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Squamous Cell Carcinoma - Science topic

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Does anyone here have a protocol for the isolation and culture of primary head and neck squamous cell carcinoma cells?
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You're welcome :)
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Hi there!
I am working with the SCC-15 (CRL-1623) cell line that I purchased from ATCC. I carefully follow the protocol recommended at ATCC . However, the cells are growing very slowly. Is growth always slow? How can I accelerate growth?
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Tongue Squamous Cell Carcinoma (SCC) is one of the most common cancer types, with a survival rate of less than 5 years in half of newly diagnosed patients. Nearly half of patients who are at the stage of diagnosis already have regional lymph node metastasis.
Check..
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I have identified some over-expressed genes associated with head and neck squamous cell carcinoma by using bioinformatics analysis. Now, I want to validate those genes at protein levels by showing IHC results available on the Human Protein Atlas database. The problem is that I can find cancerous tissues, but not normal tissues to compare with. For example, the IHC results for the GBP1 gene shows just for tumor tissues. If anyone has experience with that, please reply. Thank you.
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Yes. There are both normal and cancerous tissues (not available for all genes) that you can get their results. You need to put your gene of interest in the search box first. Then if the IHC data for that gene is available, you need to select the tissue icon (for normal tissues) and pathology (for cancerous tissues). Hope to help.
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My present project is related to oral carcinoma cell line, for which I wanted to inquire about any lab or institute that might be working on this cell line presently and if somehow I can get the working flask or cryovial for the same.
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You can order from National Centre for Cell Science (NCCS) Pune, India
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Dear Colleagues,
I have to start a study about a comparison between the metabolism of Human TONGUE Epithelial Cells (healthy cells) and human tongue squamous carcinoma cell line, after treatments.
I have the human tongue squamous carcinoma cell line but I need to buy Human TONGUE Epithelial Cells (healthy cells). Can you suggest a company where it is possible to find them? I am in Italy.
Thank you so much for your support
Andrea
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I agree that there does not seem to be a healthy tongue cell line. Almost all tongue derived cell lines are cancer cell lines from SCCs. However there is a cell line, D54, which is from a "less" diseased tongue, from a leukoplakia:
It is a cancer cell line but represent a "early oral
cancer progression" stage, so it may be more appropriate than the SCC cell lines.
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Basal cell carcinoma (BCC) is the most common form of skin cancer. An estimated 4.3 million cases of BCC are diagnosed in the U.S. each year. Squamous cell carcinoma (SCC) is the second most common form of skin cancer.
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Yes it does, and the most common classification used for this is Fitzpatrick scale.
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Hi everyone,
I am planning to do an MTT assay for the cytotoxicity evaluation of several plant extracts on A431 cell line (human epidermoid carcinoma). For this I need to use a positive standard. In the past I have used staurosporine, but it is very expensive (I am PhD Student :) ). Are there other substances that I can use that have proven to have a cytotoxic effect on this cell line? Thanks and best regards! Iolanda
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i want to buy Human Squamous Cell Carcinoma Cell Lines for my PhD research .?
One place is NCCS Pune...Can some give more suggestions..? Humble Regards
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Thankyou so much Biswajoy Ghosh
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A CASE OF recurrent sqamous cell carcinoma lower third esophagus. She received radiochemo. in the 1st presentation 3 years ago. Does she need a 2nd neoadjuvant therapy prior to surgery?
What is meant by complete response to radiochemotherapy and how many biopsies are needed to prove this? and is there any role for surgery in non complicted complete responders to radio or chemo? 
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Fully restage the recurrent disease with ct, pet and eus. If T3 and/or N+ abd three years down the line from initial treatment then further induction therapy is indicated
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These are Cutaneous Squamous Cell Carcinoma derived cell line
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Thank you for your advice
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I am in a situation where I need to freeze down freshly dissociated primary human squamous cell carcinoma cells for later use. Does anyone have any reccomendations on what media/solutions I can use for freezing to maximise cell viability and minimise cell loss when I thaw them out in the future?
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1% sterile dmso along with 10% fbs . prepare media prior storage and keep it in minus 20 degree.
note: add 1mL per cryopreservation vials.
for 10mL, add 1 ml sterile dmso with 9mL FBS,, filter and store.
