Chemotherapy - Science topic

Maybe we do not understand the underlying mechanism of the genesis of "cancer" and because of that not the therapy... The world know spontaneous healing and nobody does research on this...

Maybe we have to look for new ways to regard the (re)actions of the body and the biological meaning wihtin. Just to allow us to do new research. Only the thinkung of new ways brought mankind further, the repetition of the thinking until today not. Modern cancer therapy found out many ways, but most cancer patients die after serveral years, especially the patients who are treatet much and have a long journey in the healing system. This circumstance should be the point of thinking new ways...

In every biological being the sensation/perception of the surrounding (context) determinates reactions of the whole organism. E-Motion is Energy in motion and leads to reactions in the body ant its organs.

For example: If a shep looses his lamb, the milk ducts reacts. Under a microscope we may find a so called "ductal mamma carcinoma". This reactions forms back if the shep is pregnant again.

If you treat mouses with cigarette-smoke the lung reacts with metarmophosis according to the fear of death, the air sacs proliferate as a ancient evolutional reaction of the fear of death. Like a cancer-patient who got the idea that he/she will die soon... If you treat hamsters in the same way nothing will happen, because hamsters have no fear of getting burned according to the hamsters lifestyle in contrast to the lifestyle of mouses. A mouse needs a high sensibility for smoke, a hamster not.

Humans have the brain and its main-funktion the prediction. This ability of the brain - to scan the context and create predictions - is in humans on a high level. Old patterns of our socialisation are mixed in our daily prediction-process and if context meets imprint we call that "Emotion". Our interpretation leads to reactions of the body.

If a woman is in huge worry about her child for serveral months it is very probable the she becoms a ductal mamma carcinoma. This carcinome build back if the worry is solved in reality (the child is cured, alive not harmed any more...).

If a man looses his son and heir (in his interpretation of the death of his son) it will be very probalble that this man becomes cancer of his testicle.

I have used "swimplot" in R for a previous study, link and instructions here:

Hello Sama Yaqoo

You may please refer to the article attached below for more information.

Best.

Yes you could or you could compare treated (i.e. at IC50 dose) vs. untreated (mock treated).

Control genes are usually selected from β-actin, tubulin, GAPDH, Lamin B, PCNA, Na+/K+-ATPase, Histone H3, etc.

The following articles related to DOX-stimulated CD4+ may be helpful to you.

He@llo Malcolm Nobre

Thank you very much for answering my question

I am currently working on solid tumors in children, and I thought of taking three types of tumors and measuring some inflammatory markers for them, so I wonder to myself whether this is true or should I work on one type and do the tests

Dear Stephen Szpak, one way to do that is via "dual stimuli hydrogel". Also Gels having two LCSTs present dual thermoresponses. My Regards

Hi Stephanie Pearson, I also looked for information on chemotherapy treatment in the UK Biobank. But the web shared in the response did not work. Do you figure out this question? Could you please share it with me? Thanks!

thank you for answring my quesion dear Dr Erum Zafar

I believe it may have something to do with DAPI concentration. In your shoes, I would trust Trypan blue kit more.

Ruby,

At first, calculate IC50 of that particular drug for your cell line. Then you can treat different concentration of that drug for 8-14days.

Thanks Dear Dr for your suggestion ,I visit the website and read their guidelines which mainly about mucositis of GIT tract ,in this case endoscopy reveal no evidence of inflammation or ulcers ,biopsies where of villous atrophy ,most properly due to chemotherapy ..unfortunately trial of treatment were not so successful

Linna Green and no, I have not tested the transfection efficiency. Because of the sanctions against Iran, I am short in recourses in materials, including lipofectamine RNAimax. I thought if I perform my experiments by the general information in Thermo fisher protocol, maybe it is more efficient. But it seems I was wrong. Do you have any suggestions on how I could optimize the process by using low amounts of lipofectamine?

Dear researchers, thank you all for your contributions. Dear Mohana Krishna Gopisetty, the method you have suggested is time-efficient and problem-solving, I appreciated that. However, the cancer type we are working with is a little bit struggling. Our drug of interest is one of the members of the chemotherapy regimen which consists of other different drugs (we can say that it is given as a cocktail). Also, the relative survival rate of patients is low, diagnosis with specific drug chemoresistance takes time. (but we know that chemoresistance happens - under investigation)

Hi Lilian

No problem and Good Luck.

