Lymphoma - Science topic

Dear V H Krishna Prasad,

Check the following Institute.

National Institute of Pharmaceutical Education and Research

NIPER Ahmedabad,

Opposite Air force Station, Palaj

Gandhinagar-382355, Gujarat, India.

 +91 79 66745555 , +91 79 66745501

Their cell line repository consists of mammalian cancer cell lines, murine primary cell lines and non-cancerous cell lines. I am not sure whether you will succeed but you can always try. lf you are interested, MM.1S cell line is available at ATCC

Best.

Advices for primary T cell lymphoma isolation and culture are also appreciated.

Hello Fiona Brown-Burke

You may consider using Cultrex Basement Membrane Extract. Please refer to the link below for more information on this product.

Geltrex could be an alternative as well. Please refer to the links below.

Hope this helps!

Best.

Hello Shreyas Gujar

You shouldn’t have forgotten to keep the sample at -80 degree C before leaving the lab. Anyway, such incidences keep happening! For your information, RNA is stable in trizol which deactivates RNases. However, the sample can be kept at room temperature at this point for, at most, a few hours, or the sample can be frozen for later use at -80°C.

So, you should not proceed with RNA extraction for this sample which has been kept at room temperature for two days.

Best.

Not sure how it really works, but in papers, I've come across something called the DeLong's test used to compare different AUCs.

Hi Karol,

It's probably worth a try. Alternatively, you could also try subcellular fractionation and comparing cytoplasmic to nuclear B-cat. We have done it in colon here:

but is has also been done in some lymphoma cell lines eg here:

You will probably want to incorporate the use of a Wnt ligand and a Wnt inhibitor to give you a bit more confidence that your tecnique works and some idea about its sensitivity.

I would imagine that you are likely to run into some issues comparing between different cell lines if they cover a wide range from the endless list of lymphoma subtypes available.

Also, depending on what you find and where you aim to take your project, you may be asked by reviewers to confirm your findings more quantitatively further down the line. I would probably start optimizing this sooner rather than later.

Hello Min Gui Jang

There are differences between cancer cell lines with respect to key mutations that play a role in many different biological processes in the cell like impaired apoptosis, increased drug efflux which could cause differing drug sensitivity.

Generally, cell lines appear to respond to drugs in two broad patterns.

One group of drugs, primarily targeting machinery involved in the cell cycle, protein chaperoning or DNA repair which elicit similar patterns of response across all cell lines.

A second group of drugs, trigger responses that are specific to cell type. Different cell types respond to these drugs in qualitatively different ways. Such drugs largely target the signaling pathways that are disrupted by oncogenic mutations.

So, wherever possible, cell lines should be selected that most closely resemble the genomic alterations of the tumor subtype being studied. No individual cell line can be representative of all cancers derived from a single tissue.

I hope this helps.

Best.

CCLE RNAseq should have the details of its expression.

Dear Min!

Please You look at the article:

Signal transducer and activator of transcription 3 (STAT3) regulated by calcineurin. Calcineurin promotes the degradation of STAT3 via the ubiquitin-proteasome pathway. Inhibition of calcineurin acutely increases total levels of STAT3 as well as its activated forms, resulting in decreased levels of the tumor suppressor p53 and its proapoptotic target, Bax. In vivo and in vitro, calcineurin regulates levels of STAT3 and neurotrophin dependence. TMF/ARA 160 (TATA element modulatory factor/androgen receptor co-activator 160), the key mediator of STAT3 ubiquitination, is required for calcineurin-dependent STAT3 degradation.

Most likely, the differences between different types of cells consist in the activation of various ubiquinty ligases, which ubiquinylate proteins, including STAT3, for their subsequent degradation by the proteosome.

Dear Priscilla!

Please You look at the article:

Jordi Juncà We have just analyzed the blood of a patient with previous diagnosis of follicular lymphoma in lymph node that returned to the hospital with adenopatias and abnormal lymphocytes in blood. We performed an immunophenotyping of the blood and found 12% of medium sized cells with characteristics of follicular lymphoma: CD19 weak, CD10++, BCL-2++, CD5 neg, CD43 neg and IgM neg. However, these cells showed some positivity for post-germinal markers such as CD27, CD11c and CD39. In addition, 50% of the abnormal population showed expression of CD103 (without expression of CD25, CD123 or LAIR-1). It is the first time I see CD103 expression in a follicular lymphoma. On the other hand, I´ve already seen cases of hairy cell leukemia (very classic) with CD10 expression.

