Friday, February 6, 2015

Articles review

*Daratumumab added action to Revlimid and Decadron in Myeloma we are told!
*New important pathway :  The PLK1 disturbing spindle cell assemby...
*Blinatumomab, beneficial in refractory B cell precursor ALL....
*Potentiation of T cell  tumor recognition (of neoplastic transformation)
by  1.   Anti-CTLA4-----Ipilimumab
      2.   Anti-PD1----PEMBRO
      3.   CAR-T cell therapy
*Volarsetib in AML for older patient (research)
*Adding Everolimus to Taxol-Herceptin failed to increase disease free survival.   But it did in Her-2 negative front line!   a 7 months improvement was reported (20 Vs 13 months).  BOLERO-3 is talking!

Saturday, January 24, 2015

Cytokines and Vitamin D mysterious there a value in Cancers of the elderly!

"These sets of experiments establish clearly that combinations of recombinant cytokines and vitamins could induce substancial intramonocyte killing of M.Tuberculosis.   The mechanism involved in this killing activity is not clarified"

From M.Denis.
"Conclusions: our data imply that specific actions of 1,25 (OH) Vitamin D3 in Cytokine stimulated T-Cell functions could have a role in preventing T cells related autoimmune diseases but also predispose toward T-cell mediated allergic reactions"

        Ralph Thien  et al   (J Allergy Clin Immunol 2005;116:683-9.
F Focus on Iron,Selenium, Cupper, and Zinc
   Vitamin A  (mortality to infections),B (impacts on number of lymphocytes),C(phagocytosis),D(susceptibility in IL-6 
    diseases) ,E (dysfunction of T&B cells)   (Read Susanna Cunnigham-Rundles et al.

   When the age comes!

Don't do it again in NSCL Cancers

Clinically Negative phase III trials with Antiangiogenics (and their targets) in NSCL cancers:

1.Thalidomid  -----an Antiangiogenic drug
2.Cediranib---------VEGFR TKI
3.Vandetanib--------Multikinase TKI
4.Sorafenib---------Multikinase TKI
5.Sunitinib----------Multikinase TKI

(from C.Langer notes)

Wednesday, January 14, 2015

Castleman disease

for Castleman disease
Hepcidin, Arlet at al" The results of this unique case study (1) explain the mechanism of iron deficiency observed in some children with CD, (2) confirm in vivo the regulatory effect of IL-6 in human hepcidin production, and (3) suggest that iron deficiency is a causal link between IL-6 and anemia of chronic disease."
from conference correspodent:
Siltuximab Efficacy in Multicentric Castleman's Disease Is Independent of Baseline Symptom Burden
Multicentric Castleman's Disease (MCD) is a rare, highly symptomatic, systemic lymphoproliferative disorder driven by dysregulated interleukin (IL)-6 signaling

from Johnson :"
Fifty-three patients were randomized to the SYLVANT arm at a dose of 11 mg/kg and 26 patients were randomized to the placebo arm. Patients had symptomatic MCD and were HIV negative and HHV-8 negative.[1] In this pivotal study, which led to the FDA approval, more than one-third of patients in the SYLVANT arm had a durable tumor and symptomatic response to treatment plus best supportive care (BSC), compared to none of the patients who received placebo plus BSC (34 percent versus 0 percent; 95 percent CI: 11.1, 54.8; p=0.0012). A durable response was defined as tumor and symptomatic response (reduction in tumor size and disease symptoms) that persisted for a minimum of 18 weeks without treatment failure."
The FDA approved the drug based on these findings

A trial of Dexamethasone and Rituxan could also be given....

Saturday, January 3, 2015

about Vitamin D

Dr David Samadi:
"A University of Colorado Cancer Center study recently published in the journal Prostate presents new evidence that vitamin D may help reduce cancer-causing inflammation. Scientists found that the gene GDF-15 – known to be up-regulated by vitamin D - can help block a protein which stimulates tumor growth." (suppression of the NFkB?)

from WebMD:

" The pigment melanin reduces the skin's ability to make vitamin D in response to sunlight exposure. Some studies show that older adults with darker skin are at high risk of vitamin D deficiency."

