Cancer Biomarkers

Cancer Biomarkers

  • Luboshits Galia added an answer:
    How can I find the complete profile of specific marker production by individual cells?

    For example what proteins and receptors are produced in normal breast cells and malignant cells.

    Luboshits Galia

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

  • Lin-Lin Bu added an answer:
    NF-kB and JAK/STAT3 pathways crosstalk, (IL-6??)?

    Hello everyone.

    I am looking at studying the connection between NF-kB and JAK/STAT3 in normal and cancer cells. I am pretty certain from my research that there is a connection with IL-6. What type of tests should I propose to test this and what would some expected results be?

    Thank you!

    Connor Hoge

    Lin-Lin Bu

    “NF-κB and STAT3 – key players in liver inflammation and cancer” maybe this review could have some help for you.

  • António Maximiano Fernandes added an answer:
    Where we can order cancer aptamers?

    Sensing with the help of aptamers.

    António Maximiano Fernandes

    Great, I fail to understand aptamers until find this wonderful answer

  • Horatiu Cristian Popescu asked a question:
    Why mutant p53 expression is increased in colorectal adenocarcinoma obese- type2 diabetes mellitus patients?

    Is there a particular feature or a direct connection that can explain why immunohistochemical expression of mutant protein p53 is increased in obese and diabetics (type 2 diabetic) patients at diagnosis of colorectal adenocarcinoma compared to non -obese diabetics versus non-diabetics obese/non obese?

    Study included immunohistochemical analysis of  2 proteins Bcl2 and p53 (both monoexpression and coexpression) in 100 newly  diagnosed colorectal adenocarcinoma specimens divided  equal in 2 groups diabetics (type 2 diabetes mellitus already existing at diagnosis of colorectal cancer)  and non-diabetics .The preliminary statistics results have not indicated a significant difference between the 2 groups, in terms of Bcl2, but  indicates an increased expression of p53 only in the  diabetic-obese group compared to  non-diabetics obese or non-obese (statistically significant ) which theoretically indicates a contact point between obesity, cancer and diabetes. Interestingly moderately low degree of differentiation is associated with both diabetes and the presence of p53 positivity; G2-p53 associations is an intriguing part. Bcl2 expression was low and insignificant in both group.

  • Ishtiaq Qadri added an answer:
    Can we use any other cell surface marker in addition to CD33, CD133, CD24, CD44, CD90 DLK1, EpCAM, Ov6 for hCSC Isolation from HCV HCC biopsies?

    HCC, hepatic Cancer Stem Cells, HCV GT4, intratumoral heterogeneity, FACS

    Ishtiaq Qadri

    Dr Khedar: Thank you for your referral. My question is related to liver and hepatic cancer stem cells and it seems that Dr Ahamd;s expertise is on estrogen receptors and  p53 in the context of prostate and breast cancer. 

  • Abdul Hafeez Kandhro added an answer:
    Do low glucose conditions stabilise HIF1 alpha protein in Breast Cancer Cell lines?

    Do low glucose conditions stabilise HIF1 alpha protein in Breast Cancer Cell lines? Specifically in high glycolytic cells like MDA-MB series.

    Abdul Hafeez Kandhro

    Under normal oxygen conditions, nonmetastatic cells consume less glucose and express low HIF-1α, whereas metastatic cells constitutively express high glycolysis and HIF-1α, suggesting that dysregulation of HIF-1α may induce the Warburg effect.

    The recent discovery and study of HIF-1α have implicated a possible molecular mechanism for the Warburg effect in malignant tumors. HIF-1α plays an important role in cellular responses to hypoxia and other stresses. HIF-1α combines with HIF-1β to form a heterodimeric transcription factor that regulates the expression of glycolytic and angiogenic proteins. HIF-1α is constitutively expressed and destabilized in the presence of O2 by proline hydroxylation and is targeted for proteosomal degradation by the von Hippel-Lindau (vH-L) ubiquitin ligase. When accumulated (e.g., under hypoxia), the HIF-1 complex binds hypoxia response elements (HREs; canonically CCATG) in the promoter region of target genes.

