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1616
Existing treatments against cancer are non-sufficiently selective. Immunotherapy based treatment offers highly selective and efficient solution to this problem. A promising approach in Immunotherapy is adoptive cell therapy (ACT). In ACT, therapeutic lymphocytes are administrated to patients in order...

Existing treatments against cancer are non-sufficiently selective. Immunotherapy based treatment offers highly selective and efficient solution to this problem.
A promising approach in Immunotherapy is adoptive cell therapy (ACT). In ACT, therapeutic lymphocytes are administrated to patients in order to treat a disease. In this process antibody-type cells are generated ex vivo, and then infused to the patient. By this technology the cells can be redirected against specific tumors via genetic engineering, using chimeric receptors.
Currently ACT is logistically and economically challenging since it is limited by the used of the patients’ own cells. Another key concern is safety, due to the danger that the allogeneic cells will be rejected by the patient, or will attack the patient.
In cancer, use of tumor specific, chimeric receptor redirected allogeneic T cells can transform ACT into a standardized, off-the shelf therapy. Overall this method proposes a safe and effective adoptive therapy using allogeneic cells while avoiding the use of bone marrow transplantation (BMT).

Applications


  • Cancer immunotherapy

Advantages


  • Off the shelf, standard treatment
  • Safe
  • Effective
  • No bone marrow transplantation (BMT) is required

Technology's Essence


A novel approach for adoptive immunotherapy using fully MHC-mismatch allogeneic T cells. These cells are redirected with tumor specific non-MHC-restricted antibody-based chimeric antigen receptor (T-bodies) in the absence of Graft-versus-host disease (GVHD). In order to create a standardize treatment, the redirection of T cells can be done through an antibody-based chimeric antigen receptor (CAR), thus creating ‘universal effector T cells’. This is based on a combination of of MHC-mismatched allogeneic T-cells with an MHC unrestricted chimeric antigen receptor. These cells would recognize their target independently of MHC restriction, therefore applied as an ‘off-the shelf’ immunotherapy. Regarding the second challenge of avoiding GVHD, by using a controlled lymphodepletion the researchers were able to create therapeutic window during which the allo-T-body cells could destroy the tumor before being themselves rejected.

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  • Prof. Zelig Eshhar
1664
Neuroinflammation is well established as a key secondary injury mechanism following CNS trauma, such as traumatic brain/spinal injury or ischemic stroke, and it has been long considered to contribute to the damage sustained and fatal outcomes following brain injury. Early inflammatory events enhance...

Neuroinflammation is well established as a key secondary injury mechanism following CNS trauma, such as traumatic brain/spinal injury or ischemic stroke, and it has been long considered to contribute to the damage sustained and fatal outcomes following brain injury.
Early inflammatory events enhance brain damage, yet they provide the framework for later inflammatory events that enhance tissue remodeling and are crucial for tissue recovery.
A major unmet need in the field is a targeted treatment that would down regulate the damaging events of inflammation, while maintaining reparative functions. 
Altering between CNS microglia pro and anti-inflammatory activation states is at the core of injury-induced neuroinflammation and presents an opportunity to specifically tilt the balance towards anti-inflammatory and repair processes.
The present discovery elucidates the mechanisms that lead to injury-induced microglia over-activation and proposes IFN-? as a therapeutic strategy to induce microglia resolving state and relive inflammation. 