Is this why Prostate cancer tend to be more aggressive in Black
Is this sufficient evidence that Vitamin D deficiency should be avoided to reduce cancer
what is the role of Vitamin D in reducing certain Cytokines
does Vitamin D deficiency play a role in other cancers?
what is the role of Vitamin D in altering the Telomeres?
should Vitamin D enter the main stay of treatment of Metastatic Prostate cancers  (particularly in black)

While the NFkB may be involved, the truth is  everything  seems to happen at the Vitamin D receptor .
We know that in certain cases of deficiency (induced by Cytokines), the cell will increase the receptors to maximize its chances of capturing the Vitamin. And this may be the first move to neoplastic transformation.   Indeed increase in unbound Receptors of Vitamin D will overactivate not only the WNT but the deadly Hedgehog signaling changing the shape of the the prostate and its fate or life.   Just the BAG-1 (BCL-2 interaction) stimulation that will ensue is sufficient to beat the drum of Neoplasia.    Subsequent disruptions including  of Cav3, Raf, the RUNX and so forth will ensue.  Leading to a full fledged prostate the way this receptor also interacts with the AR (Androgen Receptor).     Avoid Vitamin D deficiency by all costs!  (The scenario where desensitization of Vitamin D receptor is the alternative is not discussed here)

Monday, December 29, 2014

Prospective study in cancer Neoplasia

We are at the break of a large prospective study that will test our understanding of neoplastic transformation.  There are obvious facts that the drop of the effect of hormones is followed by the reign of Cytokines which seems to coincide with a rise of cancers in the older population (above 50 years old).  And now we have increasingly companies that propose genes to be screened for cancer predisposition (ie.GeneID, FDA approved).
Putting these facts together,  it seems we are at the beginning of of a large prospective study that will monitor the changes in Cytokines against changes in selected genes and see what cancer will evolve over a 5-10 year period.
Cytokines tend to misbehave in the presence of certain genes (Fos, GSK, certain experiences-see related articles, G proteins -), these would play in the phosphorylation of unwanted genes.   This component must be included in the observation.
One interesting aspect to point out is that while some researchers are focusing on gene alteration detection, others such as professor Zangh at UTEP are focusing on Antibodies created as a result of the neoplastic transformation.  A recent rise in interest of lymphocytic (or activated lymphocytes) behavior in cancer may suggest the "a propos" of this last approach.

Tuesday, December 23, 2014

Options in Metastatic Her-2 positive Breast cancer

1.Pertuzumab + Herceptin + Taxanes

2.Adotrastuzumab EMTANSINE  "a HER2-targeted antibody-drug conjugate (ADC) which contains the humanized anti-HER2 IgG1, trastuzumab, covalently linked to the microtubule inhibitory drug DM1 (a maytansine derivative) via the stable thioether linker MCC (4-[N-maleimidomethyl] cyclohexane-1-carboxylate). Emtansine refers to the MCC-DM1 complex." (DRUG)


4."Data from five posters presented during the 2014 San Antonio Breast Cancer Symposium (SABCS) provide further evidence on the efficacy, safety and quality of life profile of eribulin, in the treatment of patients with locally advanced or metastatic breast cancer (MBC) and data in early stage breast cancer.

A second Phase 2, multicentre, open-label study, explores the feasibility of eribulin plus capecitabine as an adjuvant therapy in women with early-stage, estrogen receptor (ER) positive breast cancer." (drug)

Friday, December 19, 2014

New drugs on the market

From Momenta:
"Necuparanib (formerly M402) is a novel, rationally designed, oncology drug candidate under investigation in metastatic pancreatic cancer.  The use of heparins to treat venous thrombosis in cancer patients has generated numerous reports of antitumor activity; however, the dose of these products has been limited by their anticoagulant activity. Necuparanib, which is derived from unfractionated heparin, has been engineered to have significantly reduced anticoagulant activity while preserving the relevant antitumor properties of heparin. Necuparanib binds to multiple growth factors, adhesion molecules, and chemokines to inhibit tumor angiogenesis, progression, and metastasis."


" Twelve patients treated with necuparanib plus Abraxane and Gemzar completed the first 28-day treatment cycle. They had at least one follow up CT scan and were considered eligible for evaluating radiographic response. Out of them, seven patients showed a RECIST partial response and four patients reported stable disease.

Moreover, 11 out of the 12 patients showed a more than 50% decrease in CA19.9 levels (a predictive biomarker for long-term outcome and treatment response in pancreatic cancer) from baseline. The remaining patient achieved a more than 20% decrease from baseline. Overall, disease control was achieved in 92% of these 12 patients."

