Tumor Markers - Science topic

One way is to increase the upper threshold of the device and the method you are using by calibrating the measuring device with higher concentrations of standard(s). If that is not achievable depending on the type of system you are working with, another way is to dilute the samples to fall within quantifiable range. Calculate the dilution factor and use it to normalize or scale the readings. Moreover, if the two options are not feasible, think of using another method of quantification and if possible orthogonal means of verifying your measurement. I hope this helps.

Best,

Ade.

In terms of colorimetric immunoassays, this method for tumor marker detection usually uses antibodies. However, antibodies with high affinity and low cross-reactivity are very limited. Moreover, nanomaterials utilized in colorimetric methods are currently restricted to Au-NPs and MPs. In addition, because most cancers have more than one marker associated with their incidence, measuring a single tumor marker is usually insufficient for diagnosis.

Reference:

Yin, Y., Cao, Y., Xu, Y., & Li, G. (2010, December 7). Colorimetric immunoassay for detection of tumor markers. International journal of molecular sciences. Retrieved February 23, 2023, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3100837/

Dear Christian Thomsen

I really appreciate your help.

Kind regards.

A large ovarian lesion requires the use of a wide range of tumor markers to identify neighboring areas and the degree of their damage during metastasis. Check out free consultations by mail: nps@udm.ru

Diagnostic Information www.fertilityecology.ru

The best standard graph is one with the highest R2.

In ELISA, it would be curve not line. Plot the obtained absorbance against concentration and calculate R2. If it is high, the graph is good

In principle yes, but with slight modification on the recommended protocol

Hello Abdelwahab

There is still no answer to your question.

Alpha-fetoprotein is mainly produced by the liver in a developing fetus. The level of Alpha-fetoprotein is high initially and later decreases as the organ develops. In Ataxia telangiectasia patients it has been suggested that the liver is not developed fully. Based on this, there is a hypothesis that states that the defect in patients with Ataxia telangiectasia lies in tissue differentiation. This may be due to the defective interaction between the endoderm and mesoderm germ lines which under normal condition would result in the differentiation of gut associated organs like the liver.

For details you can refer to - The lancet, 300 (1972), pp.1112-1115

Thank you.

.

Diagnosis of most of the malignancies depends on the tissue diagnosis very high alpha-fetoprotein (AFP) in a cirrhotic patient or very high prostate specific antigen in a patient with enlarged prostate.

Diagnosis of most of the malignancies depends on the tissue diagnosis very high alpha-fetoprotein (AFP) in a cirrhotic patient or very high prostate specific antigen in a patient with enlarged prostate.

The role of cancer biomarkers e.g. CA 19-9 is if it is raised in a patient with a confirmed pancreatic malignancy by tissue diagnosis, is to serve as a baseline to follow up the patient after surgery or chemotherapy. Further rise or fall in the CA 19-9 will respectively indicate recurrence or disease free period.

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Hello, 96 wells plate enough as described above. If you have separation by groups which mean same experiment done in group, you can a little bit reduce the number by taking duplicates not from all samples just half from group samples.

As per one recent research:

In patients with benign diseases, abnormal serum levels of HE4 and CA 125 were found in 1.1% (3 of 285) and 30.2% (86 of 285) of patients, respectively. CA 125 false positive results were mainly found in premenopausal women with abnormal serum levels in 32.3% of the patients with gynaecological benign diseases in contrast to 22% of them found in postmenopausal women. The use of ROMA algorithm reduces the proportion of CA 125 false positive results in the total group as well as in pre- or postmenopausal women

chisquare will work for categorical variable. For continous variable you can do a correlation test and see if there is a difference in the marker level with staging

electrochemical lencece new method in detection of different biochemical and hormonal and tumor markers in serum or fluid including ascitis and plural fluid

I would like to add that anti-p53 antibodies have been reported in other human diseases (other than cancers) such as auto-inflammatory and autoimmune diseases. Therefore, reducing its clinical usefulness.

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

not only the technology does not work, but merck millipore has been selling a control designed to give the misleading impression that it does work:

1. The first bad news is: CA 19.9 is not solely dedicated to pancreatic malignancy, since it rises also in other neoplasms of upper gastro-intestinal tract or in mucinous ovarian tumors.