    To know  the relationship between HIF-1α stabilization in oxygenated conditions and the Warburg effect; by comparing glucose transport, lactate production, HIF-1α protein, and HRE-induced transcript levels in metastatic (MDA-mb-435) and nonmetastatic (MCF-7) breast cancer lines. Under a 20% oxygen atmosphere (normoxia), MDA-mb-435 cells have elevated glycolysis, HIF-1α, and HRE transcripts, whereas these parameters are measurably lower in MCF-7 cells. Hypoxia (≤2% oxygen) induced no change in the glycolytic phenotype in MDA-mb-435 cells, whereas HIF-1α, HRE transcripts, and glycolysis were profoundly induced in MCF-7 cells. But due to controversial findings have identified MDA-mb-435 cells with melanoma cells due to the expression of specific melanocyte genes and lack of expression of breast cell line genes in MDA-mb-435 sublines. To account for this possible discrepancy, renal cell carcinoma (RCC4) used, where transfection of the vH-L gene into a vH-L-null line directly modulated HIF-1α levels. Parental RCC4 cells functioned similarly to the MDA-mb-435 and MDA-mb-231 lines by expressing high levels of HIF-1α and exhibiting high glycolysis under normoxic conditions. There was a minimal effect when these cells were switched to hypoxia. Restoration of vH-L activity led to normalization of the HIF-1α response. Under normoxia, RCC4/vH-L cells demonstrated low rates of glycolysis, which subsequently increased in hypoxia. 

    You may find details in this article: "Hypoxia-Inducible Factor-1α and the Glycolytic Phenotype in Tumors"

  • Udesh Dhawan added an answer:
    How do you recognise epithelial-to-mesenchymal transformed (EMT) cancer cells in clinical samples?
    They should have reduced or absent epithelial characteristics, so how do you discriminate them from authentic mesenchymal cells?
    Udesh Dhawan

    Dear Dr. Ericsson, I have been working with something similar and I have found decreased CDH1 to be a good reference for the loss of Epithelial Characteristics and an increase in CDH2, Vimentin plus a spindle shaped morphology to know that the cells have mesenchymal characteristics. Moreover, I have also found the expression of Snail and Slug to be highly increased in the cells showing the mesenchymal characteristics since they control CDH1 gene. But in all of my experiments, I have found Twist to be downregulated. So, I would suggest that a decrease in CHD1, Increase in CHD2, Vimentin and an increase in any of these transcription factors (Snail, Slug and/or Twist) followed by an elongated/spindle morphology should be a good observation to conclude that your cancer cells have transitioned from Epithelial to Mesenchymal state.

  • Carol A Gray added an answer:
    Is there a well-established research protocol to induce prostate cancer in dogs and are there good biomarkers?

    I am part of a multidisciplinary research group at the University of Saskatchewan Canada, who are studying prostate cancer. I am wondering if there is well established research protocol to induce prostate carcinoma in dogs. We need dogs with prostate carcinoma to use for imaging studies.

    Anybody who has a protocol or can help do this and would like to establish collaboration?

    Thanks very much

    Ahmad Al-Dissi                                                                            

    Carol A Gray

    Agree with the answers above; ethically, most researchers now think that companion animals (cats and dogs) must benefit from any cancer research that involves using them, so naturally occurring cases are the only option.

  • Stefania Zuppone added an answer:
    Does anyone know about a Her2+ breast cancer cell line over-expressing uPAR?

    Hi everyone!

    I'm searching for a breast cancer cell line in which Her2 and uPAR are both over-expressed. Does anyone know about any? Thanks in advance

    Stefania Zuppone

    Thank you so much for your help and kindness!

  • Hatem A Abou-Ouf added an answer:
    Any advice on prostate Cancer cell lines, genome portal?

    Hi, I am looking for a source to get copy number data for prostate cancer cell lines such as PC3, LNCaP, DU145 , ..etc. 

    I checked Oncomine but i can not find these data. Share plz if you have a clue. 


    Hatem A Abou-Ouf

    Thanks Michele. However, i am looking for a data base that i can search/query. 

  • Fawaz Naji Saleh Al-Shaheri added an answer:
    How can I identify and evaluate patients who are at high risk to get leukemia?

