1 (line 27)
pxds = pixelLabelDatastore(im,classNames,pixelLabelID, ...
I'm trying to evaluate for mRNA expression level of ONE gene in hundreds of tumor samples. What is the method to do this?
Edit: Also, does the type of tissue I have affect which method to use? For example, frozen tissue vs FFPE tissue.
Different types of neuronal tumors occur in children such as neurocytoma and neuroblastoma. I look for any evidence and details about the mechanism by which a neuron can develop a tumor.
Tumor mutational burden (TMB) is a measure of the number of gene mutations inside the cancer cells. TMB of a tumor sample is calculated by the number of non-synonymous somatic mutations per mega-base in coding regions. The value obtained for TMB always ranges from 0 to 1 which never reaches 1. What is the minimal cut-off that can be assigned to classify TMB as High, Medium and Low?
Hello everyone,
I see a lot of papers with the spheroid generation topic. I know spheroids are used widely for simulation of tumor condition in body. Can someone say which abilities does the primary cells have which cell line do not have? like generation vascular endotheilal or producing extracellular matrix and which abilities cell line have which primary cells don not have?
Thanks in advance
I‘m doing my dissertation and the results data are all positive in the reduction of tumor size with a drug I Would like to know what method should I use or any suggestion would be really appreciated
Can you help with the referencing materials for the mathematical modelling of behavior of 'Tumor size','Toxicity', and 'Drug resistance' during the Chemotherapy cycles. ?
Thanks so much in advance.!!!
I have conducted a binary logistic regression.
There are 294 lesions and logistic regression can separate them as benign and malignant.
For this purpose three of the study parameters produced a formula. As you know it is something like:
Benign/Malign Score = 1/ 1+ exp[(Parameter1*Constant1)+(P2*C2)+(P3*C3)]
During cross validation, 80% of cases constitutes training set and %20 of them are test set.
Training and test set are formed randomly.
The constants in this formula change during each rebuild of the training and test groups as well as Sensitivity, Specificity and Accuracy.
I need help:
1- How would you suggest I manage the validation process so that I can give a single formula that everyone can use? Because the formula is changing in every single validation.
2- I want to study validation process 500 times. I am going to give arithmetic mean of Sensitivity, Specificity and Accuracy of 500 measurements. Do you offer another information to provide in the manuscript (for example min, max, 95CI of Accuracy etc.)?
Many thanks in advance to everyone who showed interest and kindness to respond.
Dear Jose,
In this article the authors claim that alpha-fetoprotein can be absorbed from GI tract into the blood (up to 11%) after per oral administration in an undigested form and travel to tumor sites carrying the non-covalently binded toxin (drug Aimpila) to destroy the tumor:
Do you believe their results?
In the previous article of the same authors the absorbency was 0.1%:
file:///C:/Users/vpak/Downloads/otsenka-internalizatsii-afp-soderzhaschego-nekovalentnogo-kompleksa-aimpila-v-modeli-izolirovannogo-otrezka-tonkoy-kishki-krys.pdf
Thank you,
Vladimir N Pak, PhD
I have T1-pre contrast MR images for three patients with gliomas however the tumors in the first patient looks darker while the tumors in two other patients look brighter. I wonder why?
Can anyone help me about this?
I upload the images.
I want to know how to look/analyze different parts in a tumor section like stroma, Ductal epithelial, epithelial lining, luminal epithelial etc etc in a breast cancer tissue slide.
Also is there any handbook/video tutorial for learning IHC slide analysis/ scoring ?
Thanks for your time!!
To find the tumor stages or growth analysis from initial stage to glioma stage which dataset will helpful.In which dataset will be able to get tumour description.
I am looking for pathological report data (text based) on histopathological analysis of cancerous tumor whole slide images. If there are any pubic (request based or otherwise) datasets available on this, then kindly inform me. It would be really helpful in my research on Computational Cancer Pathology. Thanks.
I would like to ask if someone could kindly provide me a good protocol, or suggest me a good paper with a proper description of an in vitro INVASION ASSAY to use with a neoplastic cell line.
As N-methyl-N-nitrosourea is a carcinogen used to induced mammary tumor in rats for breast cancer model development and we ran out of carcinogen what could be the possible alternative or the promoters that could help us in tumor induction imparting no other side-effects?
Las células de Schwann normalmente no están presentes en el parénquima cerebelar y es difícil explicar el origen intracraneal de schwannomas intracraneales. Muchas hipótesis han sido planteadas para explicar los shwannomas no relacionados con nervios craneales como el posible origen de células de Schwann en los plexos perivasculares: conversión de las células piales en células de Schwann, origen desde fibras nerviosas ectópicas, células de la cresta neural que han migrado erróneamente durante el desarrollo del sistema nervioso, u origen en células mesenquimales multipotenciales. Redekop y Elisevich propusieron la teoría de la embriogénesis distorsionada. [4]....
...Los shwannomas intraparenquimatosos no asociados a nervios craneales son neoplasias raras, la revisión de la literatura reporta hasta 1998 solo 35 casos descritos en los últimos 30 años [3] y 44 casos hasta el año 2004 localizados en los hemisferios cerebrales, [9] en la medula y 14 en el cerebelo. Todos excepto uno, fueron reportados como benignos, de mayor prevalencia en pacientes jóvenes y de localización vermiana.[2]....
...70 casos de schwannomas intracerebrales reportados hasta el 2011 fueron de localización supratentorial tanto en los hemisferios como en los ventrículos. De los 26 casos reportados en localización infratentorial, 11 estaban en hemisferios cerebelares, 6 vermianos y 9 medulares. Todos los casos fueron benignos excepto dos. [4]...
I'm want to deplete cells only in the periphery but do not know if they will deplete T cells infiltrating tumors