Dear Asaad Hamid Ismail thank you for your interesting and important technical question. Yes, certain kinds of cancer have been related to chemotherapy (and also radiotherapy). For more information about this, please have a look at the following useful article entitled:

How about thalidomide, celecoxib and valproic acid?

Clinical Review Prevention and Treatment with Probiotics, Thalidomide, Celecoxib and Valproic Acid for Metastatic Pancreatic Duct Adenocarcinoma.

Hello, Aicha!

1. Probably the simplest analysis for proliferation is to sow the same number of cells, treat with drugs and after the same time count the number of cells (for example, in a Goryaev chamber or using an automatic cell counter). Then, in relation to the ratio of the grown cells to the initial number, the proliferation index in% can be estimated.

2. You can use antibodies to marers of proliferation Ki-67, PCNA and use flow cytometry or immunofluorescence.

3. MTT test can also be used. The viability of cancer cells will be proportional to their proliferation. If your drugs act on proliferation, then cell viability will also change.

You should make your own resistant lines. These are something not available in cell repositories or shared by other scientists. Of course this is a costly, time consuming and tricky process.

Yes, we added as many cost as we could given the data available.

Thanks dr graymer

Complete mesocolic excision is recommended to improve dfs and local recurrence for right colon cancer

the older concept of adjuvant therapy for suboptimal clearance still holdstrue

but does adjuvant chemotherapy compensate for inadequate clearance or non cme

perecentage of salvageable recurrences after right colectomy uncertain and challenging with superior mesenteric vein involvement

would be interesting to see if any data available regards this

Gürhan Abuhanoğlu Dear Professor, Thank you for your kind information. However, I do not need any cell line, I have so many cancer and normal cell lines. I am just searching for a cancer drug-resistant tissue array for the immuno-histochemistry experiment.

Regards,

Mamun

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.

I am afraid that you cannot replace diagnostic imaging with a mathematical model. At least that is the situation in real life patients.

Have a look at this useful link.

Follow

Krishna Kumar Govindarajan

Decision making regarding use of antibacterial prophylaxis involves weighing measures of efficacy against potential negative consequences.

Measures of efficacy of prophylaxis include reductions in fever, bacteremia, sepsis, infection-related mortality, and overall mortality.

Potential negative consequences of prophylaxis include Clostridioides difficile infection, invasive fungal disease, drug toxicities, and antibiotic resistance.

In our manuscript, we describe the main schemes that caused neutropenia in our population.

I confirm the indications given by Dr. Campos-Vega. I suggest you to evaluate if your treatment could be stored at ultra-low temperature conditions (-68 ºC and below) using a proper solvent. Most treatments stored at these conditions are usually dissolved in DMSO, HBSS, PBS, or similar reagents but not the media itself since glucose and other components can form crystals and precipitate. It is always better to prepare fresh new treatments every day or evaluate several responses to your refrigerated solutions.

Chemotherapy is still very much necessary in the treatment of cancer. The use of monoclonal antibodies can be added to potentiates its effect, though can't be given as a form of monotherapy.

Nature volume 579, pages284–290(2020

Cancer recurrence after surgery remains an unresolved clinical problem1,2,3. Myeloid cells derived from bone marrow contribute to the formation of the premetastatic microenvironment, which is required for disseminating tumour cells to engraft distant sites4,5,6. There are currently no effective interventions that prevent the formation of the premetastatic microenvironment6,7. Here we show that, after surgical removal of primary lung, breast and oesophageal cancers, low-dose adjuvant epigenetic therapy disrupts the premetastatic microenvironment and inhibits both the formation and growth of lung metastases through its selective effect on myeloid-derived suppressor cells (MDSCs). In mouse models of pulmonary metastases, MDSCs are key factors in the formation of the premetastatic microenvironment after resection of primary tumours. Adjuvant epigenetic therapy that uses low-dose DNA methyltransferase and histone deacetylase inhibitors, 5-azacytidine and entinostat, disrupts the premetastatic niche by inhibiting the trafficking of MDSCs through the downregulation of CCR2 and CXCR2, and by promoting MDSC differentiation into a more-interstitial macrophage-like phenotype. A decreased accumulation of MDSCs in the premetastatic lung produces longer periods of disease-free survival and increased overall survival, compared with chemotherapy. Our data demonstrate that, even after removal of the primary tumour, MDSCs contribute to the development of premetastatic niches and settlement of residual tumour cells. A combination of low-dose adjuvant epigenetic modifiers that disrupts this premetastatic microenvironment and inhibits metastases may permit an adjuvant approach to cancer therapy.