Applications


Anti-inflammatory treatment following CNS injury

Advantages


  • Targeted therapy – avoids general immuno-suppressive side effects
  • Based on a well understood molecular mechanism
  • May allow relatively large therapeutic window – according to proof-of-concept  preliminary experiments

Technology's Essence


Resident microglia are the major specialized innate immune cells of the central nervous system (CNS). During the process of wound healing or pathogen removal, there is an induction of the microglia active pro-inflammatiry phenotype (M1), leading to a transient inflammatory response, which is resolved via local conversion to the M2 anti-inflammatory phenotype.  Following acute injury, microglia fail to acquire an inflammation-resolving phenotype (M2-like phenotype) in a timely manner, often resulting in self-perpetuating local inflammation and tissue destruction beyond the primary insult.
Prof. Schwartz and her team uncovered the mechanisms that lead to injury-based inhibition of the M1 to M2 phenotype switch.  They showed that the capacity to undergo pro- to anti-inflammatory (M1-to-M2) phenotype switch is controlled by the transcription factor Interferon regulatory factor-7 (IRF7).  Their results demonstrate that restoring Irf7 expression by IFN-? (a known IRF7 activator) reactivates the circuits leading to M2 conversion by improving the resolution of pro?inflammatory cytokines expressed by microglia ex vivo and in vivo, following acute CNS insult.
Importantly, the anti-inflammatory activity of IFN-? was demonstrated in-vivo, when administrated 24h following the primary insult, proposing a relatively large therapeutic window.

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  • Prof. Michal Eisenbach-Schwartz
1628
New generation of superior nature-inspired therapeutics for treating inflammation.Inflammation is characterized by elevated levels of TNF-?. Neutralizing TNF-? activity was shown to be beneficial for patients with chronic autoimmune inflammatory diseases such as rheumatoid arthritis (RA) and...

New generation of superior nature-inspired therapeutics for treating inflammation.Inflammation is characterized by elevated levels of TNF-?. Neutralizing TNF-? activity was shown to be beneficial for patients with chronic autoimmune inflammatory diseases such as rheumatoid arthritis (RA) and inflammatory bowel disease (IBD). However, current treatments of such conditions include general anti-inflammatory and immunosuppressive drugs that are of limited effectiveness and may cause serious side effects. Another class of drugs includes targeted therapies directed against TNF-?, that are associated with serious infections including tuberculosis (TB) and sepsis as well as increased risk of cancer in some cases. Thus, there is an urgent need for highly selective, safer and more effective drugs for inflammatory conditions that involve TNF-? as a key mediator. The present technology introduces a novel generation of candidate drugs that selectively inhibit the processing of TNF-?, thereby preventing it from exerting its pro-inflammatory properties. This technology provides a framework for the development of safer and more effective therapeutics for IBD and related autoimmune disorders.

Applications


  • Treatment of autoimmune inflammatory conditions such as IBD and RA.
  • Treatment of neuroinflammatory conditions such as multiple sclerosis (MS).
  • Treatment of other inflammatory mediated diseases such as psoriasis, systemic sclerosis and ankylosing spondylitis.
  • All MMPs and ADAMs proteases possess an autoinhibitory pro-domain and therefore this technology can be broadened to other MMP and ADAM targets.

Advantages


  • TACE pro-domain is highly potent and efficient.
  • TACE pro-domain is metabolically stable, unlike small molecule inhibitors of TACE.
  • Targeting TACE through nature-inspired protein design may constitute a safer approach to combat TNF-? induced inflammation.
  • Unlike non-specific small molecule inhibitors, which target the conserved catalytic zinc site of TACE, TACE pro-domain shares little homology to other MMPs, making it a good candidate for specific inhibitor of TACE.

Technology's Essence


The A disintegrin and metalloproteinase 17 (ADAM17), also known as tumor necrosis factor-? converting enzyme (TACE), has been defined as the major shedding protease for a broad range of substrates predominantly the key immuno-regulatory cytokines TNF-?. Cleavage by TACE renders TNF-? pro-inflammatory, highlighting ADAM17 as a rationale target for treatment of autoimmune diseases such as IBD and arthritis. A team of researchers at the Weizmann institute headed by Prof. Irit Sagi, has employed a sophisticated approach towards TACE targeting by exploiting its autoinhibitory pro-domain as a platform for the ‘smart design’ of TACE selective natural inhibitors. The therapeutic potential of TACE pro-domain was demonstrated in IBD mouse models, where TACE pro-domain administration showed significant improvement in multiple parameters such as reduced mortality and weight lost, in a dose dependent manner. Additional in vivo studies demonstrated that the TACE pro-domain is highly stable in vivo and harbors specificity towards the activated immune cells located in colon lesions. Thus, the novel TACE inhibitor presented in this technology leads to significant therapeutic effects and is beneficial in controlling inflammation in IBD disease manifestations in mice.