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Assume there is a patient with oral tongue SCC (pT3N1) underwent surgery (R0) and postop con. ChemoRT with weekly cisplatin. One month after completion a reccurence emerges in the radiated field. You want to start palliative chemo. Do you consider this patient as resistant to Cisplatin and choose other non-cis drugs? or Add something to Cis?
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Dear Reza, I appreciate for your kind attention and especially for bringing this dilemma up.
According to the published literature, the response rate for cisplatin-naïve head and neck carcinoma is approximately 50%. However, this rate is much lower in recurrent cases. There are a number of mechanisms that induce Cisplatin resistance in head and neck carcinoma (e.g. membrane transporters for cisplatin uptake or efflux, such as CRT1 and ABC transporter MRP2; DNA repair proteins, such as ERCC1 and TP53; apoptosis associated proteins including BCL-2, caspases, or MAPKs) (1). Moreover, Chang et al. showed alternate enzymatic pathway for Cisplatin resistance in head and neck carcinoma. They depict AKR1C1 induce Cisplatin resistance through activation of STAT1/3 (2).
Therefore, as is evident, due to enzymatic processes involved in Cisplatin- resistance, Cisplatin in second-line is expected to have clinical activity.
1. Galluzzi L, Senovilla L, Vitale I, Michels J, Martins I, Kepp O, Castedo M, Kroemer G. Molecular mechanisms of cisplatin resistance. Oncogene. 2012;31:1869–83.
2. Chang WM, Chang YC, Yang YC, Lin SK, Chang PM, Hsiao M. AKR1C1 controls cisplatin-resistance in head and neck squamous cell carcinoma through cross-talk with the STAT1/3 signaling pathway. Journal of Experimental & Clinical Cancer Research. 2019 Dec;38(1):245.
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Hello there,
Has anyone transfected anf of these cell lines and can suggest a protocol? We need a cell line that expresses a certain gene to try our fluorescent construct on, so we don´t mind which type of cell line it is as long as it expresses the gene we need. We already checked that, they all express the gene, but now we would like to know which one should we try first, which one is easier to transfect and more efficient. If you could suggest protocols or good cell lines in this list that would be awesome.
  • IMR-32 Human neuroblastoma cell line Neuroblast Brain.
  • HEK 293 Human embrionic kidney cell line Epithelial Kidney.
  • HT29 Human colon adenocarcinoma cell line Epithelial Colon
  • A-549 Human adenocarcinomic alveolar basal epithelial cell line Epithelial Lung
  • Hep G2 Human hepatocellular carcinoma cell line Epithelial Liver
  • Hepa RG
  • JURKAT Human T cell lymphoblast-like cell line Lymphoblast T lymphocyt
  • A-431 Human epidermoid carcinoma cell line Epithelial Skin
  • HCT116 Human colorectal carcinoma Epithelial Colon
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Dear Beatriz María Fernández Santos,
I have used HEK 293 and Jurkat. I would recommend the HEK 293 cell line. It is widely used for expression of various genes.
For example, you could try googling "hek 293 lipofectamine".
Jurkat is a T-cell line and not adherent. Generally speaking, non-adherent cell lines are more difficult to transfect than adherent cell lines.
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squamous cell carcinoma can be treated with surgical excision , radiotherapy and chemotherapy
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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
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Cancer of the esophagus is a fatal cancer. There are two histological types of esophageal cancer, namely; adeno carcinoma and squamous cell carcinoma (SCC). The incidence of SCC esophagus is common in the Asian continent and in the North Eastern part of India. Radiotherapy is the standard modality of treatment in unresectable SCC of the esophagus and chemotherapy is administered as an adjuvant or concurrent to radiotherapy. Concurrent chemo-radiotherapy (CRT) is ideal for patients with resectable SCC of the esophagus who refuse surgical resection, and also in locally advanced unresectable cases . The treatment outcomes of SCC esophagus show a high degree of residual diseases after radiotherapy alone or after CRT. However, a sub-group of esophageal SCC responds very well to a standard 50-60Gray of external beam radiotherapy with chemotherapy, and many a times without chemotherapy as well. It is seen that those malignancies that responded well to the radiotherapy initially, when they recurred after a period of two to three years, it was radio-resistant later !! Why does this happen ??
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Various molecular mechanisms and radiosensitizing stategies have been proposed.
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In a patient, squamous cell carcinoma with metastasis in the region of S1 S3. What can be the solution for the treatment of pain in the leg, the sacrum in the back.
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You are actually dealing with radicular pain from tumor invasion of the roots forming the sacroiliac plexus...!