see this article

The commonest side effects are

Nausea, Vomiting: Steps: 1. Eat small frequent meals. 2. Strong fragrance cooking may be avoided. Ondensetron and Apripitane are very effective & useful drugs

Lower immunity/ Low WBC count: 1. Take adequate rest, dont exert! 2. GMCSF/ GCSF are useful to bring back wbc count in normal limits.

Constipation: 1. Drink adequate water. 2. Have good amount of fibres / add esabgul. 3. Cremafin syrup.

Diarrhoea: 1. Avoid uncooked food. Have fresh, home cooked food. 2. Hydration, slat replacement and occasional use of antibiotics may be required. 3. Severe case with septicaemia; admission in hospital with IV fluid and salt replacement and IV antibiotics are often needed. Blood culture may help.

Hair Loss: Cooling of scalp may help. result are not predictable. Tolerance is also a big issue.

Repeated IV punctures/ Pain/ thrombosis of peripheral veins: Chemo Port insertion is great help!

Depression: Good counselling and prior information usually helps. Good friends and strong family support helps greatly. Meditation and light Yoga is also useful. Sometimes meeting cancer survivor helps to restore confidence.

Dr. Tarang Patel. Consultant Breast & Cancer Surgeon. CIMS Hospital, Ahmedabad, India

Hello Issawi, PDT depends on how and where the cancer is too. If the patiente has a big tumor, probably the doctor will operate and PDT can be used as a complementary tecnique, but if cancer is on surface and not so deeper, PDT can be used as an alternative method.

I hope it has helped you.

What is names of the journals

Hi there,

thank you for your answer and sorry it took me so long to reply. I heard of the mechanism you are describing and read some paper discussing their experiences about inducing immunotolerance to treat auto-immune diseases. I think that this might be a promising therapeutic option for patients who do not respond to established therapy. However, my question related to another group of patients. Patients with haemato- oncological diseases are prone to infectious complications during the time of neutropenia. Granulocytetransfusion (GTX) is practiced at some medical centers as ultima ratio therapy to save their lives. In my thesis I analyzed the overall survival of patients receiving GTX. On first sight it seemed as if patients receiving high doses of G-CSF tend to have a lower overall survival – that was when I thought of the immunotolerance induction caused by G-CSF. However, in a subgroup analysis results showed that patients, receiving high doses of G-CSF tend to suffer from more serious infectious complications than patients receiving lower doses of G-CSF and that this is more likely to explain the lower overall survival than the immunotolerance induction.

Of possible interest in your design is that we performed inhalation paclitaxel chemotherapy in dogs with pulmonary metastases as a preclinical trial, and our facility stopped performing it, as there was occasional leakage from the device, and the potential for handler/administration exposure was too great. Scavenging could be a major drawback.

Other facilities continued regardless and the preclinical work is published (although they did not mention the potential for exposure). Clin Cancer Res. 1999 Sep;5(9):2653-9.

Add this article

Zarogoulidis P, Chatzaki E, Porpodis K, Domvri K, Hohenforst-Schmidt W, Goldberg EP, Karamanos N, Zarogoulidis K. Inhaled chemotherapy in lung cancer: future concept of nanomedicine. International journal of nanomedicine. 2012;7:1551.

A BrdU incorporation assay, DiviTum, can be used in cell cultures, mouse and human sera/plasma. Dr Klaus Felix from Heidelberg have published results using DiviTum in pancreas PDAC:

Hello Yanfei, it is highly probable that your extract inhibited the metabolizing enzymes for irinotecan. Co-administration of certain agents either induces the metabolizing enzymes (leading to rapid clearance/elimination, decreased duration of action and perhaps therapeutic failure) or inhibits the said enzymes, leading to slow clearance/elimination, increased plasma concentration, increased duration of action and perhaps toxicity.

Was this helpful?

Kindly see this useful RG link.

I forgot to say that current studies of neo-adjuvant therapy evaluating aromatase inhibitors + CDK4/6 inhibitors look very promising...!!!