Hello Liselotte

You can use BC-1, BCP-1 and BCBL-1 cell lines. Please have a look at the research article below:

Best Wishes.

The patient will have 4 doses of the Rituximab weekly; the first dose was given over a 6 hours period by IV infusion. Prior to each dose a serial measurements of C1 esterase levels will be collected. The patient has completed the first dose and after 7 days the patients has experiences dizziness, extreme fatigue and blurred vision.

Hi

Looks that curcumin is stable in very low temperature for example -196 ^oC per week.

thawing and re-freezing at -80 ^oC

" curcumin is stable in the extracted samples during typical residence times in the autosampler and in frozen samples and standard solutions. However, repeated thawing and re-freezing of biological samples should be avoided. "

" Long-term stability was evaluated by analyzing the plasma test samples after storage at −70 0C for up to 2 months. The results showed that both curcumin and piperine were stable in the plasma matrix "

Hope it helps

Best regards

Tomasz

If the culture is in suspension, it should grow in suspension and not adhere. try to contact those who gave you the culture (it is possible that this is not a pure culture, that is, there are other types of cells or damaged). try growing cells on low-adhesion plates or dishes to avoid adhesion.

I think this will be helpful to you-

https://www.cellbiolabs.com/antioxidant-assays

https://ijpsr.com/bft-article/methods-for-determination-of-antioxidant-capacity-a-review/?view=fulltext

Also make sure the P/S concentration is 1%. Some cell death is okay. Can you post a picture of your cells in day 2 in culture here. Cells may not need 20% FCS/FBS.

Please also take a look at this link.

I am happy to help you.

I think it depends of several points: what type of lymphoma do you are suspecting, if the patient received treatment (Rituximab) or not, histologic features (e.g: necrosis). Sometimes flow cytometry is a more accurate to determine a real cut off. However, the paper below can help you.

Tumours on mucosa of bursa are considered virtually pathognomic for LL, enlargement of feather follicles ( folliculitis) only in MD, Nerve enlargement is common in MD not in LL.

I think you should fix and permeate them at different defined times. but if you do so. one questions you should be noticed : cells will be more likely aggregation by improper fixed methods and lots of them will be lost.

Hi,

in fact as for any kind of selection you will see a lag pahse. In my hands Puro selected cells took at least a week or so to recover. This is due to the selection as well as the stress coming anyhow from the transduction etc. Further due to the selection it self you reduce the number of living cells and many hermatopoietic cells have issues to proliferate in low densities. So I think this is a behavior to expect

Sven

In HIV patients, CD4 counts <100; cotrimoxazole, alternately dapsone + pyrimethamine can be given for 6 months.

Read:

I am also about to do PDX on NSG mice but I am wondering if I should use only female, only male or both male and female mice for my test and control groups. Any ideas?

Dr. Petkovic can you let us know about your therapeutic choices and the outcome of the above patient ?

Electroporation is the way to go for suspension cell lines. You can get up to 80% efficiency for siRNA knockouts with electroporation tailored to specific cell lines (for example Raji: https://altogen.com/product/raji-electroporation-kit-burkitts-lymphoma-cells-ccl-86/). Other methods can work, it's just that electroporation is particularly effective for suspension cell lines.

Check to see if Daudi and Raji (both are cell lines) meet your desired characteristics. Lymphoma lines are often suspension cell lines, and hence the most efficient transfection approach is to use electroporation (e.g. for Daudi: https://altogen.com/product/daudi-electroporation-kit-burkitts-lymphoma-cells/). Viral approaches should work as well, but electroporation is generally easier to perform and gets good results for suspension cell lines as well.

Thank you both for these suggestions!

There is a now a new opportunity to support expansion of primary cells like yours. Check this:

Please let me know if this reference/site is helpful to you:

1.  Paraaortic lymph node metastasis in patients with intra ...

www.ncbi.nlm.nih.gov › … › v.15(35); 2009 Sep 21

Sep 21, 2009 · Paraaortic lymph node metastasis in patients with intra-abdominal malignancies: CT vs PET. ... Low metabolic activity can cause a false negative PET scan ...

2. lymphoma, infection, vasculitis, and lupus

3. Early aortic endograft failure in the presence of periaortic lymphadenopathy with neurofibromatosis (von Recklinghausen's disease).Hori D et al. Gen Thorac Cardiovasc Surg. (2012)

4.  A case of IgG4-related lymphadenopathy, pericarditis, coronary artery periarteritis and luminal stenosis.Hourai R et al. Heart Vessels. (2016)  

Dennis

Dennis Mazur

The human lymphoblastoid B16 cell line expresses an IgG1 which can be observed by FACS on the surface of the cell.