A rational approach would be to use external beam radiation to the affected area, i.e. the sacrum in that case. The other part of treatment is palliating pain with opioids (fentanyl patches, sublingual or transnasal fast-acting fentanyl for breakthrough pain, etc), drugs specific for neuropathic pain, such as pregabalin or gabapentin, and NSAIDs !
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Thanks for your time for me. My query is on the radiation therapy process for a cancer patient.
How radiation simulation and marking process is done prior to radiation therapy for a cancer patient?
Any kind of explanatory video /animation/ documents from the basic level is best for me to understand it as I have absolute zero knowledge about the whole process.
Regards,
Bhaskar
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Hello
the objective of lasers is to mark the position of the isocenter on the skin or on the contention of the patient who will be treated.
Practically, the CT scan is performed and then the physician delineate the target tumour on the TPS (treatment planning system). The isocenter is then put at the centroid of the delineated tumour, and the coordinates are exported to the laser system. Laser sources move automatically to the right position and the patient, who still is on the scanner couch, is tattooed at this precise location.
The aim is just to ensure that the patient will be placed at the same place under the LINAC than during virtual simulation.
This process has nothing to do with potential movement of the patient or of the tumour.
Such movements are managed using either dedicated imaging tools on the LINAC (2D or 3D) or respiratory management systems for tumours that naturally move (typically lungs, liver).
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In treatment of non-small cell carcinoma differentiating adeno from squamous cell carcinoma is essential.When morphological diagnosis is difficult IHC is done and sometimes we get adeno and squamous cell marker co-expression by same group of cells.
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Another active regimen in both adeno- & squamous lung carcinomas with a better therapeutic index than Paclitaxel/Carboplatin in SCCs is the nab'-Paclitaxel (Abraxane)/Carboplatin combination at doses of nab'-Pacltaxel of 100mg/m2/week & Carboplatin AUC=5-6/q3weeks ! Moreover, recent data indcate encouraging results by adding Pthe anti-PD1 monoclonal antibody, Pembrolizumab to the nab'-Pacltaxel/Carboplatin, irrespectively of the level of PD-1 expression...!!!
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Preferably using Matrigel as the matrix to be invaded. Time of incubation in serum starved condition, time of culture and concentration of Matrigel bed is what I am looking for.
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Hello,
I don’t have previous experience with the cells lines you’re working with, you’ll have to test differen conditions in your lab to see which ones fits best for an invasion assay.
I’ve performed invasion assays for rhabdomyosarcoma cells, culturing them until reaching a confluence state of 70 - 80%. Then, overnight incubation with starving medium.
Matrigel concentration it’s difficult to guess. I’ll try different concentrations with your cells until getting significative cell invasion. I usually go with 4 mg/mL for a thin layer, but again, it varies from cell line to cell line.
It’s not a protocol, but I hope it sheds some light to the matter.
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The paper from Boonstra et al. 2007 (DOI: 10.1158/0008-5472.CAN-07-2064) showed that several human esophageal carcinoma cell lines were misidentifyed.
His conclusion was that TE-2, TE-3, TE-7, TE-12, and TE-13 should be regarded as one single squamous cell carcinoma cell line, however, he did not rename them.
We have been working with TE-7 and TE-13, and confirmed his results that they are genetically identical.
We have been looking for information on these cells in several Cell Banks, but they were either absent or still named as separate cell lines. Anyone knows how these cell lines have been named?
Thanks
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Hi João,
I am having your same issue, trying to figure out a bit more about these cell lines. Specifically, I am looking for a cell bank to buy this cells from, or a lab that can share those with us. Where did you guys originally obtain those cells from? Based on COSMIC, I would need TE-12, but I am not sure whether other TE-s are the same identical cell line.
Any feedback is greatly appreciated.
Thanks,
Daniele
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Dear colleagues,
I am searching an appropriate primer for diagnosis of vaginal cancers in female dromedary camels. I encountered some cases with adenocarcinoma, squamous cell carcinoma and some other types of vaginal and cervical cancers. From literature (About half of vaginal cancers in humans is associated with human papillomavirus (HPV) detection, in contrast to cervix cancer which is essentially all associated with HPV). Papillomaviruses have been detected in camels. I tried to test two samples by Prof Robert D Burk (Albert Einstein College of Medicine - NY-USA), but I had a problem in sample transportation. Now, I would like to test the other cases in home, but I do not know what is the appropriate primer that should be used.
