Oral Cancer - Science topic

Hi Omama,

The MTT or CCK8 assay can be directly performed in a 96-well plate. Alternatively, you could also culture cells in a 6-well plate, followed by trypsin digestion and transfer to a 96-well plate for the MTT assay. This is theoretically feasible. However, both trypsin digestion and MTT assay can affect cell viability. Therefore, after trypsinization, it is recommended to let the cells recover for 2-6 hours until they fully adhere, before adding the MTT reagent.

Here is a reference MTT assay protocol for your consideration:

1. Preparation of MTT working solution

Dissolve MTT powder in PBS to prepare a 5 mg/mL MTT solution.

2. Cell proliferation assay (96-well plate)

2.1 Cell seeding: Prepare a single-cell suspension in culture medium containing 10% FBS, and seed cells into a 96-well plate at a density of 1,000 to 10,000 cells per well, with a total volume of 100 μL per well.

2.2 Cell culture: Incubate at 37°C, 5% CO₂ for 24 to 72 hours.

2.3 Adding MTT: Add 10 μL of MTT solution to each well, incubate for 4 hours, then remove the supernatant. For suspension cells, centrifuge first before removing the supernatant.

2.4 Dissolving formazan crystals: Add 100 μL DMSO to each well, and shake for 10 minutes to fully dissolve the crystals.

2.5 Measuring absorbance: Measure the absorbance at 562 nm using a microplate reader to assess cell proliferation.

This protocol is provided by the MCE Technical Team Binbin Lee — hope you find it helpful!

if you have a problem, please email me: fatihah.m@umk.edu.my

CellTiter-Glo® Luminescent Cell Viability Assay， promega

KeyTec® Luminescent Cell Viability Detection Kit，KeyTec

LDH-Glo™ Cytotoxicity Assay，promega

LDH Cytotoxicity Assay Kit，yeasen 40209ES76

I personally received Mtt assay

if you are interested in learning about the basic Of this assay you can read this article

(( Proinsulin C-Peptide Enhances Cell Survival and Protects against Simvastatin-Induced Myotoxicity in L6 Rat Myoblasts))

Best Wishes.

The blue crystal shapes are probably precipitate from your trypan blue. You can spin it down or 0.4um filter it.

Hello Dr Romissaa Ali Esmail

CT and MRI are complementary in imaging oral tumours, and more broadly, for the assessment of head and neck pathology. A lot of people automatically think you only do MRI. You definitely should if you vcan and should do CT as well.

MRI is better at characterising local tumour extent as well as assessing for bone marrow involvement.

Beil CM, Kerberle M. Oral and oropharyngeal tumours. Eur J Radiol 2008;66:448–59.

It is also better at detection of perineural spread.

Caldemeyer KS, Mathews VP, Righi PD, Smith RR. Imaging features and clinical significance of perineural spread or extension of head and neck tumors. Radiographics 1998;18:97–110.

CT is readily accessible in most facilities and practices. It has faster image acquisition. It also provides better assessment of cortical bone involvement.

Stambuk HE, Karimi S, Lee N, Patel SG. Oral cavity and oropharynx tumours. Radiol Clin N Am 2007;45:1–20.

That is also a good overview of your topic.

You can get it from healthy volunteers who are willing to participate in a research work.

you will have to have their consent wit describing every step and any complication that can happen in simple words they can understand.

Of course the tissue you will biopsy will be very small and proper oral care should be done for them before and after

Dear Malcolm Nobre I really appreciate every response lead and I'm sorry not to lead a debate so as not to influence new responses. Biomarkers are very interesting, really, but would they allow us to say where the cancer actually is in a molecular stage, let's say (on the tongue? on the soft palate? on the floor?) and how to identify the real location at a stage that biomarkers theoretically allow to identify , at the molecular level or would we have to know that we have a probability of oral cancer and then wait for clinical evidence later to locate the tumor? . Westra explains this issue well. Do other methods in other areas really have great sensitivity or specificity or would it be the approach that facilitates, for example, being able to remove the entire tissue where, in the mouth, we do not have such an approach to remove the entire oral cavity.I really appreciate every direct response about oral cancer screening. who knows, one more question: could it be that many studies no longer confuse screening with diagnosis and brilliant works are lost by a mere confusion of basic concepts? very grateful

Ck 5/6, p63, p40

I completely agree with Kamis Gaballah that the answer depends on many factors, mainly the patient's biological age, co-morbidities and overall general health. In our department as a general rule, there is no upper limit, as long as the patient is able to undergo the surgery, and as long as it is with intent to cure. In a non-curable/non-operable disease we usually do not perform palliative surgery. It should also be noted that nowadays with TORS and endoscopic approaches, the recovery period and morbidity associated with oral surgery significantly improved, allowing elderly patients to benefit from these innovative techniques.