Surender,

Here's a quote I found: •Serpentine hyperpigmentation: Some chemotherapy drugs (fluorouracil, vinorelbine, and some combination regimens) given intravenously (IV) can cause a darkening of the venous pathways up the arm. This darkening over the veins will eventually fade. ◦The cause of these skin reactions is currently unknown, but may involve direct toxicity, stimulation of melanocytes (cells in skin responsible for skin color), and postinflammatory changes. Although skin reactions may occasionally be permanent,in most cases, discoloration will gradually resolve after chemotherapy is stopped.

More can be found here https://www.nccn.org/professionals/physician_gls/pdf/colon.pdf

I think the answer depends on what you intent to measure and what the details are. Chemotherapy can induce somatic DNA alterations and potentially predispose to acquired aberrant clonal expansions (https://www.nature.com/articles/gim2017196). Are you plannig to get blood samples for germline DNA testing? Hematologic malignancy testing? Cell free DNA?

Please have a look at these useful links

See this Video you will understand

Thank you all. I really appreciate your efforts for helping me. I did find the provided links informative but not to the extent I was looking for.

In fact oral sq.c. carcenoma is chemoresistans and radiosensetive, so no role for chemotherapy in oral sq. C.c.,its used for palliative therapy

For paired sample analysis you need two values per sample, pre and post treatment. If you lack one of the values for a sample you cannot analyze it by that method since it would not be paired to begin with.

J. Antes Yes, it is. You can have a try. Good luck.

Dogs with subcutaneous hemangiosarcoma are more likely to have small, localized stage 1 disease than dogs with hemangiosarcomas in other sites; therefore subcutaneous hemangiosarcoma usually carries a much better overall prognosis than visceral hemangiosarcoma and has the potential to be cured by surgery alone. On the other hand, when it is large, and particularly when it is intermediate to high grade, subcutaneous hemangiosarcoma may be more likely to recur or metastasize.

One study reported on 71 dogs with subcutaneous and intramuscular hemangiosarcoma, and found the overall survival time averaged 6 months, with 25% of dogs living a year after surgery. They found that tumour size was important; dogs with tumours <4 cm, between 4 and 6 cm and > 6 cm in diameter had survival times of 12 months, 7 months and 4 months respectively after complete surgical excision. Dogs that had clinical signs (lameness was most common) or had anemia at diagnosis lived an average of 3 months (compared with 7.5 months if neither), and those with complete surgical margins lived an average of 13 months compared with 4 months if margins were incomplete. Predictably those with metastases lived an average of less than 4 months.

In another study that proposed a histologic grading system for dogs with hemangiosarcomas; tumour grade (and specifically nuclear pleomorphism and mitotic index) appeared to predict survival time for these dogs that were treated with surgery and doxorubicin. (Grading is best done on a large, excisional specimen, rather than incisional sampling).

Adjuvant chemotherapy gemcitabine based is the most usual option

We run xenografts commercially, and you can find some examples of chemical treatment on breast cancer models (http://altogenlabs.com/xenograft-models/breast-cancer-xenograft/) and those of colon cancer ones (http://altogenlabs.com/xenograft-models/colon-cancer-xenograft/). These models are mainly necessary to confirm in vitro results on cells in preparation for human clinical trials.

Thanks! The type of tumor matters less, I'm trying to make a comparison between the accumulation of free chemotherapy vs. nanoparticle-encapsulated chemotherapy.

For some reason, the data for nanoparticles is easy to find, but free drug is very hard!

I just need a range of %ID/kg (ID-injected dose) in humans, for free chemotherapy.

Unfortunatley the clinical trial links didn't have any results...

Thanks so much for your help!

I am not a doctor, but I have spoken with countless individuals who have survived cancer through natural means (diet, colonics and supplements) to boost their immune systems and detoxify their bodies. I have had a natural health store for more than twenty-five years and have read many books and articles as well as heard testimonials on this process.

What is ironic is that now the "breakthrough" method of cancer treatment that is touted by the medical establishment is the use of the individual's own immune system. Of course they say that the immune system must be "enhanced" by their drugs in order to work. They call it CAR-T cell therapy and they will provide it for one-half million dollars with the disclaimer that the boosted immune system might attack other organs. (TIME Mag. 12/25/2017).