Thank you
Ali
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Try FAP59/64 consensus primers or CP4/5 primers.  they are often used to amplify also unknown PVs. I would recommend to perform rolling Circle amplification before subjecting DNa to PCr analysis to enrich circular DNa in the Background of liniear host DNA.
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In my institution, no routinely assessment of Human Papillomavirus (HPV) is performed in the histological examination. In relation to recent knowledge within the pathogenic role of HPV in the developing of oral squamous cell carcinoma (OSCC) and even in its prognosis, one should ask if it should be mandatory in all post-op histollogical reports, in order to administer or not complimentary treatment. What is your experience and/or thinking on it? 
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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
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I received reasonable number of photos on breast from our colleagues in Research Gate.
I am looking for following as well, please see whether you can contribute. You will be acknowledged.
1. Nipple or breast piercing/ and their complications
2. tattooing in breast skin
3. breast implants and complications
4. developmental defects in breast
5. psoriasis, hydradenitis in submammary area/ breast skin
best regards
Ranthilaka
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hi
Ranthilaka, i also need breast skin infection images .please share with me
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This baby was born by elective LSCS and detected to have mild tachypnoea, which improved within 48hrs. X ray was showing a mediastinal mass and was referred to us. He was diagnosed to have mediastinal neuroblastoma (Biopsy proven), N myc negative, Stage III.  
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Thank you for the reply. I was specifically looking for data or recommendations for management of intrathoracic neuroblastoma in a neonate. There are data or evidence for managing suprarenal neuroblastoma in a neonate, but the same is lacking in case of intrathoracic neuroblastoma
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I have been generating spheroids from HNSCC cell lines. During spheroid formation, some of the cells may not form spheroids. So how can we seperate these single cells and collect only spheroids for further experiments? Can we do differential centrifugation? If yes, what is the speed required?
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Hello Gangotri!
Unlike the spheroids, single cells require high speed centrifugation to settle down in the tube bottom. Therefore if you use a suitable low speed for short time, the spheroids will settle down in the bottom. Wherease the single cells will remain in the supernatant that can be discarded accordingly.
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I would like to analyse proapoptotic activity of a compound to be used on Actinic keratosis. Is there any cell line that might represent early phases of photocarcinogenesis?
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Dear Vieri,
I suppose you can ask professor Jean Kanitakis from Lyon.
Regards,
Aldona
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I
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You could consider using p40. A diffuse (full layered) expression coupled with malignant features on histology favours a SCC cell from a normal keratinocyte.
I think only the basal cells shows p40 positivity in normal skin.
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what is the media too, because i found two different medias one with growth factors and the other with FBS?
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thank you Dr Sabarwal
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working on SCC12 cell line
where i can get the Matrigel?
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thank you for your help
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In my present study, I am studying the expression of three genes (a,b,c) in NSCLC cases. My goal is to find out if I can classify NSCLC into adenocarcinoma and squamous cell carcinoma based on the Ct value. 
1. First I have normalized the Ct value by subtracting the Ct value of endogenous control.
2. I have used a formula to get a score (s) for each case for each gene.
Problem:
1. Should I compare original Ct value or normalized Ct value to understand if there were any significant difference between adenocarcinoma or sqouamous carcinoma for each gene? Which test should I perform (t test or mann-whitney test)?
2. Also, I want to investigate that, if there were any significant difference in Score (S) between adeno and squamous carcinoma for each gene. (Score is derieved from normalised Ct). (Again, should I use t test or mann-whitney test)?
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You must do first a normality test(Shapiro) with a qqplot to assess if the distribution is normal. If data is normally distributed, you will use T test. Either way, you will use Mann- Whitney U test
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I am working on chemoresistance of  human squamous cell carcinoma (SCC12) in the context of tumor microenvrionment, CAFs specifically. 
I have already done experiments with different concentrations of each drug (cisplatin, docetaxel and 5-FU) ranging from 0-120uM for cisplatin, 0-100uM for docetaxel and 0-500uM for 5-FU. 
I am wondering does anybody have experience with these drugs to tell me what are the physiological concentrations in patients? I have checked for concentration in plasma but I could not find a consistent answer.
I would like my results to reflect the conditions in patients.
Thank You!   
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I f you need plasma level required for treatment, please have a look of this interesting paper.
It shown minimum effective conc. as well as minimum toxic concentration of Cisplatin and Fluorouracil. 