This immunoglobulin is  very active since it is possible to kill in vitro and in vivo B16 tumor cell by injecting an antibody directed against the human IgG1.

Is there any correlation research between the development of dementia and the use of Turmeric in the diet?

Thanks all for their guidance.

Immortalization of Human Uterine Leiomyoma and Myometrial Cell Lines After Induction of Telomerase Activity: Molecular and Phenotypic Characteristics

The potential options are:

1. Brentuximab+ salvage chemo for CD30+ RR DLBCL

2. Revlimid or ibrutinib + salvage chemo for ABC type RRDLBCL 

3. CD19 CART based therapy 

4. Blinatumomab+ salvage chemo 

5. SGN 19 ADC + salvage chemo 

remeber none of the above choices are FDA approved options at current time. These all are in clinical trials. Thank you 

Hi

Which leukemia? There are several...chronic or acute; lymphocytes- T or B; myelogenic? etc...

YES

hi

I think they can be detected with the kit.

good luck

Integrating a 10kb gene by electroporation is very difficult, especially with this version of electroporator Biorad, without RF module.

It is very easy electroporate size of genes between 1 kb and 3 kb. Beyond 5kb is almost impossible.

For larger sizes of genes, it is preferable to use chemical agents such as PEI.

One note: for better electroporation efficiency, use a plasmid fresh (not frozen) to be supercoiled.

In contrast, for a chemical treatment, the more plasmid is linear (freezing and thawing) and the better the incorporation of the chemical reagent.

However, for a greater than 10 kD gene, it is more common to use a retroviral vector, such as a VLP associated with a cellular integration protein (fusion protein).

One last thing: the plasmid must be very pure (260nm / 280nm ratio = 2.0), it acts directly on the electroporation efficiency. Just as it is important: to use culture medium (serum free) to electroporate, to work at room temperature, and work quickly (no pre-incubation), for proper cell survival.

Finally 400V is the best solution, but only with all these remarks.

Hi

From Wikipedia, the free encyclopedia

Rituximab is a monoclonal antibody against the protein CD20, which is primarily found on the surface of immune system B cells. Rituximab destroys B cells and is therefore used to treat diseases which are characterized by overactive, dysfunctional, or excessive numbers of B cells. This includes many lymphomas, leukemias, transplant rejection, and autoimmune disorders. Rituximab is a chimeric molecule.The drug is on the World Health Organization's List of Essential Medicines, the most important medications needed in a basic health system.[2] It has a wholesale price of USD$159–$2,480 per vial as of 2014.[3]

Ref.

Drugs.com International brand names for rituximab Page accessed April 1, 2016

"19th WHO Model List of Essential Medicines (April 2015)" (PDF). WHO. April 2015.

Retrieved May 10, 2015."Rituximab". International Drug Price Indicator Guide. Retrieved 28 November 2015.

Thank you for suggesting these links. 

Try using Gridsearch algorithm in python

Thank you so much Andre and Grant. I will do as both of you have suggested.

Hi Lax

Before you test your drug, you should really ask how many cells you need to see your target protein in the blot, and then ask how much you can see it diminished in an siRNA knockdown. These two experiments will let you know how many cells' worth of protein need to be acquired per test point and this in turn will lead you to the cell number.

If there is a question over the expression of the protein and whether the cells are in log growth, then there is no short cut to doing a growth curve versus protein signal on the blot. Do this in the wells or flask you're planning to do the test in, remembering that for multi-well plates, it's the surface area, NOT the volume, that is important when scaling.

Good luck!

G

Dear colleague,

I personally have seen changes in bone marrow morphology in lymphoma patients prior to any chemo. Mostly, I saw changes in eritroblasts such as binuclear cell morphology, or mitotic figures. Sometimes I saw micromegakaryocytes or pseudo-Gaucher cells. This is rare events. The origin of this changes is unknown to me. My own speculations may be that malignant cells and their microenvironment may produce some cytokines, or substances that disturb regular hematopoiesis. Of course, this need to be evaluated through serious investigations. 

Assuming that the stock (14.3 M) of beta-mercaptoethanol is fresh (and stored appropriately), addition of 1.9 microliter volume to 500 ml medium would give you the desired working concentration of ~55 micromolar. However, this concentration would change upon storage of the medium. Therefore, the best practical thing would be to prepare fresh medium and supplement it with beta- mercaptoethanol before adding medium to cells.