David L Morgan, thanks for getting back. I think we're both becoming a bit confused. I confess I'd not read the last set of information that Ahmad provided carefully enough. Indeed, there are only 4 items on each occasion of measurement, and I think Ahmad might be able to combine all items into a single scale for each occasion on the condition that the items were sufficiently intercorrelated each time.

As far as the Clark and Watson article is concerned, the range from .15 to .50 refers to interitem correlations, not coefficient alpha.

I wonder how Ahmad is faring in all of this . . .

Ahmad Mahdi, feel free to get back - and sorry for my having confused matters a bit. I think a main initial issue is whether you can combine the four items to form a single scale that somehow represents anxiety/confidence.

Buen día, en el trabajo de investigación utilice productos que generaban inhibición frente al Streptococcus mutans, frente a un medicamento positivo que es la amoxicilina con acido clavulánico, que ya se conoce que hará efecto inhibidor, y efecto negativo con agua destilada, fueron medicamentos control, debes tener en cuenta, medicamentos control y medicamentos que quieres que realice el efecto para que puedas tener un mejor control de tu efecto inhibidor.

Experts have long suspected inflammation may play some role in cancer’s development. In 1863, German scientist and physician Rudolf Virchow was the first to make the connection, observing that cancer often develops at sites of chronic inflammation. But researchers have only recently pinpointed chronic inflammation as a primary risk factor for cancer and other serious health conditions. Among the reasons it’s taken science so long to confirm the relationship: Chronic inflammation causes few, if any, outward symptoms. And inflammation by itself is a sign the body is doing its job.

The concept of inflammation is sometimes tricky to grasp because it may seem contradictory. On one hand, inflammation is a healthy process, essential to the body’s ability to heal itself. When you have an infection or injury, the immune system releases white blood cells and chemicals to fight off the infection or repair damaged tissue. But when inflammation persists, or when the immune system triggers an inflammatory response when you don’t have an infection or injury—like that caused by arthritis and other autoimmune diseases—it may damage healthy tissues. “Chronic inflammation is sometimes called 'smoldering inflammation' because it's inflammation that never really resolves. It's the opposite of 'good' inflammation, which your body uses to get rid of bacteria and viruses, and then, once it achieves its goal, resolves," says Eugene Ahn, MD, Medical Director of Clinical Research and Hematologist/Oncologist at our Chicago hospital.

Today, researchers have a fairly broad understanding of inflammation’s split personality. They’ve learned that sometimes, chronic inflammation is caused by factors outside of our control, such as inherited gene mutations that raise the risk of chronic inflammation. But it also may result from lifestyle choices you may be able to change. That’s important because so-called lifestyle-dependent inflammation is on the rise. “The connection between inflammation and cancer has been apparent for a long time, but it may be that it’s now coming into sharper focus because of the increase in lifestyle-dependent inflammation we’re seeing,” Dr. Ahn says.

In general chronologic age of 70 but boilogically he is healthy, ccrt may still be considered. Case to case basis

Thank you for your suggestion Md Saifur Rahman Khan

Dear Michelle, unfortunately I did not find yet.

Please take a look at the following RG links.

Please see the following RG link.

Dear Abhirami,

you cannot easily define what you a call a 'range' threshold (basically the vaf threshold -> vaf = variant allele frequency).

The reason is that this filter depends on several important elements:

1) The fraction of cancer cells vs total cells that are present in your sample.

Are cancer cells 95% of the total? 50%? 5%? This heavily impacts on the vaf of somatic variants you should expect to find in your sample.

2) Somatic mutations can be present in all cancer cells as well as in small subclones.

So the point is: are you interested in detecting only 'first hit' mutations that likely occurred very early in the history of the tumor and are likely to be present in approx. 100% of cancer cells?

Or instead are you interested in detecting somatic mutations occurring possibly in very small subclones?