Here's an idea - let people keep their one-half million dollars and use a small portion of it to buy organic vegetables and supplements, and maybe pay a practitioner to monitor their progress. Their naturally tuned-up immune systems will love all of their organs rather than attack them.

How gullible do we have to be to believe that we should pay the medical community one-half million dollars to use our own system that is in place naturally?

Positivity (positive attitude) leads to the hope of improving the disease and in my opinion it really accelerate the speed of recovery from a disease.

For curing cancer pranayam (breathing practices) and meditation are really beneficial.

You may be interested in the psychological reactions children with ALL exhibit:

In general, it can be said that 5-FU has been applied in various chemotherapy regimens in a variety of malignacies, such as bolus doses in 5-day regimens 400-425mg/m<2> in colorectal cancer, that is of no current use, single bolus doses 500-600mg/m<2> in CMF or CAF in breast cancer, regimens that are rather of no utility today, high-dose continuous infusion schedules 500-1000mg/m<2> x 4-5 days in head & neck carcinomas (with CDDP) or stomach cancer (DCF regimen), low-dose continuous ampulatory infusion via portable pump, such as in ECF in advanced gastric cancer (replaced currently by oral Capecitabine; ECX) or colorectal cancer during early 90's, in the De Gramont schedule as a 46-hr infusion after Leucovorin (LV) (mFOLFOX or FOLFIRI regimens in the treatment of colorectal cancer), and at 2600mg/m<2> as 24-hr infusion after LV and Docetaxel (FLOT regimen) in advanced gastric cancer...!!!

Here is a reference, may be it helps you: Kim MK, Kyong-Ah Y, Myung WS, et al. KRAS mutation in cell-free DNA was correlated with treatment response to gemcitabine/cisplatin chemotherapy in patients with pancreatic cancer. Poster presentation at: AACR Annual Meeting 2016; April 16-20, 2016; New Orleans, LA.

Bridge chemotherapy is chemotherapy given in the time between leukapheresis and infusion of CAR T cells. This period is required for the manufacture the CAR T cells, which may take months due to the limited proc=duction capacity. In the mean time, the tumour of the patient may progress and requires treatment. This is the bridge chemotherapy.

In the present scenario, immunotherapy is used along with chemotherapy upfront in adult ALL by addition of Rituximab to chemotherapy in CD20 + adult ALL. Blinotumomab is used as single agent in relapsed refractory ALL in adults and children.

At this stage, we don't have evidence to say if immunotherapy can be used alone in upfront setting in paediatric patients. Hopefully clinical trials will be able to answer this question in future.

Sorry Ladislaus but besides the salary and in spite of regulations, kickbacks are there all the time...and mainly from big pharma.

Hi Go,, high dose of cyclophosmamide rarely can cause Myocarditis and heart failure. Cardiac side effect are common with doxorubicin but high dose cyclophosmamide can rarely also cause Myocarditis and heart failure. lt is usually occur within 10days of chemotherapy and does not occur because of cumulative effect. Cardiac side effect are because of Endothelial damage and leakage of fibrin and fluids in interstitium. Histopathology usually reveals acute pericarditis and haemmorragic Myocarditis which may be fatal. Congestive heart failure is the common manifestation and arrhythmia is rare. Following link might help you ..thanks

I am appreciated for your kind comment.

It has been shown that CD44 variant 8-10 (CD44v), produced by the alternative splicing machinery regulated by ESRP1 protein, contributes to the attenuation of high level of redox stress in the tumor microenvironment.

My colleagues and I have demonstrated that CD44v interacts with and stabilizes the protein xCT at the cell membrane. This latter protein, together with CD98 heavy chain, forms an antiporter known as system Xc(−) that exchanges intracellular glutamate for extracellular cystine. Cysteine as well as glycine and glutamate are essential substrates for synthesis of GSH. CD44v8–10 thus promotes GSH synthesis by increasing the import of cystine and thereby increasing the intracellular concentration of cysteine. The elimination of ROS by GSH inhibits the activation of p38 MAPK signaling and thereby prevents ROS-induced senescence, apoptosis, or differentiation of cancer cells. The CD44v8–10–xCT–GSH axis thus protects CSCs from redox stress.

Ref.

* Inversed relationship between CD44 variant and c-Myc due to oxidative stress-induced canonical Wnt activation.

Biochem Biophys Res Commun. 2014 Jan 10;443(2):622-7.