2. The second bad news is: although not ideal, CA 19-9 remains still the most reliable and best validated marker of pancreatic cancer. Some useful overviews you can find under:

Shah UA, Saif MW. Tumor markers in pancreatic cancer: 2013. JOP. 2013 Jul10;14(4):318-21. doi: 10.6092/1590-8577/1653.

Buxbaum JL, Eloubeidi MA. Molecular and clinical markers of pancreas cancer.JOP. 2010 Nov 9;11(6):536-44.

Zhang Y, Jiang L, Song L. Meta-analysis of diagnostic value of serumCarbohydrate antigen 199 in pancreatic cancer. Minerva Med. 2016 Feb;107(1):62-9.

3. The good news is, you can improve the quality of your diagnosis and prognosis using easily and widely available parameters, which reflect the systemic response to tumor, e.g. thrombocytosis, C-reactive protein, neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR) or modified Glasgow Prognostic Score (mGPS). However, they all are also not specific regarding pancreatic disease.

Martin HL et al. Prognostic value of systemic inflammation-based markers in advanced pancreatic cancer.Intern Med J. 2014 Jul;44(7):676-82. doi: 10.1111/imj.12453.

Chadha AS et al. Paraneoplastic thrombocytosis independently predicts poor prognosisin patients with locally advanced pancreatic cancer. Acta Oncol. 2015Jul;54(7):971-8. doi: 10.3109/0284186X.2014.1000466.

Miyamoto R et al. Platelet × CRP Multiplier Value as an Indicator of PoorPrognosis in Patients With Resectable Pancreatic Cancer. Pancreas. 2017Jan;46(1):35-41.

4. If you do not forget about numerous pitfalls regarding the interpretation of tumor markers and soft markers (e.g. false positive results in non-expected malignancies or in inflammatory states), you will really benefit from considering both of them, as I used to do in respect to ovarian tumors (see Watrowski et al., “Usefulness of the preoperative platelet count in the diagnosis of adnexal tumors” or “Simple laboratory score improves the preoperative diagnosis of adnexal mass", both papers are available on at researchgate).

 CTC research has much promise in early stages of cancer although more sensitive technologies are currently being researched.  CTC research holds promise in molecular tumour characterization and identification of treatment targets in the nearest future.

Overall, PSA is the most widely used.

Microscopic recurrence may not be picked up on CT and MRI scan. But one also needs to know what was the presurgery level of AFP and to what extent it has rebounded. Also the etiology of cirrhosis, especially hepatitis C, can itself cause raised AFP levels even without cancer but again the level is important. SPECT or PET scan can identify microrecurrence.

 which sequence did you order?

Thanks Kevin 

The CDTN and UFMG, Belo Horizonte -Brazil (Centro de Desenvolvimento da Tecnologia Nuclear and Universidade Federal de Minas Gerais) has animal PET  ,and humans PET-CT , you may wish contacting them       http://estatico.cnpq.br/programas/inct/_apresentacao/inct_medicina_molecular.html

Best regards,

Priscila Santana

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

Hi,

Your STR marker ID are incomplete they should in the format D13S317. Once you get the complete ID you will be able to know where they match in the genome (if that is what you look for).

the number after "D" corresponds to their chromosomal location so in this case chromosome 13.

I am not sure about the number following "S" but I don't think there is any correlation with base pair size or chromosomal location. I would suspect some chronological identification.

I hope it helps,

Best,

High Lipase Numbers with no symptoms - hyperlipasemia

Posted over a year agoFor over 3 years I had flucatinig lipase numbers ranging from 1-4x over limit. The first was found incidentally while completely asymptomatic. When discovered I was given ultrasound, ct scans with constrast, ca19, colonscopy, celiac test, liver, kindey, cbc, hep, etc and all were fine. I do not drink and do not have a family history of pancreatic cancer.

Gastros diagnosed me with benign condition. However 2 years later for reassurance I had MRI on pancrease which again was normal. My gastro and his team tell me not to worry and there is nothing wrong with pancreas.

 However I read these reports and it looks like I need EUS test is the test I need, which is not common here in USA. My gastro refuses to send me get one because he does not feel it's necessary. Reports below state that my so-called benheing condition is not so benign and pancreatic disease are found over 50% of time with further testing with EUS with people with Asymptomatic Pancreatic Hyperenzymemia. Some days my test are normal and some days they over slighlt over limit or 1x over limit. I have no symptoms whatsover.