3) As a side note: the vaf of your mutation is also influenced by the copy number status of the target genome

So as a rule of thumb I suggest to:

1) With the help of a pathologist try to identify the fraction of cancer cells that are present in your sample(s)

2) Define the goal of your research: identification of the main driver mutations (likely high vaf) or also subclonal variants (possibly very low vaf) ?

So, just as an example: assuming that the fraction of cancer cells in your sample is 80% and you're interested in relatively high vaf mutation, say vaf > 10%:

Target vaf = 0.10 * 0.80 = 8% (not taking into account copy number)

Note that, assuming that your interested in subclonal variants, the lower limit of the vaf is somewhat arbitrary and is limited by the NGS strategy you used for the analysis (i.e. amplicon-based? capture based? UMI? ..).

That said, after the identification of your bona fide driver somatic variants, you can for example:

1) Annotate them with tools such as FATHMM, Polyphen, Provean etc to predict if the variant you detected is damaging

2) Query tools such as our OncoScore to quickly assess if your target gene is associated with cancer

3) Match your variants with already existing variant databases, such as Cosmic, TCGA etc to test if your variant is already known

Fingers crossed for you project, best regards,

Rocco

Hello, Antioxidants & Oral mucosal lesions: The evidence in support of a chemopreventive role for the so-called antioxidant nutrients, β- carotene and vitamin E, against oral cavity cancer. In several epidemiologic studies, low intakes of vitamin E, carotenoids, or both have been associated with a higher cancer risk.

Kindly go through the following RG links and PDF attachments.

Dear Mandana Donoghue, there are changes in this edition concerning oral cancer. With respect to T category depth of invasion (DOI) has been added with cutoff points of less than 5 mm, 5-10 and more than 10 mm, the other change in T category is the removal of T0. Concerning the N category the main addition is the extranodal extension (ENE). Other changes have been made concerning the other head and neck malignancies, new chapters have been added. check this article

Tea tasting is the process in which a trained taster determines the quality of a particular tea. Due to climatic conditions, topography, manufacturing process, and different clones of the Camellia sinensis plant (tea), the final product may have vastly differing flavours and appearance

The temperature difference between cancerous and normal cells could be variable. Although there is this common concept that tumor cells tend to have slight increase (maybe 1 degrees celsius). Similarly with the manipulation of the cellular processes by the cancer cells, a major temperature and pH change within the tumor micro environment could easily effect them which is not usually the case in normal cells as they is a buffering system to protect the cells. So yes there is atmost 1-2 degrees difference between the cancerous and normal cells as usually quoted in literature

I appreciate professor Aseem for his excellent answer which summarized the subject.

Hi Cesar,

This can mean multiple things actually.

The one solid conclusion is that when the data set is read, the gene appears many times and is well connected to interactions with other genes.

From there it is much less obvious, however. There are many reasons the gene can be found so often in the network: It might be inherently important in the pathogenesis of cancer -- but not uniquely so and could be important for other things. Add to this the possibility that the gene ended up being essentially a fad in research (although an important one).

An example is the proto-oncogene p53 (aka TP53), which although critical in cancer pathogenesis, is likewise researched very heavily. That does not mean it's a good target for a drug; it just means it's important and central in cell function.

You may wish to consult Hainaut & Weiman (2005) for more on the p53 example: https://books.google.com/books?id=tH4te5w-3BUC&dq

Best wishes and best of luck in your research.

hi.  Im looking for the same.  Cell line of oral ca which is positive for ck19 and EpCAM. And i thought i could get it from India.  Please share the provider in case you have found any

HPV subtyping should be done. p16 status, while a good surrogate for HPV related disease in the oropharynx is not a reliable surrogate in oral cavity tumours. We subtype all oropharynx also and to date all are HPV 16

Dear Rachana,

I've similar problem. may I ask you how you test viability of explants? and if you could find a solution?

It all depends on the proteins you are looking at post-treatments.  In order to provide you with positive controls, you need to indicate which proteins you are looking at. 

 80 mmol/L for 24 h 

http://www.sciencedirect.com/science/article/pii/S0009912099000545 

Tissue as such can not be stored for deriving primary culture. However, alternatively, what you can do is:

1. Dissociate tissue with sterile blade upto 1mm in size and obtain fragments, followed by washing in serum free culture medium

2. Seed fragments in 10% serum containing medium with antibiotics

3. Culture for extended period of time (7-30 days) with periodic observing for presence of necrosis- This is how PDX tumor models are developed

This process may give you some time buffer in case you can't handle multiple tissue samples in one go.