    How I can evaluate patients whom at high risk to get leukemia, , I'm asking about lab technique by which I can expect if patients at risk to be leukemic?

    Fawaz Naji Saleh Al-Shaheri

    You are welcome and best of luck.

  • Piero Tosi added an answer:
    Can all malignant tumors (cancers) metastasize to other organs?
    Cancers metastasize via seeding through blood or lymphatic vessels.
    Piero Tosi

    I agree with Jarad and Momma, with the exception for glioblastomas in very rare cases.

  • Mehrdad Payandeh added an answer:
    What is the new tumor suppressor gene for prostate cancer?

    For evaluation of tumor response and toxicity in prostate cancer cells.

    If we want to check the cancer cells response to the adjuvant radiation therapy or combination of three or two modalities in prostate cancer, what biomarker could help us? What is the newer and recent androgen receptor?

    Mehrdad Payandeh

    Ki67 level and mitotic index

  • Steve Mcclellan added an answer:
    What stemness genes can be used for cell classification using expression data?

    I have sequenced tens of single cells of bladder cancer, and got the gene expression profile of each single cell. I am trying to speculate the cancer stem cells mixed in these cells using clustering method, which needs a priori list of "stemness genes". If there are some available common or specific stemness signatures can be used in this analysis? Many thanks.

    Steve Mcclellan

    The ES markers Nanog, Sox2 and Klf4 are relevant to CSC and can be used to differentiate stem versus non-stem cancer cells.  Please see our most recent paper using SmartFlare to detect CSC (you can download it in my profile).  Other relevant markers are players in the Wnt, notch or sonic hedgehog pathways as these are unregulated in most CSC.  Other surface markers are CXCR4 (Cd184) and MDR1 (CD243) and Muc1 (CD227).

    Kind regards,


  • Kulvinder kochar kaur added an answer:
    Cancer a mere matter of luck? Or is there something under-appreciated?

    It has been all over in the news lately: The majority of cancer is obtained by bad luck, not by lifestyle or inheritance. See attached. 

    Really? The data appear solid and they make sense, but the conclusion seems a bit premature: the observations are based on established risk factors in the USA and I assume (let the experts please come forward!) that these risk factors are based on occurrence. This means we do not see all those cases where the patient's immune system adequately takes care of the anomaly. 

    How does occurrence of cancer relate to failure of the patient's immune system, and can we monitor this based on adequate biomarkers? How will the statistics and the conclusions change when this factor is included in the analysis?

    Kulvinder kochar kaur

    thanks for the reference will read it and get back

  • Tahmina C Islam added an answer:
    Can cancer come from any type of cell or are there some cell types that never produce cancer?
    Some cells seem to produce cancers more frequently than others. There are > 200 distinct human cell types; do all of these produce cancers under some circumstances? If not what is special about cells that never produce cancer? Why do some cells produce cancer relatively frequently while others do not? How well is this predisposition toward or against cancer development understood?
    Tahmina C Islam

    Wonderful discussion and a very nice question,Just adding some points to the discussion. With the development in high throughput techniques and specific molecular, biological, clinical research coming together, many aspects of cancer initiation-formation, biology, progression are unravelling such as cell type specificity, stem cell origin of cancer, transcriptions factors for pluripotency vs differentiation, genetic errors and mutations, epigentic and immunological factors along with socioeconomic factors, ethnicity, and geographical location (diet) regarding the incidence and understanding of cancer.

    I think the cells that are most prone to cancers depends on their exposure to the hits involved in cancers and also their proliferative and differentiation status.
    1. So epithelial cancers are the commonest such breast, prostate, lung, colorectal.
    2. then Melanoma, Lymphoma, Leukemia, the list varies with the location in the globe, ofcourse.
    3. Neuoblastomas is a rare cancer that occurs in the children, while most brain tumours develop from cells that support the nerve cells.
    4. And many rare tumours that are found in the 'rare list' are very specific such as Merkel cell skin cancer, Angiosarcoma of the heart. Very well differentiated cell types are may be not switched back to pluripotency easily or may be these cell types not easily exposed to triggering mechanisms as are the cancer stem cells.
    I would like to bear in mind the basic cell types and the location of their stem cell type in our body keeping in mind their normal functionality and derailment from it, by DNA damage and also their normal proliferative and apoptotic signals (as the damaged cells are may not be cleared) regulates how common or how rare a tumour may be. Ofcourse other factors mentioned above do come into play.

