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JUST PURE BIOLOGICAL SCIENCE!

WE ESCAPED SMARTLY IN THE MELI-MELO OF AGING JUST TO DIVERT OUR ATTENTION ON GENES INVOLVED IN ALZHEIMER. DON'T ASK ME WHY, BUT WE DID. WE CAME OUT MORE PUZZLED THEN ANYTHING ELSE!

MANY QUESTIONS THOUGH:

Many of the striking things and questions

1.Can calcium inhibitors slow down Alzheimer progression?
2. Is Namenda's role to slow down apoptosis in neurons by giving non specific stimulation to Glutamate receptors ?  Or this really by counterbalancing or increasing the effect of cholinesterase inhibitors? We know that when the disease is advanced and cell death has occurred, Namenda does not do much.
3. Can S100B be a more reliable way of monitoring Alzheimer's progression?
4. Does Alzheimer reflects a deficiency of Macrophage function and therefore Colony stimulating factors a way of treatment?
5. What is the effect of GM-CSF on NG2 glial cell and can this slow down Alzheimer?
6. What can slow down tau-protein phosphorylation, will ubiquitination work in detoxifying cells ?
7. What is the effect of disrupting the exosome, could this cause abnormal cell to be cleaned up earlier...? ....before plaque build up!
8. What is the real relation between Vit. D and DAG (diacyl glycerol), the phosphorylator, APOE and Presenilin?

Many question to struggle with...but the challenge is thrown at you, let's go to work!

FYN, A CRAZY GENE...

IT DOES NOT KNOW WHEN TO STOP INTERACTING
IT IS INVOLVED IN CRAZINESS (ALZHEIMER'S)
BUT YET IT KEEPS DOING ITS THING.
CAN WE STOP IT ELECTIVELY?
WE ARE WORKING HARD!

FYN

From Wikipedia, the free encyclopedia

Jump to: navigation, search

FYN oncogene related to SRC, FGR, YES
PDB rendering based on 1a0n.
Available structures PDB Ortholog search: PDBe, RCSB [show]List of PDB id codes
Identifiers
Symbols	FYN; SLK; SYN; p59-FYN
External IDs	OMIM: 137025 MGI: 95602 HomoloGene: 48068 ChEMBL: 1841 GeneCards: FYN Gene
EC number	2.7.10.2
[show]Gene Ontology
RNA expression pattern
More reference expression data
Orthologs
Species	Human	Mouse
Entrez	2534	14360
Ensembl	ENSG00000010810	ENSMUSG00000019843
UniProt	P06241	P39688
RefSeq (mRNA)	NM_001242779	NM_001122892
RefSeq (protein)	NP_002028	NP_001116364
Location (UCSC)	Chr 6: 111.98 – 112.19 Mb	Chr 10: 39.37 – 39.57 Mb
PubMed search	[1]	[2]
This box: view talk edit

Proto-oncogene tyrosine-protein kinase Fyn is an enzyme that in humans is encoded by the FYN gene.^[1]
This gene is a member of the protein-tyrosine kinase oncogene family. It encodes a membrane-associated tyrosine kinase that has been implicated in the control of cell growth. The protein associates with the p85 subunit of phosphatidylinositol 3-kinase and interacts with the fyn-binding protein.

Interactions

FYN has been shown to interact with:

• ADD2^[6]
• Alpha-tubulin 3C,^[7]
• BCAR1^[8][9]
• Cbl gene^[10][11]
• CBLC^[12]
• CD36^[13][14]
• CD44^[15]
• CDH1^[16]
• CHRNA7^[17]
• Colony stimulating factor 1 receptor^[18]
• C-Raf^[19]
• CTNND1^[16][20]
• DLG4^[21][22]
• Dystroglycan^[23]
• EPHA8^[24]
• Fas ligand^[25][26]
• FYB^[27][28]
• GNB2L1^[29][30]
• GRIN2A^{[21][22][31][32]}
• ITK^[33][34]
• Janus kinase 2,^[35]
• KHDRBS1^[36][37]
• Nephrin^[38][39]
• PAG1^[40]
• PIK3R2^[41]
• PRKCQ^[42]
• Protein unc-119 homolog^[43]
• PTK2^[44][45]
• PTK2B^[46][47][48]
• RICS^[49]
• SH2D1A^[50][51]
• SKAP1^[28][52][53]
• Syk^[11]
• Tau protein^{[7](ALZHEIMER LOCATED HERE PEOPLE!)}
• TNK2,^[54]
• TrkB^[55]
• TRPC6^[56]
• Tyrosine kinase 2^[57]
• Wiskott-Aldrich syndrome protein^[58][59][60]
• ZAP-70^[61]