Hello, 

Why not PCR with primers for TCR beta chain, do electrophoresis and then collect monoclonal PCR product?

Did you ever test RNU44 and RNU48 as normalizers? U6 is usually low expressed normalizer and I usually do not recommend it.

PS: di solito ci si riferisce con Housekeeping genes ad mRNA analysis, mentre normalizers per microRNAs.

Dear Christine, 

The authors to these papers are here on RG. Consult them: 

Dear Raju,

You could may be try the P388 so-called "leukemia" cell lines, which behave like a lymphoma when injected subcutaneously and not i.p. as classically done with this model.

I never performed actual lymphoma characterization of this model, in which I was interested for its aggressive behavior as an actual metastasizing process to the liver.

This model is described in the attached article. May be it could of help for you.

Best regards

Robert

The effect of the mitogen per se may not last that long, but once the cells started proliferating, the cytokine produced by them keep them going. If you do [3H]-thymidine incorporation assays using ConA stimulated T cells (so starting with a defined number), the cells keep going for up to a week, before being burned out (and undergoing apoptosis), In vitro, there is a lot of interefrences from other cytokines (IL-10, TGFb), other cells, and within stimulated cells, you will have activation of SOCS at given timepoints as well. In addition, that may nt be fully applicable for B cells, T cells need more than one signal to proliferate, otherwise they develop anergy.

Hope that helps

Dirk

Hi,

This may be useful to someone: LP-1 cells (multiple myeloma cell line) are highly positive for Notch2.

I think it depends on the promoter whether your GFP will be expressed less over time. A CMV promoter for example tends to get methylated in lymphoma cells and therefore lower expressed with time. I have good experiences with EF1alpha promoters in my B cell lymphoma cell lines regarding high long-term expression.

I am not aware of comercially available GFP lymphoma cells though, sorry.

In fact it is not quite true that all circulating B cells are killed by Rituximab.

Approximately 10% of circulating B cells, CD19 +, CD20 low, are still active even after treatment with metotrexate.

It is these cells that are responsible for the ADA response which follows. Although the majority of B cells have disappeared from the circulating blood, we have reactivated residual B cells with HuBBB, in sufficient quantity to identify cells producing ADA, and then clone a number of them.

This is also the case with Infliximab and RoActemra which although causing a significant lymphopenia let escape B cells capable of producing ADA directed against these drugs.

Dear Go, 

You find the researcher here on Rg so you can contact them with your questions:

Am J Surg Pathol. 2011 Jul;35(7):1080-4. doi: 10.1097/PAS.0b013e31821ddaec.

A case of hairy cell leukemia with CCND1-IGH@ translocation: indolent non-nodal mantle cell lymphoma revisited.

Chen D, Ketterling RP, Hanson CA, Colgan JP, Zent CS, Viswanatha DS.

From the abstract: Herein, we report a patient with clinical and cytogenetic features of INNMCL with overlapping morphologic and immunophenotypic features resembling hairy cell leukemia (HCL). After failing the chemotherapeutic regimen for MCL, he received a HCL-directed therapy and achieved durable response. This case suggests that CCND1-IGH@ may rarely occur in other mature B-cell neoplasms such as HCL.

Zhonghua Bing Li Xue Za Zhi. 2009 Nov;38(11):769-73.

[Clinicopathologic study of 15 splenectomy specimens of patients with hairy cell leukemia].

[Article in Chinese]

Li ZQ1, Chen HS, Liu EB, Sun Q, Fang LH, Sun FJ, Zhang PH, Yang QY, Qiu LG.

Abstract

OBJECTIVE:

To investigate the clinicopathologic features, diagnosis, differential diagnosis and the prognosis of hairy cell leukemia (HCL).

METHODS:

Fifteen splenectomy specimens of HCL patients were investigated retrospectively using HE and immunohistochemistry in correlation with the follow-up information.