Wednesday, December 10, 2014

Cytokines after age of 45

Now it is true that the Cytokines are able to induce cancers
the question is is it through the FAK gene or the BCAR3,TENC1
or directly through the MDM2,
or through pathways (ie. the LYN-CD22-SHP-1 pathway for lymphocyte )(wikipedia)whatever the connection, a number of amplification gene will be soon engaged to commit and amplify the process Myc, NPM1, Cyclin B1,
other supportive activities will be amplification of transcription factors
suppression of promoters of Tumor suppressor oncogenes
and some of the elongation genes (for telomeres)
disturbance of Mitochondrial genes and Ubiquitination genes
all these steps open an opportunity for a therapeutic intervention.
the way to treating cancer provide so many opportunities, soon we will be working at finding the best way to articulate and sequencing them!

Tuesday, December 2, 2014

New targeting Chemotherapies

Eribulin in Breast cancer
Tipiracil in Colon cancer
Ramucirumab and Paclitaxel (or FOLFOX) for Gastric cancer
Panobinostat for Myeloma
Pembrolizumab for lung cancers
Afatinib +chemotherapy for non small cell lung cancers that is EGFR with Mutation Del-19
Bortezomib +chemotherapy VR-CAP for Mantle cell
Nivolumab for Metastatic Renal cancer
anti-BRAF and Anti-MEK for Melanoma

Sunday, November 30, 2014

Recent Big news!

*Recent trial suggested that Jakafi in combination with Xeloda may be useful in second line therapy against pancreatic cancer particularly those induced or accompanied by strong inflammatory response as suggested by high lebel of CRP (C-reative protein) (Targeted Therapy).
*With over 20% success in patents with NSCL cancers, Nivolumab /Pembrolizumab and other anti PD-1/PD-L1 continue to impress researchers and are bound to change the therapeutic approaches in this disease.  Soon everyone will be screened for these antigens as response rates seem to correlate with their presence.
*Does inhibiting Cytokines inducing cachexia in cancer able to change overall survival rates in cancers.   What is the relationships between these Cytokines and Mitochondrial changes and telomeres?

Tuesday, November 25, 2014

After the Cytokine period in a life cycle

First we have a Conception, birth and growth lasting from birth to 10 to 15 years, this period is full of "growth" but seems dominated by the HLA (Histocompatibility build up) but also organ maturation. Trying to establish what is oneself seems to be the priority.  Fight against infections seem to be the determinant event. Here women are the most "build"up in preparation for receiving the child, a foreign entity.

Then come 15 to 25 years of "Hormone reign"when most of the purpose is turned to reproductive function. The testicular cancer happen at this stage.  And in women, infection driven cancers (cervix) will mark this period.  Autoimmune and metabolic diseases will mark this period.

After the reign of the Hormones, after Menopause, commences the "years of the Cytokines".  This last another 20 years. One important fact during the years of the Cytokines, Hormone receptor desensitization with marked endothelial effect in women and does have profound epigenic and nuclear effects at cellular level.  Most cancers will happen here as Cytokines induce them.  In developing countries, most do not reach this period.  The cytokine period obviously last all life long as cancer can happen any day but during the years of 50 to 70, cancer risks are clearly higher but so are arthritic conditions that fully fall on the lapse of the Cytokines.  Mental disturbances also fall on the Cytokines.  Those who are lucky have a good c-fos, c-jun, Fas, FOXO-1, Daf-1 and the Telomeres (families of genes), will enter the new 10-20 years with still the Cytokine but less intense, like the one that make lose weight and muscle tone, the one that induce dementia and further CNS disturbances....

Saturday, November 22, 2014


 In this world of infections, Ciprofloxacin has gained prominent place and is widely prescribed and many antibiotics have similar effect of immunomodulation on mainly the monocytes and of course the lymphocytes.  Widespread use of these antibiotics call for further discrimination at genetic levels.  Ciprofloxacin has been known to amplify several genes including the NFKB, JUN B, C-Myc, AP-1, NFAT, c-fos, c-JUN, fra-1.   The NFAT amplification has the most of the attention here...This amplification calls for a check on the GSK3B  because a secondary amplification of this gene hits many critical genes in the initiation of cancers!  And in a profoundly obese population, the GSK3B has to be assumed to be profoundly disturbed in terms of level.  A high amplification of this gene not only affect key genes but is associated with marked phosphorylation of other genes particularly when interacting with SGK3.   And phosporylation of genes has been implicated in the expansion neoplastic transformations.  i.e the story of Casein Receptors and their relation with breast cancers.
Concurrent amplification of NFAT and GSK3 may be dangerous
1.when interacting with AR- --(Androgen Receptors) because Prostate Cancer may result
2.MUC 1, because Colon cancer may result
3.P53 and the Catenin, the NOTCH, all implicated in various cancers (Breast,tuberous etc..)