 So far I seen 4 gastros and they all think I have too much anxiety and not to worry but they are unaware of the latest studies.

Take care when using proteins/genes from HIF pathway to check hypoxia in cancer, a lot of them will present altered pathway. HIF role in cancer is still under discussion. Anti 4-hydroxynonenal antibody will be a nice option.

I totally agree with Dmitry.... especially in cases of ER/PR/HER2 i have personal experiences as well... as far as lymph nodes are concerned there may be difference of expression not only between inguinal and cervical lymph nodes but also in different areas of the same lymph node...???

hope the answer is helpful.

Hepatic tumor cells are widely known to express embryonic antigen characterized by AFP. Notably, serum titers of AFP and PIVKA-II are often used to assess the tumor aggressiveness and therapeutic response. Staining with anti-AFP antibody is also recommended.   

sorry no

I dont know, sorry. Best wishes.

Maybe this articles could be of help for you : 

I destroy with hot snaring or HBFP any polyp under 10 mm whatever anticoagulation without any significant bleeding. Bleeding risk was a false problem. Anyway, heparin can be stopped easily or blocked in very special cases by using protamine. If anticoagulation can't be stopped and if you are very very anxious, you can put a plastic snare at the base, take a biopsy and in case of any question, control the site which could have been spotted with a tattoo!  

But much ado about almost nothing!

you can run protein antibody array and compare the expression in normal versus malignant tissue

MMP9. See papers by Marsha Moses.

Any investigation should be done only if it alters the treatment and the prognosis. By ordering the CA you have committed yourself to the patient and yourself that the results will influence your further action. Therefore,in this patient, you have to do further evaluation.

If the present knowledge is that it is not something that is not important, you will have to explain to the patient that it was important when you ordered it and now the literature says that it is not important. This will be a difficult thing to do. Moreover you will be in trouble if she develops symptoms and signs of recurrence.

In future cases, you may take a ploicy decision whether to do this investigation as a routine follow-up one.

This principle is true for all investigations except may be a few basic ones such as TC, DC etc.

Narayanan

That's a very important but difficult question. And probably best studied with respect to epithelial (E) and mesenchymal (M) markers. I agree with Ruhul: micrometastasis are very frequently found and they are typically M, while in macrometastases E markers are expressed. The question is: are these M cells 1) becoming E via an mesenchymal to epithelial transition (MET, e.g. via INDUCTION by the microenvironment) or 2) are dissociated SELECTED E cells attracted to the micrometastases which basically may represent a good microenvironment themselves for the E tumor cells due to cooperation (Tsuji, Cancer Research 2009, Cleary, Nature 2014 )? The answer may strongly depend upon the tumor type. But for breast cancer we have a manuscript in preparation that stable MET and thus induction is much less likely than cooperation and selection - this is  supported by single cell data, fluorescent cell tracking, functional videomonitoring and importantly, patient data,

To answer your question about markers: multiple markers capable to discriminate the E from the M phenotype at the micrometastatic site should be used, which described the STAGE and level of aggressiveness with E markers relfelcting aggressive and M markers reflecting less aggressive.

thank you sir .

Glutamate is exported from the GBM cells in exchange for cystine via the amino acid transporter system Xc-, which features the xCT transporter subunit (also known as SLC7A11). Increased glutamate in the tumor microenvironment leads to brain edema, the main cause of death in GBM patients. Tumor microenvironment affected by the functional inhibition of xCT with administration of sulfasalazine (SSZ), one of the DMARDs for patients with rheumatoid arthritis or ulcerative colitis, has strongly suggested the pathological significance of GBM-induced neurotoxicity and its impact on the development of peritumoral brain swelling. Cysteine uptake contributes to the synthesis of glutathione (GSH), which significantly decreases the accumulation of intracellular ROS.

xCT transporter is stabilized at the cellular membrane by binding to CD44 variant 8-10 (CD44v8-10) in epithelial cancer stem cells (CSCs). Epithelial-mesenchymal transition (EMT) causes increased number of CSCs with the altered splicing pattern from CD44 variant to CD44 standard isoform. That is why some researchers make misunderstanding that mesenchymal tumor cells no longer depend on CD44v-xCT-GSH axis. However, I have demonstrated the experiments to investigate into the expression amount of xCT in U251 GBM cells by quantitative RT-PCR and WB analyses. Mesenchymal GBM cells tend to express much higher amount of xCT at the cellular membrane without CD44v8-10, in comparison with HCT-116 colon cancer cells, well-known as high level expression of CD44v8-10. That is why GBM cells robustly exhibit the released glutamate and cysteine uptake, thereby affecting the microenvironment and redox stress.