References (WIKIPEDIA)

WITH THIS MANY INTERACTIONS, IT IS A CRITICAL GENE, BUT WATCH OUT NOW, IT NEEDS TO BE HANDLED WITH CARE.  HIT IT ONLY IN A VERY SELECTIVE FASHION NOW! OR YOU LOSE THE HOST!

 

another crazy gene

 

Androgen receptor has been shown to interact with:

• AKT1,^[38]
• BAG1,^[39][40][41]
• Beta-catenin,^{[42][43][44][45][46][47]}
• BRCA1,^[48][49]
• C-jun,^[50]
• Calmodulin 1,^[51]
• Caveolin 1,^[52]
• CDK9,^[53]
• COX5B,^[54]
• CREB-binding protein,^{[55][56][57][58]}
• Cyclin D1,^[59][60]
• Cyclin-dependent kinase 7,^[61]
• Death associated protein 6,^[62]
• Deleted in Colorectal Cancer,^[63]
• EFCAB6,^[64]
• Epidermal growth factor receptor,^[65][66]
• FOXO1,^[67]
• GAPDH,^[68]
• Gelsolin,^[69]
• GNB2L1,^[70]
• GSK3B,^[71]
• HDAC1,^[72]
• HSP90AA1,^[73][74]
• HTATIP,^[72]
• MAGEA11,^[75][76]
• MED1,^[77]
• MYST2,^[78]
• NCOA1,^[43][79][80]
• NCOA2,^{[42][57][75][81][82]}
• NCOA3,^[81][83][84]
• NCOA4,^{[38][82][85][86][87][88][89][90][91]}
• NCOA6,^[92]
• NCOR2,^[42][93][94]
• NONO,^[57]
• PA2G4,^[95]
• PAK6,^[96][97]
• PATZ1,^[98]
• PIAS2,^[99][100]
• PRPF6,^[101]
• PTEN,^[102]
• RAD9A,^[103]
• RANBP9,^[104]
• RCHY1,^[105]
• Retinoblastoma protein,^[106][107]
• RNF14,^{[82][85][108][109]}
• RNF4,^{[98][110][111]}
• SART3,^[112]
• SMAD3,^{[113][114][115]}
• Small heterodimer partner,^[116]
• Src,^{[102][117][118]}
• SRY,^[119]
• STAT3,^[120][121]
• SVIL,^[122]
• Testicular receptor 2,^[123]
• Testicular receptor 4,^[124]
• TGFB1I1,^[85][125]
• TMF1,^[126]
• TRIM68,^[127]
• UBE2I,^{[42][43][128][129][130][131]}
• UXT,^[132] and
• ZMIZ1.^[133]

 wikipedia! remember what we said about short stature

this one also is that kind, lack of it lead to short stature so it it is a powerful gene, suppression here cures prostate cancers!

Medscape Medical News from the:

NCCN Issues New Treatment Guidelines for Penile Cancer

Roxanne Nelson

Mar 22, 2013

Drug & Reference Information

• Penile Cancer
• Urogenital Squamous Cell Carcinoma
• Pelvic Lymph Node Dissection

Hollywood, Florida — The National Comprehensive Cancer Network (NCCN) has issued new treatment guidelines for penile cancer.
"The first thing people ask me is why develop guidelines for such a rare cancer," said Philippe  E. Spiess, MD, genitourinary oncologist at the H. Lee Moffitt Cancer Center in Tampa, Florida.
In 2010, an estimated 1250 new cases of penile cancer were diagnosed in the United States and there were about 310 related deaths. Penile cancer accounts for 0.4% to 0.6% of all malignant neoplasms in the United States and Europe.