Do we check the status of this gene? no, we are still waiting for clinical trials...can't wait to live in the next century when all this will be done!  don't take my words for them!


GSK3B has been shown to interact with:

Wednesday, November 19, 2014

cancer detection movement is on the rise

It is generally thought that cells undergoing Neoplastic transformation will exhibit mutation, amplification or some form of new pattern in their genes, and based on this new pattern, observer can diagnose or even anticipate the behavior or prognosis of the cancer.   But each time, the question that come to mind is, which genes in which cancer?  And with 25,000 genes , the task is not a slim one.  And to make matter worse, Neoplastic cells do not remain static!  They are in constant flush, trying to survive their environment.
We know for example that prostate cancers grow on Androgen stimulation which has become the focus of most prostate cancer treatment with "abiraterone Acetate which blocks androgen synthesis, and Enzalutamide which block the Androgen Receptor" (Nina Sharifi).  We also know now that In their struggle to survive, the prostate cancer cells will acquire the enzyme 3 Beta-Hydroxysteroid dehydrogenase-isoenzyme to self produce DHEA and ultimately DHT.

While it is important to focus on these important driving mechanisms, it is also important to remember that cells use their potentials to fabricate these important enzymes!  Other supportive genes continue to play important supportive roles that also need to be disturbed.  And that remains a further challenge.  At certain times, the supportive role could be the overwhelming activity and detection may be skewed !
Professor Klein proposed 17 Genomic Prostate Core
1.Androgen signaling:
2.Stromal response
and there are
4.Cellular organization
and 5. Reference  (see article:"Genomics for active surveillance now in Practice")

We, at CRBCM, although reserved on the content as most of these reports may be limited, approve of this model of reporting detection as no single gene could actually reflect cellular activities all the time.   The fact is that the Genomic core does not speak about other genes such as the MED1,RAD51, CHEK1, DAPK, MLH1,TIMP3, PPARGs, TMPRSS, ERG, ETV1, SMADs,NBN or miRNAs  even though we know they are into play!

Despite our reservations, it is clear and exciting  to see the vibrant stand for cancer detection  in the general population and of course in targeted markets!   We are meeting today at UTEP to discuss what will be tested in collected blood samples...our bank has already 25 vials of blood samples the first week since we launched this study.  And more people are coming to donate...
CRBCM, progressing  slowly despite adversity!

Tuesday, November 18, 2014

Progression even in cancer detection

The study of cancer particularly as it comes to genes, gene alterations and their quality and quantity  modifications is one of the most exciting field of scientific research.  The cell, even the neoplastic cell, continue to be alive meaning undergoing constant changes and molecular transformations.  Often times, these transformations seem purposeful and clearly directed.  And often times the direction intends to reach "survival".  Less often though, the ultimate purpose is clear death ie when the Telomeres are shortened or the Caspases are engaged.
It is obvious that cancer detection should follow these transitions because some genes may not be over-expressed all the time, and some are even depressed during the neoplastic transformation.  The shear number of cells may affect secreted membrane proteins (such as the Prostate specific membrane Antigens (PSMA) to influence detection (by antibody) but often the predominant ongoing cellular phenomena can only be detected by studies of gene amplifications.
There seem to be 3-4 phases of cancer progression that require adapted detection:

1. The initial phase
where an amplified gene is inducing changes that will initiate the Neoplastic process,
ie effect of smoking on the MDM-2 gene and resultant effect on the P53.
ie. Viral effect on the Src or CSK genes,  this of course before the FUS gets into the frey! YES1! Rho gene...

2.The period of proliferation, that is when the MYC gene is involved to amplify all the genes
but not only the MYC but NPM1, Cyclin B1, and of course the many genes of proliferation

3.Metastatic phase (initial or during disease recurrence) here comes the Ros gene

4. Cellular death where Telomere and Mitochondrial phenomena come into play

we still have to wonder about the NCOA, the EZH2, ATRX, and MED1, TIMP3, where do these fit?