You can also cryo preserve these fragments.

Ohk. Thank you alot.

As Rose said, it could be a mycoplasma infection, or cells have reached replicative senescence and won't proliferate further. If these are primary cells then I suggest not using them at higher passage (depending on cell type, primary cells shouldn't be used beyond P5-9).

Hello Heba,

As mentioned by previous respondents, different cell lines will reach confluency in different times depending on their cell-cycle time. You need to optimise your seeding rates to achieve the desired level of confluency within a convenient period, normally 24 to 48 hours. Remember that the cytotoxicity of your drug may be profoundly influenced by the cell density.  Generally the greater the confluency the lower the toxicity. This may be either because the dose per cell is decreased when there are more cells/well, and/or because cells may cooperate in detoxification of the drug via inter-cellular connections. So you must optimize cell numbers and then standardize if you wish to compare data between experiments. You could titrate a fixed concentration of drug against different levels of confluency to determine the optimum cell number.

Thanks Deepika,

I have gone through the details of commercially available kits. But I believe none of them are optimized for deaggregated cells. I would look forward to inputs from people who have hands on experience as literature available regarding such model is also scarce.

Have you tried contacting the Royal Marsden Oral Maxillofacial team in London? They may have the most up to date information. 

Head and Neck Unit | The Royal Marsden NHS Foundation Trust

The Royal Marsden's Head and Neck Unit focuses on the management of, and ... Mr Cyrus Kerawala, Consultant Maxillofacial / Head and Neck Surgeon ...

Hello Zohaib,

That is a conclusive list by Manwar, but I would also like to add that you knidly have a look at journals, especially dated ones, as most historical references have not been digitalized, so difficult to find.

Good luck!

Venk

I totally agree (with early T2 I meant T1  border T2 non ulcerate)

try to extract spectra from different regions (intensity related differences) e.g some from blue or orange regions and post here. We can check for DNA damage, protein content etc...then we can take a call.. 

Dear Essam A. Al-Moraissi,

The components of Carnoy’s solution are absolute alcohol 6ml, chloroform 3ml, glacial acetic acid 1ml, ferric chloride 1gm. It is a tissue fixative that penetrates bone to a depth of 1.54 mm. It should be applied post enucleation to fix and kill the remnants of epithelial cells as well as to prevent recurrence of the lesion.

A histological examination is very much needed for the diagnosis of KCT.

Excision of overlying mucosa can contribute remarkably to reducing recurrence rate of KCOT however, that should not be considered a general rule. Each case should be taken on it's own merit. A lesion that is completely within the cancellous space of bone, distant from the bucal or lingual plates of bone (In the mandible for example) should not require such excision. On the other hand, a lesion that has come very close to the labial or lingual plate or has even perforated the plate would benefit from such excision. These are two extremes of the situation. You can be sure there will be the dicey cases with which you have to weigh the sides carefully or engage the use of frozen section.

The clinical and radiographic features of Keratocystic odontogenic tumors (KOT) are not pathognomonic. It is difficult to distinguish KOT from other lesions, however in most cases, the pattern of radiological destruction do not correlate with clinical examination, i.e radiologically KOT may be an extensive lesion,however clinically they might be minimum bone expansion especially when the lesion is in mandible.

There is still confusion in the literature.  KB has not existed since at least 1962, when it was deposited at the ATCC (Lavappa 1978).  It was cross-contaminated when it originally established.  KB is a subline of HeLa cells.  Unfortunately, there is confusion by the term "contaminated" by HeLa.  It does not mean that it is a mixture of two or more cell lines.  It means, in this case, HeLa contaminated the KB culture very early (sometime between 1955 and 1962) and took over as the principal / only cells in the culture because it grows so vigorously.  All known samples of KB are HeLa by genetic testing, even though they may differ in phenotype.  Different isolates of KB can also vary in phenotype.  There are over 100 cell lines with different names and probably phenotypes, but they are all sublines of HeLa.  Cell lines, when used for any biological/biomedical research, should always be authenticated by either STR or SNP genotyping, not by phenotyping them.