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Does anyone have knowledge or experience dealing with the effects of testosterone, estrogen and/or aromatase inhibitors on squamous cell cancer of the thymus. We are involved in a case where the liquid biopsy tested positive for both estrogen and androgen receptors.and are trying to understand the possible connection and therapeutic implication
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Hello,
This paper actually proposes an improved prognosis with ER overexpression:
Li SY, Wang YX, Wang L, Qian ZB, Ji ML. Cytoplasm estrogen receptor β5 as an improved prognostic factor in thymoma and thymic carcinoma progression. Oncol Lett. 2015 Oct;10(4):2341-2346.
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i read about tumor marker and enjoy about its very important role in early diagnosis and help in assessment of therapy and recurrence probability,so i need to know if there is specific tumor marker for SCC effecting oral mucosa?
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I don´t know the existence of any efficient tumor marker related to the diagnosis and follow-up of pa¡tents with SSC at the oral mucosa
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We are trying to isolate squamous cells from oral squamous cell carcinoma. 
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 Thank you Hala for your reply. Actually I was looking for a some commercially available culture medium that I could use for my research with squamous cells. Whether DMEM, IMEM or Epi cell growth medium or something else?
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the esophageal cell lines are not available with nccs.
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The attached article could may be help you.
Best regards
Robert
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I try to find CAFs of squamous cell carcinoma of the head and neck or lung. I found one company in the US selling CAFs of lunch squamous cell carcinoma but they don't deliver them in Europe. Do you know if it is possible to obtain such CAFs from other research institutes or commercially?
Many thanks! Have a nice WE,
Sandra 
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I am not sure, In our lab we use cancer associated fibroblasts which we culture from dissociated primary HNSCC tumours. If you have links with a surgical team to obtain samples maybe this could be an option for you? Hope this helps & good luck!
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We have a quick (in vivo) biopsy to lab transfer time, we wash three times, use multiple types of medium with different concentrations of antibiotic, EGF, cholera toxin etc. Others in the lab have also used irradiated 3T3 feeder layers. 
Any tips or is it just a matter of needing large numbers? We must have explanted 50 different patient samples by now.
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Andrew, I've done this with oral SCC quite successfully (I don't know about their HPV status but I don't think that would matter).  I think we collected about 45 biopsy samples from SCCs of tongue, floor of mouth etc.  We managed to culture most of them and only lost a few through fungal contamination and a few that just refused to grow.  (When I say "we" a lot of this work was done by Simon Broad, the lab manager and tissue culture guru from the Watt Lab, where I wrote my PhD).
I collected the samples from theatre and kept the processing simple. 
1. Quick wash in PBS + betadine 10%
2. Quick wash in 70% ethanol.
3. Repeat wash in ethanol.
4. Rinse in PBS.
5. Digest in trypsin EDTA (0.05%) (you can leave it overnight at 4C or a couple of hours at 37C)
6. Chop it up manually with a scalpel.
7. Neutralise the trypsin with your culture media (We used FAD + FCS + HICE + P&S).
8. Spin 3min 1200 rpm.
9. Aspirate then resuspend in media.
10. Plate on irradiated J2s. 
11. Change the media every other day.  After 10-12 days you'll start to see colonies.
12. Once established most SCCs don't require the feeder layer.
We tried straining the digested tissue to get rid of the fibrous stringy bits, but essentially that's not necessary and might actually help to just leave some ECM in the mix!
Let me know how you go.
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How do you handle growth delay data from mice that develop ulceration over their SC tumors following rapid growth rate; include data until exclusion or totally exclude data? 
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Dear Anders,
I do not think that you can exclude any tumor from your statistical analyses, even if they are ulcerating.
WHich type of model are you using?
How big are the tumors when you are ending the experiment?
When do you see the first appearance of ulceration?
Best regards
Robert
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I'm looking for a rat oral cancer cell line to produce tumor in the oral cavity (preferably in the tongue) of healthy (immunocompetent) SD or Wistar rats. For Eg: oral squamous cell carcinoma cells.
It would be helpful if you can answer any or all of the following:
1. Do you have/know a cell line which I can use.
2. Can a cell line derived from a different strain used? For Eg: A cell line derived from Wistar rat can be used to produce tumor in SD rats?