    How a stem cell becomes a cancer stem cell having the multipotent capacity by acquiring genetic modifications is vital, as clonaity of cancer has shown that origin of the tumour goes back to a primary cancer stem cell. It is important to be hit by one or multiple mutations by triggering agents in the environment (bacterial, viral or toxic) and the cells proliferative capacity allowing it not to be able to repair the damage or other enzymes or molecules in the repair pathways being ineffective. Also, epigenatic mechanisms may come into play along with the genetic aberrations in the mutihit process of cancer formation and progression.

    The refs below in cancer biology, progression and pluripotency factors may help further understanding.
    2.Cell. 2006 Aug 25;126(4):663-76. Epub 2006 Aug 10.
    Induction of pluripotent stem cells from mouse embryonic and adult fibroblast cultures by defined factors.
    Takahashi K1, Yamanaka S.

  • Valentine Comaills added an answer:
    Does anybody have a good antibody to detect human cells in mouse xenograph model?

    my cells are human breast cell line GFP/luc but my GFP signal is very low. I cannot find a good anti-GFP to detect it (I also tried TSA amplification, it is not working). Anti-Luciferase antibody from abcam is very unspecific. I tried anti human mitochondrial MAB1273B from millipore and do not get signal. I am thinking to buy the MAB1281 from millipore anti nuclei human, but I read bad comments about this antibody. Any suggestions? Thank you very much in advance.

    Valentine Comaills

    Hi Nora,

    when I say overfixed, it is because I have a lung metastasis, that clearly is from my primary site (confirmed by pathologists with H&E stain), but i cannot stained it for my antibodies, I fight as crazy for it, but nothing... some collaborators also tried to do FISH on it and cannot do it... I put my sample in formalin overnight, but it seems that this piece get overfixed..(other sample were fine). but if you already stained with other thing your sample and have signal, your sample should be perfectly fine... I think the MAB1273 is weak so need to have a good sample to begin with.

    Good luck!


  • Holger Zeitler added an answer:
    Is there a role of CA 15-3 as a biomarker for breast cancer in the surveillance of a properly selected group of ”high risk” women?

    As a radiologist, interested in cancer imaging, i came across a publication
    (Atoum, 2012), that could show correlation between elevated CA 15-3 and stage II-III breast cancer.

    Of course CA 15-3 cannot detect early stage breast cancer and is therefore not recommended in screening (Duffy, 2006). 

    But sometimes it can be challenging to find a 2-3 cm diffusely infiltrating breast cancer in asymptomatic - especially premenopausal - women with dense tissue (Buist, 2004. Kolb, 2002).

    A serum marker might be helpful to select patients for further evaluation, e.g. Breast-MRI, tomosynthesis or ultrasound, in order to find “medium size” breast cancers, that otherwise would go undetected by mammography for quite a while with worsening prognosis.

    + 4 more attachments

    Holger Zeitler

    Hi Christina, thank you for that interesting information:
    imaging methods might be less sensitive than CEA and CA-15-3 to predict recurrences in advanced breast cancer.
    a little bit like mammography screening in women with very dense breasts,
    or ultrasound screening for HCC detection in patients with liver cirrhosis:

    not 100 % sensitivity and specificity ....

    there is a paper, which may be interesting in that context: Alpha-Fetoprotein Measurement Benefits Hepatocellular Carcinoma Surveillance in Patients with Cirrhosis