Cell lines when propagated in culture can evolve by adaption, selection, mutation to change their phenotype.  There are many different isolates of KB, which can also vary in phenotype. By genetically authenticating your sample of a cell line you will know whether you are working with the cell line you think you have.  Then other researchers can reproduce your findings by authenticating their samples of the cell line that has the same name.  Besides cross-contamination of one culture by another (due to poor technique), another means of cell line mix-up is be mislabelling of flasks / petr idishes. 

I highly recommend visiting the website of International Cell Line Authentication Committee (ICLAC.org), where there is a list of many (438) known imposter cell lines, like KB, which do not have any known authentic stocks in the world, plus some 35 imposter cell lines for which there exist some original authentic stocks.  There are also many useful references and guidelines available on the website. 

Many journals are starting to require authentication of cell lines prior to publication.  Furthermore, in the United States, the National Institutes of Health (NIH) will be requiring of all grant applications, submitted on January 25th, 2016, or later, the authentication of reagents used for the proposed study, including tthe authentication of cell lines.  This will be considered as a zero-tolerance policy by the NIH leadership, according to a meeting at the NIH in September 2015.

Dear hala thank you so much for the link. 

Haitham, you are absolutely right,there is no proof yet about the role of RT for recurent non malignant ameloblastoma. Most of them were case report with max 10 in case series. For my case, we ll 'try' to give 50Gy RT. My patient has got left total max with itf clearance and orbital exenteration and right subtotal max. I cant risk her to have recurrence on her right eye. After considering the risk and benefit,we ll give it a try. Knowing that my institute have a lot of ameloblastoma case in a year (more than 100), we ll propose a clinical trial to see the role of RT for certain aggresive cases. Thank you so much for sharing your case with us.

I concur that visual inspection is the most feasible in resource-crunched regions. However, it is effective to target the high-risk population especially males - tobacco chewers, alcohol drinkers, etc.

Our article published in peer-reviewed Journal "Communicative & Integrative Biology". A few major points discussed in the paper:

(1) Brain is not the source of consciousness.

(2) Consciousness is ubiquitous in all living organisms, starting from bacteria to human beings.

(3) The individual cells in the multicellular organisms are also individually cognitive entities.

(4) Proposals like “artificial life”, “artificial intelligence”, “sentient machines” and so on are only fairytales because no designer can produce an artifact with the properties like internal teleology (Naturzweck) and formative force (bildende Kraft).

(5) The material origin of life and objective evolution are only misconceptions that biologists must overcome.

You should be able to find viral miRNAs in deep sequencing of a small RNA library. The challenge is in the bioinformatics. This is not my area of expertise, but obviously if you simply align your sequence data to human sequences then you will not find viral miRNAs. Then an additional question is whether you are simply looking for known viral miRNAs from known viruses (easier),  novel miRNAs from known viruses (harder), or novel miRNAs from novel/unknown viruses (much harder). 

 Dear Vinoth, 

Check this link out: 

In Karachi, Pakistan (South) oral cancer is very common. The reason being oral tobacco and betel nuts in various forms ( Pan, Guttka, Citi, Panprak etc). We do elective neck dissection Level I to III or IV in all T stages. However there is no need for level V elective neck dissection even in T3 or T4 oral lesion. As observed in our study

Article: Need for Level V Neck Dissection in T3-T4 Oral Squamous Cell Carcinoma 

The healing of biopsy site involves upregulation of growth factors, that given the upregulation of receptors on tumor cells.  Cases of rapid growth of lesion at biopsy site and extraction sites are seen clinically in cancer patients, supporting this potential.  

There is little doubt anymore that certain HPVs are associated with a subset of oropharyngeal cancers. It is also likely that they are the cause of these cancers since the patients generally do not show excessive alcohol consumption or a history of smoking, nor other etiological factors that may associate with HNSCC/OSCC.

Furthermore, HPV-positive oropharyngeal SCCs show several common features ranging from histology to molecular markers (undifferentiated, high p16, low cyclin D1, rarely p53 mutated, RB1 low or absent, very aggressive growth and can have distant metastases...). 

Taken all this together, HPV-positive OSCCs with the above features are a group of their own: this is not trivial since these tumors tend to be less aneuploid and and respond very well to conventional radio-therapy. Their treatment therefore could be in theory be adjusted: I personally think they could skip radiation therapy (which may have more long-lasting negative side effects; Otolaryngol Head Neck Surg. 2015 Jun 29. 