3. Any method to transform healthy cells to tumor cells and use them for syngeneic tumor development?
4. Mention any special points / precautions to be considered to develop this type of syngeneic tumor model.
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30 year old gentleman, squamous cell carcinoma tongue,
excised at a peripheral hospital 3 month back; no neck dissection done.
HER - pT1, RIGHT lateral border, tumor thickness 0.2 cm, all margins close.
No adjuvant therapy received.
Now patient has LEFT level 1, hard, fixed node; RIGHT neck - no nodes; Tongue - NO LESION FELT.
FNAC of RIGHT neck node -SCC
MRI tongue - ill defined lesion 0.5 cm along LEFT lateral border; to co relate clinically.
How will you proceed?
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Radiologist's answer
If the tongue lesion is not palpable at all, I am not sure if you should treat based only on the MRI findings. MRI can show positive findings in inflammation as well ; also accessory salivary tissue can also enhance. The MRI probably needs to be reviewed as well.
One avenue I would try at my institute, not as a general rule, but specifically in this case, only to resolve my clinician's dilemma is an intraoral ultrasound at the site where MRI shows enhancement. If there is a neoplastic lesion, it would be seen as a hypoechoic well defined lesion and maybe the clinician can attempt a biopsy in this region. However the clinician might not opt for this and may simply observe the tongue.
This morning I attended a lecture of Prof Ross Kerr from New York who is visiting TMH and he spoke of emerging adjunctive techniques in oral cancer detection--which though are not widely or readily available in the field---but a possibility in future. 
Regarding PET , we have had cases where PET has been positive , but MRI negative.
PET has no role at all for detecting or staging the primary. Its only value in this case would be to map the extent of nodal disease in this established N+ neck (only if needed) .  
The metastatic left neck node need not be from a new primary -it could be related to the original primary , as it is known that after a neck dissection, nodal relapse is expected in the contralateral neck due to lymhatic diversion. 
I guess treatment for the neck is definitely warranted , but treating the left tongue would be an overkill without a biopsy confirmation of squamous cancer at this location. 
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IN recent times.i.e. in the last ten years, there have been numerous case reports on Head and Neck Squamous Cell Carcinoma which may have HPV as one of the contributing/causative agents.
I have also seen one patient with  OSCC wherein there was no history of tobacco usage., and/or trauma/ sharp teeth etc.
I want inputs from all those doctors/researchers/health care workers/caregivers who have seen similar cases.
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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.
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I am attempting to me a RDEB patient SCC cell line from a  frozen tissue sample. I have a couple of protocols saved but none of them are specific to SCC or RDEB.
Thank you for any help you can provide! 
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Just keep me updated, I try to guide you when they are there
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Would you consider SCC growth rates time dependent?
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I think that cutaneous squamous cell carcinoma (SCC) includes manysubtypes with widely varying clinical behaviors, ranging from indolentto aggressive tumors with significant metastatic potential.
I suggest you to see "Cutaneous squamous cell carcinoma: a comprehensive clinicopathologic classification" Part one. J Cutan Pathol. 2006;33:191–206
Warm regards
Matteo
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In many Arab countries, obstructive uropathy constitutes a major cause (40%) of end stage renal disease mostly due to renal calculi and schistosomiasis. Schistosomiasis, due to S. mansoni and S. haematobium, is an endemic common disease in a number of Arab countries. Both types have their negative impact on the kidneys. While obstructive uropathy is a common complication of S. haematobium, distinct patterns of glomerular lesions, including membranoproliferative glomerulonephritis and focal segmental glomerulosclerosis, are associated with infection by S. mansoni or S. japonicum. However, with the widespread use of praziquantel, the prevalence of Schistosomiasis decreased over time. In Egypt, the incidence of squamous cell carcinoma of the bladder decreased while that of transitional cell carcinoma increased after mass treatment of Schistosomiasis. In South America, a change in the distribution of glomerulopathies associated with nephrotic syndrome was observed along with a decline in the occurrence of severe forms of schistosomiasis.
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However, roughly CKD prevalence worldwide is estimated at 8-16%.
References:
1          (CDC) CfDCaP: National chronic kidney disease fact sheet: General information and national estimates on chronic kidney disease in the united states, 2014: Atlanta, GA: US Department of Health and Human Services, Centers for Disease Control and Prevention, 2014,
2          Jha V, Garcia-Garcia G, Iseki K, Li Z, Naicker S, Plattner B, Saran R, Wang AY, Yang CW: Chronic kidney disease: Global dimension and perspectives. Lancet 2013;382:260-272.