RESULTS:

(1) The male to female ratio was 2.75:1, age ranged from 36 to 68 years with a median of 47 years. The most consistent clinical feature at presentation was marked splenomegaly (100%). Other symptoms included anemia (80.0%), thrombocytopenia (60.0%), leucocytosis (53.3%), pancytopenia (20.0%) and the absence of B-symptom. (2) The proportion of hairy cells was (14.6 +/- 7.2)% in periphery blood and (47.3 +/- 23.8)% in bone marrow. The positive rate of TRAP assay was 62.5% in bone marrow; 85.7% for TPA test and the detection rate for RLC was 25% by transmission electric microscopy. The frequency of bone marrow involvement was 100%. (3) The average weight of 15 spleens was (3012 +/- 1974) g. The size of 6 spleens ranged from 16 cm x 10 cm x 5 cm to 32 cm x 20 cm x 14 cm. The white pulp of spleen showed a characteristic atrophy feature or even absent due to leukemic infiltration, predominantly involving the red pulp with some sinusoidal pattern. "Blood pool" change was an infrequent feature (3/15 cases). The nuclei of leukemic cells were round (13 cases) or bean-shaped (2 cases), nucleoli inconspicuous or disappeared. The abundant cytoplasm and prominent cell border resulted in a "fried egg" appearance. By immunohistochemistry, leukemic cells were positive for CD45RA, CD20, PAX-5, CD25, CD11c, Annexin A1 and cyclinD1, but negative for CD3 and CD43. (4) 13 cases (86.7%) have been followed-up and all are alive. Among them, 9 cases are living well more than 5 years and 7 more than 10 years.

CONCLUSIONS:

Splenomegaly is frequently the first manifestation of patients with HCL and occurred predominantly in the middle to elderly adults. Definite diagnosis of HCL requires a combined histological and immunohistochemical assessment of the splenectomy specimen, bone marrow biopsy and aspirate.

Mod Pathol. 2000 Dec;13(12):1308-14.

Immunohistochemical detection of cyclin D1 using optimized conditions is highly specific for mantle cell lymphoma and hairy cell leukemia.

Miranda RN1, Briggs RC, Kinney MC, Veno PA, Hammer RD, Cousar JB.

Hairy cell leukemia with translocation (11;20)(q13;q11) and overexpression of cyclin D1. Ishida F et al. Leuk Res. (1999)

Cyclin D1 expression in non-Hodgkin's lymphomas. Detection by immunohistochemistry.

Zukerberg LR, Yang WI, Arnold A, Harris NL

American Journal of Clinical Pathology [1995, 103(6):756-760]

Thanks Béatrice. 

Regards,

Muhammad

Hello Anke,

you could use lysates from NPM/ALK positive cell lines, such as SU-DHL-1, Karpas299 or SUP-M2.

Most simply to cut solid tumors with forceps to very small pieces in clock glass or in special blender. and dispergs (suspend )   it in norrmal saline or Henks solution  with syringe abd ubject subutaneouksy it the flank side of miuce or rat.

I don't have the references available offhand, but there's good evidence in myeloma, acute leukemia, and B-cell lymphomas that tumor phenotypes can change on relapse.  This may be due to genetic instability of the primary tumor, emergence of pre-existing chemo resistant  sub-clones after therapy, or competition among subclones for environmental niches in the patient. 

Hello Angeliki Pournara and Jacqueline Salotti,

I appreciate your kind suggestions.

First of all, I will plan to treat actinomycin D or cycloheximide with or without MG132 in the presence or absence of poly (I:C) to get an idea about stability of IRF7 transcript and protein.

Thank you.

Nayoung

Why not use the mail address I attached to get a good answer

GPR is a Microsoft Excel based algorithm for Global Pattern Recognition (GPR) for PCR/qRT-PCR based techniques. If your GPR fold change for a gene is 96.45, means that the said gene is expressed at 96 fold higher level (compared to control).

Basically you are measuring deferentially expressed genes from multiple replicates ( from at least two conditions/samples).

See some of the links below:

https://www.bhbio.com/BHB/(S(pbw4hguf2capymwtwa13fam5))/GUI/SP/Gpr.aspx?AspxAutoDetectCookieSupport=1

Hope this information is helpful.

Hi, I

Thank you for your replies.

am using the RPMI1640 from Hyclone and FBS is from Gibco. I have tried to count and seed cells as per recommendation. I try to keep them at 3*10^5 cells / ml. Anyway, i have thawed a new vial and I hope it survives because from your suggestions it seems there should not be a problem. 

Many people will tell you that the tissues should not be formalin-fixed more than 24 or 36 hours otherwise the tissue will get too hard, or IHC staining will not work, but in my opinion this is just something that gets repeated over and over as dogma, but not actually based on fact. I have obtained good section quality and very good IHC staining in tissues that have stayed in formalin for months. As long as you use a proper heat retrieval protocol prior to IHC staining, my experience has been that many epitopes remain adequately antigenic to get proper staining. Perhaps some delicate markers, present in very low amounts, might be affected by long fixation, but this should be tested empirically, before declaring that tissues have been fixed too long to be of any use. 