HPV-Positive Oropharyngeal Carcinoma: A Systematic Review of Treatment and Prognosis. Wang MB, Liu IY, Gornbein JA, Nguyen CT; similarly HPV-positive skin cancer does also not benefit from radiation therapy: J Cutan Med Surg. 2015 Jul;19(4):416-21. doi: 10.1177/1203475415576859. Epub 2015 Mar 18.

Deleterious Effect of Radiation Therapy on Epidermodysplasia Verruciformis Patients.

de Oliveira WR1, da Cruz Silva LL2, Festa Neto C1, Tyring S3.). In contrast to many clinicians, I think chemo alone may do the "trick" for these patients. But this is just an educated guess with the side-effects in mind. I am sure not many clinicians may agree with this judgment. But the literature seems to go against radiation therapy for these patients (HPV-Positive Oropharyngeal Carcinoma: A Systematic Review of Treatment and Prognosis.).

So, these HPV-positive HNSCCs of the Waldeyer's tonsillar ring are special in their molecular profile, their histology, the personal history of the patient (smoking, alcohol) and their favorable response toward conventional therapy despite aggressive growth and high level of metastasis. These tumors should be put in their own category and treated differently from the "classical" HNSCCs.

Thank you very much Rolando. It will help me a lot.

The important point is cell density on your plates at the initial point.

If your cells reached confluency and after that you wounded them - their attachment to the plastic could be distorted.

In fact, there are 2 different moments to keep in mind - attachment of the cells to plastic and adherence between the cells. If you have low density of the cells - adherence to the plastic dominates, when the cells reached confluency - cell-cell adhesion increases and at some moment may become stronger than adhesivity to the plastic... (This "critical point" strongly depend on your cell type). In such a case, you could state the cells as "thin film" and if you will wound it, it will lose a contact with underlayer plastic...

so, I would advise to check confluency, adn start a scratch assay at the confluency not more than 80-90%.

Thank you Dr.Jinesh. Key components of E cigs are - NAB: N′-nitrosoanabasine; NAT: N′-nitrosoanatabine; NNK: N′-nitrosonornicotine; NNN: 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone.

Ingredients are almost same as normal cigarettes but in extremely reduced doses.

Thank you for your suggestion. 

Dear   Anuj

I could imagine.  

Best

Prash

I give Tablet. Artane 2mg twice a day, can step up to three times a day (max 6mg). Daily dose is not so effective. One can see the secretions lesser and wound more dry within Day 3 of administration. If for some reason this is not enough, I inject Botox into the salivary gland. Hope this helps, thank you.

The best method to assess nitrites and nitrosamines in saliva is Gas Chromatography. I am hereby attaching articles on various techniques. hope these might help you.

I would suggest to do a mycoplasma testing, immediately!! I have worked with them extensively for xenografts and face these problems. Normally they are good till they reach a confluency of 50-60%. However as soon as they reach to getting confluet they came off. Its know fact that  many times when you recieve the cell line from ATCC , for eg. , they are mycoplasma+  these has to be rectify.

Dear Khan

In order to calculate sample size of the case-control study, you should know the prevalence of the disease (oral cancer) in the study population, then choosing the Confidence level, yo will be able to calculate it by online calculators like suggested by Ishag Adam.   

Hope it helps.

Isn't the first question to be asked does any screening method improve the outcome in patients with oral cancer rather than which screening method should i use?

For patients in the general population I think the answer is a clear no for an organized program (this is also the consensus of the american preventative services taskforce ), for high risk individuals there is some data to suggest a benefit but if we are serious we should institute a confirmatory large trial in such patients to confirm. In the meantime perhaps opportunistic screening of high risk individuals

See Screening programmes for the early detection and prevention of oral cancer.

Brocklehurst P1, Kujan O, O'Malley LA, Ogden G, Shepherd S, Glenny AM. Cochrane Database Syst Rev. 2013

Main results: A total of 3239 citations were identified through the searches. Only one RCT, with 15-year follow-up met the inclusion criteria (n = 13 clusters: 191,873 participants). There was no statistically significant difference in the oral cancer mortality rates for the screened group (15.4/100,000 person-years) and the control group (17.1/100,000 person-years), with a RR of 0.88 (95% CI 0.69 to 1.12). A 24% reduction in mortality was reported between the screening group (30/100,000 person-years) and the control group (39.0/100,000) for high-risk individuals who used tobacco or alcohol or both, which was statistically significant (RR 0.76; 95% CI 0.60 to 0.97). No statistically significant differences were found for incidence rates. A statistically significant reduction in the number of individuals diagnosed with stage III or worse oral cancer was found for those in the screening group (RR 0.81; 95% CI 0.70 to 0.93). No harms were reported. The study was assessed as at high risk of bias.