Dr. Philippe Spiess

Dr. Spiess presented highlights of the guidelines here at the NCCN 18th Annual Conference.
There is a high degree of heterogeneity in the way penile cancer is treated in North America and globally, he explained. "The standard of care remains complete tumor excision and eradication of negative margins."
However, there has been increasing consideration of less or noninvasive management of primary penile tumors, based on stage and grade, he added.
Less and Noninvasive Therapy
For carcinoma in situ and superficial verrucous carcinoma, a British study showed that 5-fluorouracil or imiquimod produced response rates of 60% to 70% at 5 years (World J Urol. 2009;27:179-187). In this setting, CO₂ and Nd:YAG laser ablation can also be used, although retreatment rates are quite high (about 20% to 30%), explained Dr. Spiess.
Total gland resurfacing and wide local excision with circumcision are also options.
There is some evidence for the use of topical therapies. In a recent retrospective review of all primary and recurrent cases of penile carcinoma in situ treated with topical 5-fluorouracil and imiquimod over a 10-year period (Eur Urol. 2012;62:923-928), "the response rates were excellent," said Dr. Spiess. "A complete response was seen in 57% of the patients, with a partial response in 14%."
No response was seen in the remaining 29.5% of patients, but none of the patients recurred or progressed. Toxicity was also low; 10% of patients reported local toxicity and 12% reported an adverse event.
Another study, looking at penile-preserving surgery for patients with penile Tis and PT1 tumors, found that there was a recurrence rate of 21.4% in both subgroups (J Urol. 2011;186:1303-1307). At 5 years, 13.8% of patients had a late recurrence, but none of the patients with pTis tumors had progressed to invasive or metastatic disease.
"These patients can recur fairly late, so it is important to follow them for at least 10 years," Dr. Spiess pointed out.
"As far as penile-preserving therapy, the take-home message is that clinical stage is everything," Dr. Spiess explained. However, he went on to emphasize that "it has to be a patient with a small superficial lesion, where you can obtain negative margins. If you can't, then you need to look at more radical options in surgery."
Another treatment option is brachytherapy. A recent French study found a 10-year penile recurrence rate of 20% and a 10-year inguinal recurrence rate of 11% (Int J Radiat Oncol Biol Phys. 2009;74:1150-1156). However, "centers of excellence that have experience with penile brachytherapy are few and far between," he cautioned. "That's why the guidelines...are somewhat cautious in making recommendations until we see a wider experience using penile brachytherapy."
He emphasized the importance of stringent surveillance after radiotherapy to the penis; up to 40% of patients who receive radical radiotherapy will eventually need surgery for disease recurrence. Surgery in this population can be challenging because irradiated tissues are brittle and poorly vascularized, making them less than ideal for grafting.
Sentinel Node Biopsy

Learn about evolving data on EGFR mutation and ALK rearrangements in NSCLC. It can impact your decision to test for biomarkers.

Review the data

OC468500PROF-E 10/12

Information from Industry

Dr. Spiess discussed the concept of sentinel lymph node biopsy in penile cancer, which was proposed more than 30 years ago. One study reported a false-negative rate of 18% using a combined preoperative injection of technetium-99m labeled sulfur colloid and isosulfan blue dye (J Urol. 2002;168:76-80).
A more recent prospective study found a sensitivity of only 71%, with 2 false-negative results reported (J Urol. 2007;177:2157-2161). But a review found that false-positive results can be minimized with preoperative ultrasound and fine-needle aspiration cytology on suspicious nodes (World J Urol. 2009;27:197-203).
However, this technique has not yet been embraced in this setting. "We are somewhat cautious about promoting this technique, although clearly it is something very interesting and something that can be used at a center that has high expertise in sentinel lymph node biopsy," said Dr. Spiess. "At this point, it is not being widely used in North American centers."
National Comprehensive Cancer Network (NCCN) 18th Annual Conference.

 

ON THE CPRIT FRONT THE DANCE GOES ON!