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Can anyone tell me about positive control tissue of c-fos in Immunohistochemistry for human oral squamous cell carcinoma. Please help me.
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Maybe this site can give you the wanted information.
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I am looking for squamous metaplasia in human tissue. I wonder if anybody used a specific marker (antibody) to identify metaplastic squamous cells by immunohistochemistry.
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What comes to my mind almost immediately is TP63 or p63. This protein is "primarily" expressed in squamous epithelia, is expressed at high levels and there are good antibodies against it. It has an expression pattern similar to Krt14 and Krt5. Is it perfect? probably not. Another problem I see with p63 is the specificity of the antibodies since there might be problems with p53 and p73. There are so many different isoforms of those and p63 itself. 
If there is differentiation then one should be able to detect Krt4 and Krt13 (for mucosal epithelia such as the oral squamous epithelium). These are pretty specific squamous epithelial markers and more restricted than p63/Krt14/Krt5. I am sure there are better ones but these are good for starters. There are good antibodies for all of them, they are all highly expressed and easy to detect.
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Is it possible to define any relationship between cutaneous squamous cell ca and atrial myxoma? We have seen both tumors in the same patient. We haven' t seen any report about this simultaneous occurance. However there are some reports about the simultaneous occurance of the squamous cell ca of the lung and myxoma.
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Dear Demir it is a very interesting and difficult too, answer with yes or no. The association of tumors could happen in genomdermatosis some syndromes like DNA instability synd, Blooms or Familial  Multiple tumor synd, Cowdens or Poiklodermatous;  Dyskeratosis congenita but other syndromes deserve revision like:
Carney complex ( LAMB - Lentigines, atrial myxoma, mucocutaneous myoma, blue nevus syndrome NAME - Nevi, atrial myxoma, skin myxoma, ephelides syndrome) is a genodermatosis (PRKAR1A gene, called type 1 alpha) inherited in an autosomal dominant pattern. The disorder is characterized by an increased risk of several types of tumors. Affected individuals also usually have changes in skin coloring (pigmentation). Signs and symptoms of this condition commonly begin in the teens or early adulthood. Individuals with Carney complex are at increased risk of developing noncancerous (benign) tumors myxomas in the heart (cardiac myxoma) and other parts of the body. Some people with Carney complex develop a rare tumor called psammomatous melanotic schwannoma. This tumor occurs in specialized cells called Schwann cells, which wrap around and insulate nerves. This tumor is usually benign, but in some cases it can become cancerous (malignant). Almost all people with Carney complex have areas of unusual skin pigmentation. Brown skin spots called lentigines may appear anywhere on the body but tend to occur around the lips, eyes, or genitalia. In addition, some affected individuals have at least one blue-black mole called a blue nevus.
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In very severe psoriasis patient with currently diagnosed squamous cell carcinoma,
should ignore the dermatological problem? because PUVA side effect is SCC and that patient is already resistant to other topical treatment.
I am doing research for my EBP question . Any suggestion please. 
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I think you could try, after surgical excision of the SCC, acitretin or methotrexate.
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Three patients with pulmonary squamous cells carcinomas submitted to pneumonectomy had relapses in single cervical lymphnodes respectively after three, nine and twelve months after the operation. We undertook radical monolateral cervical lymphadenectomies and the three years follow up didn't detect any relapse in all the cases.
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We identified seven gene signatures, and combined them with the clinical parameters age and stage, we could differentiate patients into three risk groups and predict patient survival probabilities at 10 and 15 years post-surgical resection, which were extensively verified using 6 other datasets from five different countries.
This breaking new study published in the first issue of EBioMedicine which is a high quality peer review journal under editorial leadership of Cell Press and The Lancet.
Please read the whole paper. Here is the linker:http://www.sciencedirect.com/science/article/pii/S2352396414000140
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Smoking is a strong risk factor of esophageal cancer, what about passive smoking? 
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Hello, Nazir, according to Duan et al's population-based case–control study with 2474 participants in Los Angeles County, there was no evidence that passive smoking had
any appreciable effect on oesophageal or gastric adenocarcinomas.
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Five-year survival of oral cancer varies from 81% for patients with localized disease to 42% for those with regional disease and to 17% if distant metastases are present. Generally, due to late-stage diagnosis, fewer than 50% of patients with oral and pharyngeal cancers survive more than 5 years. This rate has remained disappointingly low and relatively constant during the last few decades. Therefore there is need to create awareness for oral cancer screening so that the deadly disease can be diagnosed at an early stage.