Nat Med. 2008 Jun;14(6):629-32. doi: 10.1038/nm1772. Epub 2008 May 11.

Small interfering RNA-mediated xCT silencing in gliomas inhibits neurodegeneration and alleviates brain edema.

Savaskan NE1, Heckel A, Hahnen E, Engelhorn T, Doerfler A, Ganslandt O, Nimsky C, Buchfelder M, Eyüpoglu IY.

Cancer Cell. 2011 Mar 8;19(3):387-400. doi: 10.1016/j.ccr.2011.01.038.

CD44 variant regulates redox status in cancer cells by stabilizing the xCT subunit of system xc(-) and therebypromotes tumor growth.

Hi,

It depends if you are talking about established (clinically used) test, or if you talk about recent achievement not yet certified.

From my knowledge most countries rely on Feccal occult blood test (FOBT) as a first screening, followed by coloscopy when the test was positive.

Some countries go directly with Coloscopy.

These program are usually recommended for the population above 50 or the population at risk. Be aware I'm talking mostly about Europe and North America, I have no knowledge about how it works in other countries.

Recently the use of FIT started to replace regular guaiac FOBT, since it does not require specific fastening prior to the test. 

In terms of molecular biomarker, some commercial kits are available but not necessary certified.

- Cologuard (http://www.cologuardtest.com/) which has been approved by FDA, use a mix of FIT, genetic (KRAS...) and epigenetic alterations BMP3, NDRG4) in stool

- Colosure (http://www.hopkinscoloncancercenter.org/CMS/CMS_Page.aspx?CurrentUDV=59&CMS_Page_ID=59EB34A4-86A8-475B-8E10-87A0AAA8CFA8) which test VIM methylation in stool.

- epi-procolon (http://www.epiprocolon.com/en/) which test SEPT9 methylation in plasma and serum.

In terms of non validated markers you can find a good number of paper with the use of DNA methylation in stool or plasma/serum. the publication in attachment is one example among other...

Most of the test have decent specificity, and if you need higher sensitivity you will need to go with the molecular test. As individual marker methylation of SEPT9 was reported to show good sensitivity and specificity.

Hope it helps,

Best,

VE1

were selected for their potential utility as diagnostic markers

Melanoma Marker antibodies for your research by isotype, epitope, applications and species reactivity.

a unique system for rapid identification of Melanoma Marker Antibodies. 

Melanoma (LHM 3) sc-53370 mouse IgG1 FL (h) WB, IF human

Melanoma Marker (HMB45) sc-59305 mouse IgG1 FL (h) IF, IHC(P) human

Melanoma Marker (2G12) sc-69646 mouse IgG1 FL (h) WB, IF human

Melanoma Marker (NKI/beteb) sc-52704 mouse IgG2b N/A IF, IHC(P) hu

Melanoma Marker (NKI/C3)sc-52351 mouse IgG1 N/A WB, IP, IF, IHC(P) hu

Melanoma Marker (PNL2) sc-59306 mouse IgG1 FL (h) IF, IHC(P) human

Wouldn't it be more informative to do a IHC stain for the same tumormarkers on the specimens? Or is it a matter of quantification?

Outliers are the goal for biomarker seekers, all the time. The key is how to find out the outliers. With the development of Bioinformation, outliers can be found more easily. However, I don't think all outliers appeared have been researched or noticed. So, reviewing results of others' research may be a way. Besides, new findinds always depent on new technology. If the current technology truly block the further finding, maybe the shortage of them should be improved.

another way is broading the area you focus, like the project, namely RIOK, started recently.http://www.r10k.org/R10K/About_R10K.html

R10K update: NGS of immune repertoire for biomarker discoveries (P3241)(J Immunol)

hi

Sequence: H-pGlu-Gln-Arg-Leu-Gly-Asn-Gln-Trp-Ala-Val-Gly-His-Leu-Met-NH2

good luck

Thanks for the suggestion.I have seen some kits based on some assay method but i require something simple and cost effective like colorimetry. can u suggest any such kits if u know.