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04/09/2013 08:11 PM

CPRIT executives grilled by lawmakers

By: John A. Salazar

Executives for the Cancer Prevention and Research Institute of Texas were being grilled by state lawmakers Tuesday. The organization is currently under criminal investigation and an audit showed millions of dollars in scientific grant funds went out, but results weren't coming in.
For House committee members, Tuesday’s meeting was all about trust, transparency, and accountability.
"How can we expect public trust to be reaffirmed?" Republican committee member Dan Flynn said.
Four months after a criminal investigation began on the Cancer Prevention and Research Institute of Texas, Transparency Committee members continue to look for answers.
Questions surrounded the non-scientific grant approval for Dallas-based Pelaton Therapeutics, worth $11 million dollar.
Suspicions of grant-rigging went public in November of last year.
"When it appeared that the grant report was missing information or inaccurate, I immediately called for an investigation,” Jimmy Mansour, CPRIT chairman, said.
The CPRIT chief told the committee that $3 million dollars of that public money grant will not be recovered.
"And that is regrettable that much is lost," Mansour said.
To date three people have left CPRIT while under criminal investigation. Committee members want to know if only those three misled the entire agency.
Committee members also wanted to know how public trust could be restored in the CPRIT executives, the same executives who brought scrutiny to the cancer agency.
They also criticized the renaming of the fundraising entity of CPRIT, the CPRIT Foundation. That name change came about two weeks ago. Committee members said any money raised by the foundation needs to be returned to the state.

• 
  
• 
  

==============================================
How can this organization survive such a lengthy, protracted war and come out winning?
One thing for sure it will never be the same and will come out weaker and slim!  another win for cancer and another impediment to the CURE.   The cure is with us, we just complicate our minds with politics and favoritism.  What a waste!  I still pray for CPRIT...SAVIOR PLEASE COME UPON THIS ORGANIZATION!...

ACTIVITIES AT CRBCM

*COMPLETED INDIANA WORK
BACK IN EL PASO, TX
Initiated therapy for Angiosarcoma with trial of Avastin alone at this point thanks to drug company help.
will try 3-4 infusions and reassess.  Votrient still an option.  But remember (OUR PT developed severe skin reaction to taxanes and had received MAID)
-------------------------------------------------------------------------------

J Am Acad Dermatol. 2010 Oct;63(4):e83-4. doi: 10.1016/j.jaad.2009.09.035.

Dramatic improvement of inoperable angiosarcoma with combination paclitaxel and bevacizumab chemotherapy.

Fuller CK, Charlson JA, Dankle SK, Russell TJ.

--------------------------------------------------------------------------------------------

 

Avastin alone has proven to be effective.

 

 Case Report"Scalp Angiosarcoma Remission with Bevacizumab and Radiotherapy without Surgery: A Case Report and Review of the Literature, " DE YAO et al.

=========================================================================

*Also we are searching for a surgeon who would consider resecting a Pancreatic cancer with mesenteric VEIN NOT ARTERY involvement.  we are shrinking the tumor with chemotherapy and Radiation, will reassess result radiologically.  Call me if you can help!

=============================================

DON'T LOOK FOR ME THIS WEEK-END

WILL BE HARD AT WORK!

Prostate Symposium

Dear Dr.Mutombo Kankonde,

Below is the link for the agenda for the Prostate Symposium research event on April 13, 2013 in Las Vegas.  Below you will find the agenda link and hotel information:  

Agenda_ProgramBook_CCProstate_LasVegas_4-1-13.pdf

Meeting Information:

Mandarin Oriental

3752 Las Vegas Blvd South

Las Vegas, Nevada 89158

(702) 590 8888

Meeting: Ballroom B, 3^rd Floor

WILL LOSE SOME MONEY BUT THAT COMES WITH THE TERRITORY!  BELIEVE ME IT'S HARD TO MISS THE ACTION, WILL TRY TO BE GOOD COLLECTED AND UNDER CONTROL.

THANKING THE ORGANIZER FOR INVITING ME, WILL LEARN PLENTY OF GOOD STUFF FOR THE BLOG AND FURTHER RESEARCH!

==================================================

WILL PUBLISH OUR BLOG STATISTICS AS SOON AS WE HIT 15000 REVIEWS WHICH WE PROJECT WILL BE IN 2-3 DAYS AT CURRENT PACE OF ATTENDANCE!  CRBCM, WE ARE HARD AT WORK!

T-DM1 IS NOT ALONE AND TARGET THERAPY WILL LEAD US TO NEW MEDICATION EVERYDAY : GET THIS!