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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.
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I am doing research in oral cancer. I need any specific marker present for Oral squamous cell carcinoma. Please kindly send me these details.
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Based on the surface area of about 1.9 m2 and 3.5 million new cancers per year (Squamous cell carcinoma and basal cell carcinoma) the ectocervix has a very high cancer rate per m2 surface area: about 0.00075 m2 and about 12000 new cases per year. If you oversimplify and calculate the ratio of tumors/m2 in the USA you get enormous differences. Do these differences represent a higher susceptibility of the ectocervix or cervix compared to epidermis; or a different exposure to carcinogens (in case of the ectocervix HPV)?
Within the skin, are melanoma rare or more common than epidermal tumors taken into account the low number of melanocytes compared to keratinocytes (they at least are exposed to the same carcinogen)?
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Interesting question, Thomas. 
In the epidermis we might speculate that we should count only the basal keratinocytes (which are likely the origin of both SCC and BCC in epidermis), not keratinocytes in all other layers since generally these move outwards and are shed.
Textbooks say that there is about one melanocyte per 10 basal keratinocytes in humans. 
In the UK, the incidence of melanoma is about 1/10 that of non-melanoma skin cancer, although records are patchy for NMSC.  So you could say that the incidence per cell is probably about the same for these two specific cell types.  Although it may vary with the wavebands of UV.  More UVB relative to UVA near the equator.  And there is probably more evidence that UVA is a carcinogen for melanoma than for NMSC.
And of course for both these types it varies with skin colour, other genetic factors, and sun exposure.
(And I'd agree about HPV and the high cancer rate of cervical cells.  It's not high in people not exposed to HPV.  Keratinized epidermis is relatively protected against viruses.)
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I want to down-regulate gene of interest in SCC cells but this cells are hard to transfect. I have tried using Xtreme gene as well but got 10-15% transfection.   
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We normally use SAINT-18 for hard to transfect cell ines. This compound was used by Cambrex/Lonza in there no longer commercial available Primefect Reagents.
It now sold under the name SAINT-18 by SYNVOLUX
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Seeing only some early esophageal Ca cryotherapy publications.  Also, who is the best current manufacturer of the device?  Any recommendations?
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Wonderful!  thank you so much Wolfgang.
Warm regards,
Christine
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Any suggestions are welcome.
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Moh's surgery may not be absolutely necessary (too time consuming), the resection may include cartilage per primum and the reconstruction can be relatively simple (without flap surgery - see Head & Neck 36, 735-738,2014)
Ultimately, each case has to be evaluated seperately.
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After primary culture from one tumor sample (of squamous cell carcinoma of cattle ) I found a lot of small round shining apparently nucleated (fine adjusted inverted microscope) cells partly in suspension & partly attached to collagen coated t-25 flasks on the consecutive 3rd & 4th day. Before processing the primary culture the tumor tissue was well detached from vascular tissues. These cells are also increasing in number. When I performed percoll gradient differentiation of cells collected from the flask at different gradient (30%,40,60,80,90%) the cells took the gradient in between 30-40%. Can these be stem cells? Or rather should I ask how to get stem cells from this type of sample? Seeded them in gelatin coated flasks.
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thanks sir. last time I used a proportionate mix of trypsin & stem-pro accutase from life technologies & it worked well.
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Does anyone know of a protocol for establishing oral squamous cell carcinoma cell lines?
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paul Harrison from Glasgow identified the profile of mortal and immortal cells that can keep growing sponteously in routine culture. other people either tranfecting cells, heat shock cells or they starve the cells but all these will change the genetic make up so the cell line requires a detailed characerisation after such manipulation
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Type and volume of surgery, radio and chemotherapy.
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Protocol below
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Most of these are squamous cell carcinomas, and very well-differentiated, with lymph nodes of neck also involved.
There is always a boy-friend or girl-friend in the picture.
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Dear Arnavaz,
There really is no debate about the association between HPV 16/18 and head and neck cancer. Mainly affects lingual and palatine tonsils. Much higher in younger males and there is a definite association with oral sex. Very good research at John Hopkins, USA Dept ORL, Westera W, Pai S, Also see clinics of North America Aug 2012.
Please see links below. We are running a conference in Galway, may 17th.
Ivan.