    • Source
      [Show abstract] [Hide abstract]
      ABSTRACT: Liver cirrhosis is a major risk factor for hepatocellular carcinoma (HCC), and all liver study societies recommend HCC surveillance in patients with cirrhosis. However, no ideal modality for HCC surveillance has been determined. The aim of this study is to assess the effectiveness of α-fetoprotein (AFP) measurement in HCC surveillance. In this retrospective analysis, all patients with cirrhosis, who received HCC surveillance through ultrasound (US) and AFP measurement between January 2002 and July 2010, were followed up until June 2013. The performance effectiveness of surveillance using AFP, US, or both in HCC detection was compared. Overall, 1,597 patients were followed for a median duration of 4.75 (range 1.42-12) years. Over the 8563.25-person-year follow-up period, 363 patients (22.7%) developed HCCs. For HCC detection, the area under the receiver operator characteristic curve of surveillance AFP was 0.844 (95% confidence interval: 0.820-0.868, P<0.001). When the traditional cutoff value of 20 ng/ml was used, the sensitivity and specificity of AFP were 52.9% and 93.3%, respectively. US exhibited a sensitivity and specificity of 92.0% and 74.2%, respectively. A combination of US and AFP exhibited a sensitivity and specificity of 99.2% and 68.3%, respectively. By using cut-off at 20 ng/ml and AFP level increase ≥2 × from its nadir during the previous 1 year, the combination of US and AFP yielded a sensitivity of 99.2% and an improved specificity of 71.5%. The complementary use of AFP and US improved the effectiveness of HCC surveillance in patients with cirrhosis.Am J Gastroenterol advance online publication, 14 April 2015; doi:10.1038/ajg.2015.100.
      The American Journal of Gastroenterology 04/2015; 110(6). DOI:10.1038/ajg.2015.100
  • Ana Rita Pedrosa added an answer:
    Which IHC markers are the best to show epithelial-mesenchymal transition on FFPE tumor samples?

    I testing this on in samples of normal skin, actinic keratosis, in situ and invasive SCC of skin. I used Vimentin, E-cadherin and N-cadherin, but I have problems with interpretation of my staining results. Vimentin is quite intense and easy to interprete. E-cadherin in invasive SCC is pale or there is no staining in samples that do not show vimentin expression. In in situ lesions is focally lost (in actinic keratosis in regions where atypical cells are). N-cadherin is pale and seen only in few tumors. Different authors used different combination of markers. I was wondering which one or which combination is enough and safe to say wheter EMT is present or not?

    Ana Rita Pedrosa

    Dear Martina,

    I used successfully, E-cadherin and the EMT transcriptions factors, Snail and Slug. The latest factors are seen as small dotted points inside the tumor cells. In my case, frozen-mouse prostate samples, the areas which exhibited tumorigenic transformation with a considerable degree of dysplasia had loss of E-cadherin and positive staining for the mesenchymal factors referred. In the skin you will probably have a lot of vimentin staining, due to the presence of myofibroblasts?

    Hope this helps you...

  • Neeraj Verma added an answer:
    What is the scientific and most acceptable way to give doses of carcinogenic compound to a mice dermally?

    In my experiment I'm giving the doses of DMBA/TPA, with my compound of interest, what would be the best and most widely accepted scientific way to give doses and treatments?

    1: Trim the upper dermal hairs and give the doses with the Pipette?

    2: Remove the hair with the hair removal creams and then apply the doses?

    3: What could be other suggested way?

    Neeraj Verma

    Either you can use hair removal cream.

    Apply the hair removal cream (VEET) carefully on the mice skin and then slowly take out the hair using cotton. 

  • Sinan Ibaguner added an answer:
    What are the clinically used biomarkers to detect Diabetic Pancreatic Carcinomas?

    There are many biomarkers for the detection of pancreatic cancers, leading the pack is CA 19-9 whose sensitivity and specificity is less than optimal. In clinical settings, are there any other markers that has proved more useful in detecting diabetic pancreatic cancers?

    Sinan Ibaguner

    Particularly in heavy drinkers &/or smokers screening of ESR & CRP must be done periodically in order to diagnose pancreatic cancer at treatable stages.

  • Shyam Bandari added an answer:
    Any suggestions on the problems with the Western blot analysis on Myeloma patient serum derived exosomes?

    Helloo all,

    I have Isolated exosomes from myeloma patient serum using Exoquick kit (SBI)..and I confirmed the size using Nano sight (50 to 200 nm)..Till this point all fine but I have an issues performing western blot on these samples, when I add WB loading buffer and heat the sample...sample is getting viscous (gluy) I was unable to proceed further ....does any one have suggestions to circumvent this problem ?? 