* Alternative splicing of CD44 mRNA by ESRP1 enhances lung colonization of metastatic cancer cell.

Nat Commun. 2012 Jun 6;3:883.

* Therapeutic strategies targeting cancer stem cells. (Review)

Cancer Sci. 2016 Jan;107(1):5-11.

Sincerely yours

Go J. Yoshida MD, PhD.

Very interesting project! And thank you Aftab Ahmad for sharing your article.

Unfortunately, I might have a subject at hand who just recently have been diagnosed with metastases. Previously succesful treated for breast cancer. Nonetheless, it would be interesting to propose fasting during her (likely) chemotherapy in order to have an efficient treatment with limited side effects. Any protocols on fasting and age limitations? Subject is 76yrs old.

The more chemotherapy you give to a patient more heterogeneity you will find in the tumor. This is because chemotherapy works as the "unnatural" selection process. Which is darwinian selection of the more resistant clones to chemotherapy.

Dear Mr. Chukwurah,

do you have a reference to support your statement?

You should use the "calculadora amostral", available online. Put your data in blanks and you will have a idea about your "n".After you have some results of your new experiments (pilot model), put your data again and check if the "n" is enough

We are not going to see the end of classical chemotherapy drugs any time soon.

Newer methods like direct targeting of proteins implicated in cancer, does not mean that usual chemotherapeutics are outdated.

Probably we shall see the old drugs used along with direct targeting and immunological targeting.

A deeper knowledge of chemoresistance may improve in the next future the outcome of classical treatments.

Better bioavailability will also be an important factor in order to deliver better results.

For radiotherapy to work, oxygen is needed as most of the damaging effects on the DNA level of the cell/tumorcell is due to the production of reactive oxygen species. So less oxygen, less damage/efficiency.

Hi Dr Tomas

I mean a patient with aspergillosis and he needs transplantation.

I think the following information helps you:

Tankyrase 1 inhibitior XAV939 increases chemosensitivity in colon cancer cell lines via inhibition of the Wnt signaling pathway as was written by Professor Xueyun Zhong (gdqylkp@163.com gdqylkp@163.com). Hans Clevers writes about the consequences of Wnt deregulation in colorectal cancer (clevers@niob.knaw.nl clevers@niob.knaw.nl)

Hello

We have no clinical evidence of its utility in patients in Latin America. In our hospital we are characterizing the expression of the PD-L1 and we are using it in second line, this due to state regulation.

Probably the most reliable and clinically most relevant way of verifying registration results is to ask experts to identify the same landmark points in both the fixed and moving image and then compute the distance between the fixed and transformed moving points.

Similarly, you can segment relevant structures in both the fixed and moving image and compare the fixed segments with transformed moving segments. Hausdorff distance (mean, 95th percentile) is a good metric, tells you how well the surfaces of the segments are matched. Some people use Dice Similarity Coefficient for segment comparison, which is a very poor metric, as its value is highly dependent on shape of segments (but it's very easy to compute, probably that's why many people still report that in papers instead of Hausdorff distance).

Both point and segment based evaluation can be performed in 3D Slicer (http://www.slicer.org - free, open-source medical image visualization and analysis software).

For segment-based evaluation, install SlicerRT extension and use Segment Comparison module (it can compute both Hausdorff and Dice metrics).

For point-based evaluation, you create two markup fiducial lists, apply the computed transform to the moving list, harden the transform, and compute distances in Python - or save transformed point positions to file and compute distances in Excel, R, etc.

If you have any questions, post it to http://discourse.slicer.org, you typically get expert help within a few hours.

Hi Kartik. We have preliminary data showing that glioblastoma cells are rendered susceptible to chemotherapeutic drugs after alterations in the lipid metabolism, including the in GCS. There are some published research related to this. E.g.:

 Yeh,S., Wang,P., Lou,Y., Khoo,K., Hsiao,M. and Hsu,T. (2016) Glycolipid GD3 and GD3 synthase are key drivers for glioblastoma stem cells and tumorigenicity. 10.1073/pnas.1604721113.

 Lee,E.C., Lee,Y.S., Park,N., So,K.S., Chun,Y. and Kim,M.Y. (2011) Ceramide Induces Apoptosis and Growth Arrest of Human Glioblastoma Cells by Inhibiting Akt Signaling Pathways. 19, 21–26.