"DMUC5754A consists of a monoclonal antibody against the protein MUC16, found on ovarian cancer cells at high levels, and a toxin linked by a cleavable linker. Approximately 80% of ovarian cancer patients have tumors that have high expression of MUC16 (also known as CA-125), according to Liu. The toxin is the microtubule-disrupting agent monomethyl auristatin E (MMAE). The antibody directs the toxin specifically to ovarian cancer cells to kill them. Because the antibody delivers the toxin specifically to the ovarian tumor, an especially potent toxin can be used, one that would be too toxic as a general cytotoxic agent that would also affect healthy tissue." NEWS FROM GENENTEC SOURCE

 

Home » CONFERENCES » AACR 2013

CONFERENCE REPORT  AACR: Antibody-Drug Conjugate Shows Promise in Platinum-Resistant Ovarian Cancer By Anna Azvolinsky, PhD1 | April 9, 2013 1Freelance Science Writer and Cancer Network Contributor. Follow Her on Twitter Washington, DC—A novel therapy has shown activity in treatment of difficult-to-treat, advanced, platinum-resistant ovarian cancer. The drug, DMUC5754A (Genentech), is part of a new class of drugs called antibody-drug conjugates. The phase I trial results were presented at the American Association for Cancer Research (AACR) Annual Meeting, held April 6–10 in Washington, DC by Joyce F. Liu, MD, MPH, of the Dana-Farber Cancer Institute and Harvard Medical School in Boston. Ovarian cancer as seen on CT; source: James Heilman, MD, Wikimedia Commons “Overall the drug was well tolerated, with a toxicity profile that is comparable to other therapeutics currently used in clinical practice,” Liu told Cancer Network. “We think the results are very encouraging in a patient population where response to other therapies is limited.” (MORE: AACR: Anti-PI3K/MEK Inhibitor Targeted Therapy Combo Shows Activity) DMUC5754A consists of a monoclonal antibody against the protein MUC16, found on ovarian cancer cells at high levels, and a toxin linked by a cleavable linker. Approximately 80% of ovarian cancer patients have tumors that have high expression of MUC16 (also known as CA-125), according to Liu. The toxin is the microtubule-disrupting agent monomethyl auristatin E (MMAE). The antibody directs the toxin specifically to ovarian cancer cells to kill them. Because the antibody delivers the toxin specifically to the ovarian tumor, an especially potent toxin can be used, one that would be too toxic as a general cytotoxic agent that would also affect healthy tissue. The results from the phase I trial also showed that those patients who had the highest expression of MUC16, the target of the antibody portion of the drug, derived the most benefit from the treatment. This is likely to facilitate the selection of only those patients who are most likely to benefit from treatment in future trials. Platinum-resistant, advanced ovarian cancer has an unmet need and is difficult to treat. Patients currently have few treatment options. Platinum-based chemotherapy remains the standard way to treat ovarian cancer, and platinum resistance is a major treatment challenge. The phase I trial evaluated various doses of DMUC5754A in advanced ovarian and pancreatic cancer patients. DMUC5754A was administered at doses ranging from 0.3 mg/kg to 3.2 mg/kg every 3 weeks. Forty-four patients with advanced, recurrent, platinum-resistant ovarian cancer enrolled; of those, one complete response and four partial responses were reported. All patients who responded were treated with a 2.4 mg/kg dose of the drug and had high MUC16 expression in their tumor cells. Six additional patients had minor responses. Fatigue was the most common adverse event at all dose levels, occurring in more than half of all patients. Other common adverse events were vomiting, decreased appetite, nausea, diarrhea, and peripheral neuropathy. Peripheral neuropathy was manageable and reversible in most patients through dose delay and dose reductions, according to the researchers. Grade 3 adverse events included fatigue and neutropenia, both occurring in 9% of patients. Neutropenia and uric acid release were the only dose-limiting toxicities during the study. Both occurred at the maximum 3.2 mg/kg dose. Other serious drug-related adverse events were small intestine obstruction in two patients, hypocalcemia in a single patient, and neutropenia in a single patient. “Neuropathy, which was an anticipated potential toxicity of the drug, did occur, but was manageable and typically reversible with dose reductions or delays,” said Liu. The role of MUC16 in cancer development and progression is not yet clear. The protein is a large transmembrane protein that is found in abundance on ovarian cancer cells but not healthy tissue. Researchers speculate that the protein may help ovarian tumor cells bind to mesothelial cells that line the peritoneal cavity. The encouraging activity and safety profile of the antibody-drug conjugate warrants further trials in ovarian cancer patients, according to the study researchers. “I think the major remaining question is how this therapy compares against the standard treatments that we use in platinum-resistant ovarian cancer,” said Liu. Discussions for further development of DMUC5754A, including a phase II ovarian cancer trial, are ongoing.