    Shyam Bandari

    Thank you all.... I have diluted my sample and performed the western blot.. and the results look fine, I could see the protein of my interest.....once again Thank you all 

  • Peter Kloehn added an answer:
    Which antibodies attached to gold nanoparticles are used to detect breast cancer?

    Gold nanoparticles synthesized by Citrate reduction method and loaded with anti cancer drugs are used to target cancer cells. Which antibodies are used for detection of these cells and how these antibodies will be attached to the surface of AuNPs?

    Peter Kloehn

    Best to use therapeutic antibodies used to treat breast cancer, as these antibodies are FDA approved. Commercial antibodies are not validated and may show substantial off-target effects. ERBB2 is overexpressed in breast cancer tissue and can be targeted by Trastuzumab and Pertuzumab. Also, the EGFR is overexpressed in breast cancer and can be targeted by Cetuximab, Panitumumab, Nimotuzumab and 806.   

  • Sunil Badve added an answer:
    Are there some complete and authoritative databases for cancer biomarkers?

    As we know, it's a time-wasting work to curate biomarkers of some specific cancers from massive literature and they may be incomplete for us. Therefore, I want to know whether there are some complete and authoritative databases for cancer biomarkers? By the way, noncommercial and publicly available databases may be better.

    Sunil Badve

    there are others such as KM plotter - which are tumor site specific

  • K.Kamil Reza added an answer:
    Why are long non-coding RNAs are important for cancer diagnosis?

    I would like to know about the non-coding RNAs as cancer biomarkers

    K.Kamil Reza

    Thanks for the answers

  • Svetlana Boudko added an answer:
    What immunohistochemical markers would you use to define a Granular cell tumor of breast as benign or malignant?

    Notwithstanding the Smith-Fanburg criteria, what immunohistochemical markers would you use to rule out malignancy?

    Svetlana Boudko

    Dear Narayanan

    I mean Granular cell tumour (breast), can tubular structures be seen there?


  • Sunil Munakomi added an answer:
    Can anyone suggest a reliable glioma marker?

    We're looking for a nice marker to detect tumor cells within glioma tissue. The tissue will be dissociated into a cell suspension. After that, we want to stain the suspension with a mixture of antibody-conjugates for flow-cytometric analysis to get an idea of the cellular composition of the tumor...

    Can anyone suggest a marker (either extra- or intracellular) that is only/mostly expressed by tumor cells?

    Sunil Munakomi


  • Jan Voskuil added an answer:
    Does anybody know of a good human Snail and Twist antibodies for IHC?

    I am interested in looking at the expression of some EMT markers in human breast tumor samples. It's difficult to find good antibodies. Especially in the case of Snail (Snai1), most papers list the company that produced the antibody but not the catalog number. Often times there are several antibodies from one company. Looking to see if anybody tested and identified ones that work well for IHC on FFPE samples. Thank you!  

    Jan Voskuil

    I completely sympathize! Publishers need to demand authors to specify the catalog numbers. Everest Biotech has a goat peptide antibody shown fit for IHC in mouse: EB07405. However, batch has changed and the confirmation came from the former batch (another thing to worry about!). You should give this one a try and if you get stuck let us know.

  • Björn L.D.M. Brücher added an answer:
    What are the consequences differences of plasma DNA and DNA from HCC tissues?

    What will be the consequences out of this?

    Extract by Florent Mouliere / Montpellier and Nitzan Rosenfeld / Cambridge:

    Circulating tumor DNA (ctDNA) is now widely investigated as a biomarker in translational and clinical research. However, despite the growing field of clinical applications, the biology of ctDNA remains unclear. In trying to learn about the origins of ctDNA, nature provides us with very few clues. One of the important accessible parameters is the size of those DNA fragments. In addition, a well-informed model of these sizes and biases can help design more efficient and accurate diagnostic methods. In PNAS, Jiang et al. take an important step in that direction.