Hi,

I think that you have to perform the DNA extraction first by precipitation from saliva ( using  RIBO-prep Kit) and then you can use АmpliSens HPV HCR-genotype Kit. With this kit you can easily do the detection of the 12 most common High-Risk HPV types with no cross detection with Low-Risk HPV genotypes.

Regards.

Nadia

Thank you Lakshmanan

miRNA-491-5p and GIT1 were also suggested.

Other:

Regards,

Joachim

current concepts of oral submucous fibrosis may not support the use of arecanut and may associate osmf with elevated copper  content in oral fluids.  In our day to day practice, we come across  most of the osmf cases associated with arecanut just like how we see more cases of leukoplakia associated with use of tobacco either in smoking or in smokeless form though idiopathic leukoplakia has also been reported.

With my  clinical experience I would like to state that osmf is definetely associated with arecant and the elevation of copper content is connected to it

I have a try.

p53 (i believe you are referring to p53 tumor suppressor gene) is a gene that often triggers apoptosis (programmed cell death) in cancerous cells. ~50% of cancerous growths have mutations that have occurred in the p53 region. Essentially a cancerous mutation will occur in a divided cell, then p53 will trigger cell death. However, if p53 mutates nothing (usually) happens. If that mutated cell then has a new cancerous mutation then the dysfunctional p53 gene now won't trigger cell-death and if other bodily defenses fail to kill the doubly-mutated cell then cancer will occur. I wouldn't say that p53 is specific to just oral cancer, as much as it's a very general anti-cancer gene that serves as a first line of defense.

For reasearch purpose use sacacae biotechnology 

Hi Cajouste. In epidrmoid carcinoma you will find dysplastic and in severe cases anaplastic squamous epithelium invading the connective tissue.

Dear Anas

Thank you for your help. I am very appreciated

Regards

Maysaa

Thank you WZ. Well, it seems that the longer and the higher concentration of the 4NQO treatment, the more severe the cancer will be. Best of luck to all of us.

Fortunately, most of my OLP patients get remission more than active disease. To answer your question two of my patients ( a man and a woman) have been visiting me on a regular basis for relief of symptoms (erosive type). They are content with treatment but they wish to know the cause of the disease.

Dear colleague,

I do not know how useful it will be for you, but I suppose that spectrofluorometric assay of oxidatively modified protein and/or lipid products may be the case. Due to a relatively small volume of saliva and high sensitivity of spectrofluorometric analysis it is possible to estimate a high number of products. A couple of methods are described in the articles below

Thank you, Dr. Samapika Routray.

I wrote to Luiz Kowalski with regard to head and neck cancers but he did not answer yet. You mentioned a sarcoma trial which is very interesting. In this context, please allow me to recommend a book edited by Aigner/Stephens: "Induction Chemotherapy: Integrated Treatment Programs for Locally Advanced Cancers", published in 2011.

@tarun: I want to make an automated device for oral cancer detection, that can help for mass screening purpose. If there will be a change in thermal profile between normal cells and cancer cells in oral cavity, then it will be easy to develop the device. To know more about thermal profile I want to read some publications related to thermal profile of cells or if any publication related to thermal images of oral cancer also enough. Do you have any idea...

Normally we strave the cells for at least 6 hrs (3 hrs each using serum free medium)

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My master Ruth Tramontani always said to us: "Watch from WHAT tissue the lesion came and it will be more simple to diagnose it." So, in oral cavity, we mostly have epitelium and conective tissue... following this line, most of the lesions in oral cavity arise from epitelium or conective tissue (wich includes dense conective tissue lesions, like Fibroma) According to Neville, Regezi, Boraks, and my clinical experience the most common is Fibroma. Thanks for asking, the most simple questions are the more Important!

There is no one set questionnaire which covers all the questions. Besides the history the clinical factors for oral cancer may include recurrent ulcers in the mouth which are non healing, any discolouration or change in pigmentions of the oral mucosa and lymph nodal involvements and of course history of habits.