In a retrospective review of Lung cancers , use of Beta blockers may provide survival advantage

*In a retrospective review of Lung cancers , use of Beta blockers may provide survival advantage.

*Ruloxitinib, still the success story in JAK driven diseases.  For JAK driven disease to be seen more in Hematologic malignancy, the receptors for hematologic growth hormones must be stimulated.
COMFORT-1 showed 41.9% of patients on Ruxolitinib had spleen reduction  but in COMFORT-2, only 28% had spleen reduction by week 48.

The JAK inhibitors are now being tried in Pancreatic cancers!

*Obstruction to Cure is not only found in limitation of progress in science, but in man made complications such disparities in funding availability and managed care obstruction to access to known medications!  Cure escapes us for our own doing, in a summary!

*In Breast Cancer, Inhibitors to CD4,6 are proving to be a new approach when given with Letrozole

*In Prostate cancer don't be too eager to use Steroids with enzalutmide.  Steroids may "activate androgen receptors promoting the cancer".   I should confess this point is a bit controversial since that's what we do, stimulate to better kill with chemotherapy (Taxotere-Cabazitaxel).  But the logic may not work for another hormone used for killing.

*In Tivo-1,
they found no survival advantage for TIVOZANIB Vs Sorafenib in patient with Renal Cancer.
Tivozanib is said to be more potent and selective for VEGF receptors!  PFS was superior though with TIVO!

*Check this out!  The global multikinase inhibitor Regorafenib (blocks VEGFR1,KIT,TIE2,PDGFR and RET) got approved for GIST.  patients received 160 mg PO daily x21 Q28. Watch for fatigue hand foot sundrome diarrhea, loss of appetite,HTN,weight loss,rash and fever.  and being an anti-VEGF, bleeding and intestinal perforation of course!  rare cases of Coronary attacks!
*New kid on the block, RAMUCIRUMAB TRIED IN GASTRIC CANCER!

(READ TARGETED THERAPY NEWS)

New Software Identifies and Stratifies Risk Posed by Lung Nodules

Apr. 8, 2013 — A multidisciplinary team of researchers at Mayo Clinic has developed a new software tool to noninvasively characterize pulmonary adenocarcinoma, a common type of cancerous nodule in the lungs. Results from a pilot study of the computer-aided nodule assessment and risk yield (CANARY) are published in the Journal of Thoracic Oncology.

"Pulmonary adenocarcinoma is the most common type of lung cancer and early detection using traditional computed tomography (CT) scans can lead to a better prognosis," says Tobias Peikert, M.D., a Mayo Clinic pulmonologist and senior author of the study. "However, a subgroup of the detected adenocarcinomas identified by CT may grow very slowly and may be treatable with less extensive surgery."

CANARY can noninvasively stratify the risk lung adenocarcinomas pose by characterizing the nodule as aggressive or indolent with high-sensitivity, specificity and predictive values.

CANARY uses data obtained from existing high-resolution diagnostic or screening CT images of pulmonary adenocarcinomas to match each pixel of the lung nodule to one of nine unique radiological exemplars. In testing, the CANARY classification of these lesions had an excellent correlation with the microscopic analysis of the surgically removed lesions that were examined by lung pathologists, Dr. Peikert says.

Lung cancer is the leading cause of cancer-related deaths in the United States.

"Without effective screening, most lung cancer patients present with advanced stage disease, which has been associated with poor outcomes," Dr. Peikert says. "While CT lung cancer screening has been shown to improve patient survival, the initiation of a nationwide screening program would carry the risk of overtreatment of slow growing tumors and would be associated with substantial health care costs. CANARY represents a new tool to potentially address these issues."

 http://www.sciencedaily.com/releases/2013/04/130408133044.htm