Dear Dr. Khaleque, it's hard to believe, that SOLITARY EXTRANODAL lymphoma is T-cell lymphoma/leukemia requiring ALL-like treatment. This type of lymphomas is very aggressive, so localized stage is very-very unlikely! The precise morphological examination is crucial for the treatment decision. But... If it's impossible technically (hospital haven't required morphology lab) CHOP-like chemotherapy is more 'universal' treatment.   

Imatinib is soluable in water, ethanol and DMSO. Just prepare a stock and store @ -20°C. Create dilutions while storing @4°C.

In this case I would suggest  Fugene HD, which usually works as the charm. Though you would need to do titration assay to find out what ratio (plasmid/reagent) will work the best in your system. Good luck!

Thanks for suggestion and help and about demographic of Montreal you are absolutely right. Our patients are mainly European descendants and control population is checked samples of phase 1 data of 1000 gene project. I have asked bioinformatician who provided us the data for help but I was not lucky to receive help or advice. Is there any other way that can help me interpret these findings correctly? 

I am not an expert on Raji cells, but for sure serum starvation induces a G0/G1 block in their cell cycle. From the adhesion point of view, G1 phase is characterized by a general increase in the formation of Focal Adhesions after mitotic detachment and rounding. Thus, this could be the reason for the increased adhesion to the substrate. I think you could use trypsin to detach them (as routinely done to split epithelial cell lines), or you can starve them in no-adhesive conditions. For instance, you could use poly-Hema to coat the flask and avoid cell attachment.

Dear Avinash,

By checking the references to these papers you may find something useful:

Spectrochim Acta A Mol Biomol Spectrosc. 2014 Apr 5;123:241-8. doi: 10.1016/j.saa.2013.12.063. Competitive interactions of anti-carcinogens with serum albumin: a spectroscopic study of bendamustine and dexamethasone with the aid of chemometrics.

Wang Y, Zhu R, Ni Y, Kokot S.

Investigation of bendamustine HCL in a phase 2 study in women with resistant ovarian cancer. Baker AF, Roe DJ, Laughren C, Cohen JL, Wright HM, Clouser MC, Cui H, Alberts DS, Chambers SK. Invest New Drugs. 2013 Feb;31(1):160-6.

Bendamustine pharmacokinetic profile and exposure-response relationships in patients with indolent non-Hodgkin's lymphoma. Owen JS, Melhem M, Passarell JA, D'Andrea D, Darwish M, Kahl B. Cancer Chemother Pharmacol. 2010 Nov;66(6):1039-49

Competitive interactions of anti-carcinogens with serum albumin: a spectroscopic study of bendamustine and dexamethasone with the aid of chemometrics. Wang Y, Zhu R, Ni Y, Kokot S. Spectrochim Acta A Mol Biomol Spectrosc. 2014 Apr 5;123:241-8.

Bendamustine HCL for the treatment of relapsed indolent non-Hodgkin's lymphoma. Weide R. Ther Clin Risk Manag. 2008

Ask Nicola Gökbuget, Frankfurt, Germany, goekbuget@em.uni-frankfurt.de

I wonder if you have checked EBV DNA by PCR in peripheral blood, EBER, CD20 and CD30 on the colonic biopsy.

Thank you! I'll try the butyrate trick.

You have to treat your patient as acute lymphoblastic leukemia with extranodal involvement.

Just in case someone following this question., I got an answer from specialist in oncology. Generalized lymph-adenopathy is more related to Lymphoma while nasopharyngeal carcinoma is mostly comes with nasal bleeding, headache, hearing impairment as well as vision problem.

As regard heart biomarker and chest RT, I would suggest to give a look at

N-terminal pro-B-type natriuretic peptide plasma levels as a potential biomarker for cardiac damage after radiotherapy in patients with left-sided breast cancer.

D'Errico MP, Grimaldi L, Petruzzelli MF, Gianicolo EA, Tramacere F, Monetti A, Placella R, Pili G, Andreassi MG, Sicari R, Picano E, Portaluri M.

Int J Radiat Oncol Biol Phys. 2012 Feb 1;82(2):e239-46

Check this out:

Hematological Oncology

Special Issue: 12th International Conference on Malignant Lymphoma, Palazzo dei Congressi, Lugano, Switzerland, June 19–22, 2013

Volume 31, Issue S1, pages 151–200, June 2013