Saturday, November 15, 2014

Amplification of NCK-2 gene is/could be a strong Bio-marker of cancer recurrence

One thing for sure the return of cancer is physiologically one of an extraordinary undertaking in cancer biology.  Indeed as cell reconstitute, reoganization has to occur at several cancer cell levels including the Cytoskeleton.   One of the little known gene that comes into play is the NCK2 gene, a ligand protein /gene that direct to exacerbation of Actin polymerization and " The protein has no known catalytic function but has been shown to bind and recruit various proteins involved in the regulation of receptor protein tyrosine kinases. It is through these regulatory activities that this protein is believed to be involved in cytoskeletal reorganization" wikipedia.    We suggest, It is strong signal that the cancer is back!



Friday, November 14, 2014


A 54 Year old hispanic male presented with rectal bleed at an area hospital
and was admitted.  A subsequent Colonoscopy reported fragments of Colonic Adenocarcinoma.

The patieent underwent a partial colectomy which revealed an Enteric type Adenocarcinoma Grade 2 (moderatelly differentiated invading the Muscularis  propria and into the pericolic fat without involvement of the Serosa
13 nodes obtained none with Metastatic disease
the liver contains a calcified granuloma

we elected to observe this patient
since chemotherapy will not benefit him by adding more than 5 % survival rates
Only those with poorly differentiated carcinoma..."T4, perforation or Obstruction, and less than 10 nodes removed, and angiolymphatic invasion" ASCO.

Another rising star! BLINATUMOMAB

Should we use this for Burkitt lymphoma?
It is normally reviewed for Philadelphia negative ALL...involving the T-cell...

"Blinatumomab received the FDA's Breakthrough Therapy designation earlier this year (OT 8/10/14 issue), which was enacted as part of the FDA's 2012 Safety and Innovation Act to expedite the development and review time of a potential new drug for serious or life-threatening disease where early clinical evidence suggests the drug may demonstrate substantial improvement compared with existing therapies." From Oncology Times

Wednesday, November 12, 2014

Blood draw for research

Blood draw for our research is advancing at higher pace than expected
every one is eager to participate, It is incredible that patients and family are lining up for donation
everything voluntary and consents signed!  It seems that the idea of participating in an UTEP driven study has energize "the base".  El Paso is energized!  Thank you to the donors!

Tuesday, November 11, 2014

CRBCM, Collecting blood samples from volunteers at large from broader cancer studies

With collaboration from the Biomedical Research At UTEP, (DR Zangh), CRBCM has launched today studies investigating the role of cytokines in the production of cancers.  We are collecting blood samples from Volunteers at large, and our cancer patients are going to participate.  The theory is that when after age 55, or post Menopause in women, people enter the age of the "Cytokines" which seem to play a major role in the Neoplasm occurrence.  Collecting blood samples may give us levels of various Cytokines in patients currently with cancers, or who might develop cancer of the next 5 to 10 years.  Also the samples give us opportunity to have genetic testing for cancer screening.  This is an exciting time in cancer...further discovery awaits!   It is worth mentioning that 80% of our population is of Hispanic origin in El Paso!

Friday, November 7, 2014

On the road again! Back to learning again in Vegas!

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Wednesday, November 5, 2014

Here Come CRBCM to Beijing....NOone own science!

CRBCM has been invited to Beijing!
by professor Baofo Yu
 FROM:JN BAOFA CANCER HOSPITAL   DATE:2010-05-22 16:46:50  
            Dr. Baofa Yu
BaoFa Yu, M.D
Home Address:    
4443 Governor Drive
San Diego, CA 92122
Tel: (858)597-0219, 858-336-4363 
Fax: 597-0219, Email:

CRBCM working on Cancer Research using all means!!!!

Tuesday, November 4, 2014

proposed track in Neurofibromatosis: what we know about the FUS?


NF1----Ras---ERK---MAPK----Myc---Let-7---XPO5---ILF3----FUS---/TLS-RELA SPI-1

let-7 affects Exportin 5
This FUS explain the diversity of sarcoma that may result:

According to Atlas of Genetics and Cytogenetics

" t(12;16)(q13;p11) chromosomal translocation. It produces the fusion protein FUS/ATF-1.
Disease Angiomatoid fibrous histiocytoma (AFH).
Hybrid/Mutated Gene FUS was interrupted at codon 175 (exon 5) and fused to codon 110 (exon 5) of ATF-1, resulting in an in-frame junction with a glycine to valine (GGT to GTT) transition.
Entity t(7;16)(q33;p11) chromosomal translocation. It produces the fusion protein FUS/CREB3L2 (also known as BBF2H7).
Disease Low grade fibromyxoid sarcoma (LGFMS).
Hybrid/Mutated Gene The breakpoints in the fusion transcripts are produced between the exons 6 or 7 of FUS and the exon 5 of CREB3L2.
Entity t(12;16)(q13;p11) chromosomal translocation. It produces the fusion protein FUS/DDIT3 (also known as CHOP).
Disease Myxoid liposarcoma (MLS).
Hybrid/Mutated Gene 9 different types of fusions between the genes FUS and DDIT3 have been reported. The most frequent rearragements join the exons 5, 7 or 8 of FUS with the exon 2 of DDIT3.
Oncogenesis The unequivocally relation between FUS/DDIT3 and the MLS was shown by the generation of a transgenic mouse model expressing FUS/DDIT3 from a housekeeping promoter.
Entity t(16;21)(p11;q22) chromosomal translocation. It produces the fusion protein FUS/ERG.
Disease Acute myeloid leukemia (AML).
Hybrid/Mutated Gene The junction of both genes is produced between the exons 6 or 7 of FUS and the exon 9 of ERG,or between the exon 8 of FUS and the exon 7 of ERG."   

Monday, November 3, 2014

Beyond the Myc!

Now as it seems to be suggested the mechanism of Cancer development seems to be multiple but one recognize that stimulation of the Myc or one of its variations seem to still the center piece of many neoplastic transformations.   From Burkitt to Small cell cancer, the most aggressive cancer seem to act through this gene.   Even Watson the DNA man went after the Myc as a potential drive for neoplasm.  Myc can increase proliferation by acting through general proliferation factors (transcription factors) but in specific diseases, it can act specifically on downstream genes to drive the neoplastic transformation by using the Leucine unzipping prong (opening the nuclear machine to proliferation) or by opening the Ribosome to protein production needed in the neoplastic transformation.

Our interest in this area stems from our involvement with one family of 4 members that we suspect have  Neurofibromatosis.  NF1 has not been established yet but all members have development issues and lipomatous lesions and imaging has suggested diffuse Neurofibromas.   One member developed Breast cancer, a BRCA was negative,  One member has gait disturbances and speech impairement, and the member with several lipomatous lesions, came to our attention for cough.  CT chest suggested a new peripheral nerve sheath tumor that we are following.  NF1 is a tumor suppressor of the Ras of which amplification will reach the Myc.  The Myc has interactions with BRCA but also several other genes

Thursday, October 30, 2014

New Interesting case at CRBCM

A 47 Year old young Hispanic woman has been referred to us because a 1 year history of abdominal pain and lately has had Hematochezia.  An EGD and colonoscopy were performed and Biopsy in the stomach and the Colon revealed Burkitt Lymphoma. The patient Bone Marrow biopsy is still pending (it is my understanding that a first attempt by the pathologist failed-it should not happen!?  Now patient is asking for general Anesthesia-always a twist to some cases).  Lumbar tap cytology pending!
questions about this case
1.EBV titer?
3.or just plain old Allopurinol
4.Rituxan-HyperCVAD  Vs standerd ALL protocols
5.And now for intrathecal treatment -she is asking for general Anesthesia
6.How to prepare for transplant in patient with lack of Insurance
7. Echo Vs MUGA

Case unfolding, will update you

Sunday, October 26, 2014


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Saturday, October 25, 2014

Imput on Non Hodgkin lymphoma

3 distinct groups of lymphoma
1.Germinal center
2.Activated B cell
3.Primary Mediastinal B cell lymphoma  (closer to Hodgkin disease)

when activated B cell, the prognosis is worse

somatic mutation may also influence outcome

Hans model   CD10     BCL-6   and MUM-1/IRF4   model to determine cell of origin

The Germinal Center B cell  lymphoma respond well to R-EPOCH  (CD10+, BCL-6+, MUM-1 -negative)
whereas the Activated B-cell lymphoma may be better of with Ibrutinib based treatment

Germinal Center responds better to Revlimid than Activated B cell lymphoma

Addition of Velcade allows to conquer the the resistance due to Activated B Cell Lymphoma

Those c-MYC positivity are the worse...and may need upfront transplant...or a clinical trial

Certificate for 'Advances in the Management of Lymphoma and Chronic Lymphocytic Leukemia' at OMedLive

Certificate for 'Advances in the Management of Lymphoma and Chronic Lymphocytic Leukemia' at OMedLive