    We used massively parallel sequencing to study the size profiles of plasma DNA samples at single-base resolution and in a genome-wide manner. We used chromosome arm-level z-score analysis (CAZA) to identify tumor-derived plasma DNA for studying their specific size profiles. We showed that populations of aberrantly short and long DNA molecules existed in the plasma of patients with hepatocellular carcinoma. The short ones preferentially carried the tumor-associated copy number aberrations. We further showed that there were elevated amounts of mitochondrial DNA in the plasma of hepatocellular carcinoma patients. Such molecules were much shorter than the nuclear DNA in plasma. These findings have shed light on fundamental biological characteristics of plasma DNA and related diagnostic applications for cancer.

    The analysis of tumor-derived circulating cell-free DNA opens up new possibilities for performing liquid biopsies for the assessment of solid tumors. Although its clinical potential has been increasingly recognized, many aspects of the biological characteristics of tumor-derived cell-free DNA remain unclear. With respect to the size profile of such plasma DNA molecules, a number of studies reported the finding of increased integrity of tumor-derived plasma DNA, whereas others found evidence to suggest that plasma DNA molecules released by tumors might be shorter. Here, we performed a detailed analysis of the size profiles of plasma DNA in 90 patients with hepatocellular carcinoma, 67 with chronic hepatitis B, 36 with hepatitis B-associated cirrhosis, and 32 healthy controls. We used massively parallel sequencing to achieve plasma DNA size measurement at single-base resolution and in a genome-wide manner. Tumor-derived plasma DNA molecules were further identified with the use of chromosome arm-level z-score analysis (CAZA), which facilitated the studying of their specific size profiles. We showed that populations of aberrantly short and long DNA molecules existed in the plasma of patients with hepatocellular carcinoma. The short ones preferentially carried the tumor-associated copy number aberrations. We further showed that there were elevated amounts of plasma mitochondrial DNA in the plasma of hepatocellular carcinoma patients. Such molecules were much shorter than the nuclear DNA in plasma. These results have improved our understanding of the size profile of tumor-derived circulating cell-free DNA and might further enhance our ability to use plasma DNA as a molecular diagnostic tool.

    Jiang P et al.: Lengthening and shortening of plasma DNA in hepatocellular carcinoma patients. Proc Natl Acad Sci U S A. 2015 Feb 2. pii: 201500076.

    Björn L.D.M. Brücher

    well pointed out.

    We also have this discussion at the web group of theTheodor-Billroth-Academy on LInkedin and Reinhold Kiehl, Hossein Rahmati Roudsari and Jan Voskuil made very important points and I try summarizing those:

    -tumor markers as CEA or CA19-9 should be used for follow-up-never for making the diagnosis, as the overall accuracy is too small. Further tumor markers are expressed proteins on surface membranes and we learned from epithelial cysts that such can mimick a cancer, spleen cysts very high CA-19-9 had been observed without any association of any cancer, nor during follow-up

    Therefore, we by now do not know 

    - the influence and value and accuracy of detectable DNA
    -when the best time is measuring it and how the values are influenced
    -how storing would be best and how the interobserver variability might be
    -when free DNA is measurable, how do such values differ after treatment
    -are they proven being related to the observed cancer or assumed to be
    -microRNA#s had been observed in ling cancer patients assuming having impact on spread and even cancer development but again: assumed!
    -to my knowledge no standard protocol is accepted or suggested determining free DNA so far

    Additionally Ijaz Jamall added a valuable insights deepening he comment from Hossein Rahmati Roudsari and Jan Voskuil (copy and pasted):

    Ijaz Jamall: "I agree with Dr. Rousdari and Jan: one key factor to consider in measuring anything in the blood is its half-life and how to "normalize" the thing being measured - per ml blood or serum, per g protein, etc. because essentially we are measuring a concentration as opposed to a mass and dilution and binding kinetics or changes in hydration or albumin content can make huge a difference. In fact, diurnal variation can itself make a huge difference"

About Cancer Biomarkers

A biological molecule found in blood, other body fluids, or tissues that is a sign of a normal or abnormal process, or of a condition or disease. A biomarker may be used to see how well the body responds to a treatment for a disease or condition. Also called molecular marker and signature molecule. A cancer biomarker pertains to any biomarker that fits the aforementioned definition but only for cancer, and no other disease.

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