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  • Prof. Irit Sagi
1546
Improvement of protein production by modulating the tRNA pool. For maximal heterologous expression of proteins per host cell, the optimal level of expression of genes needs to be addressed. The science and art of expressing a gene from one species in another often amounts to modifying the codons of the...

Improvement of protein production by modulating the tRNA pool. For maximal heterologous expression of proteins per host cell, the optimal level of expression of genes needs to be addressed. The science and art of expressing a gene from one species in another often amounts to modifying the codons of the gene, and supplementing the host with specific tRNAs. Yet the full challenge of heterologous expression is not only to maximize expression per host cell, but also to minimize the burden on the host. The outlined invention describes a universally conserved profile of translation efficiency along mRNAs, based on the adaptation between coding sequences and the tRNA pool, to improve heterologous gene expression and thus protein production.

Applications


  • Improvement of the yield and success rate of recombinant protein production.

Advantages


  • Protein expression levels can be artificially increased
  • Minimization of the burden on the host

Technology's Essence


The translation efficiency profile of a gene is defined, for each codon position, as the estimated availability of the tRNAs that participate in translating that codon. The profile is high at codons that correspond to abundant tRNAs and low at codons that correspond to rare tRNAs. In this invention it is predicted that the first ~30-50 codons of genes appear to be translated with a low efficiency “ramp”, while the last ~50 codons show highest efficiency. The “ramp” serves as a late stage of initiation and is an optimal and robust means to reduce ribosomal traffic jams, thus minimizing occupation of free ribosomes, ribosomal abortions and, ultimately, the cost of protein expression. Implementation of appropriate ramping in heterlogous proteins, given the host?s tRNA pool, might improve the yield of expressed recombinant proteins.

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  • Prof. Yitzhak Pilpel
1633
The ErbB family consists of four structurally related receptor tyrosine kinases. Excessive ErbB signaling is associated with enhanced tumorogenesis, and as such serves as a major therapeutic target in a wide array of solid tumor cancers. A member of this family, the human epidermal growth factor...

The ErbB family consists of four structurally related receptor tyrosine kinases. Excessive ErbB signaling is associated with enhanced tumorogenesis, and as such serves as a major therapeutic target in a wide array of solid tumor cancers. A member of this family, the human epidermal growth factor receptor 2 (ErbB-2/HER2), is overexpressed in a variety of human cancers, including breast and gastric tumors. ErbB-2/HER2 amplification correlates with elevated metastatic activity and poor prognosis. An innovative and highly potent approach for cancer treatment is proposed here, based on delivering novel nucleic acid-based entities called aptamers targeting ErbB-2/HER2. Remarkably, the antitumor effect exerted by the multimeric anti-ErbB-2/HER2 aptamers is twofold stronger than that elicited by currently available antiErbB-2 monocolonal antibodies.

Applications


  • A novel class of molecules for the treatment of human cancers exhibiting excessive ErbB-2/HER2 signaling.
  • Combination with other therapeutic modalities may predictably enhance the antitumor activity of the aptamer.
  • Aptamers may also be harnessed as carrier molecules to deliver toxic loads into cancer cells.

Advantages


  • Unlike traditional methods for producing monoclonal antibodies, no organisms are required for the in vitro selection of oligonucleotides. This facilitates the selection and chemical design process of aptamers.
  • Aptamers are produced chemically in a readily scalable process.
  • Non-immunogenic.
  • Unlike other oligonucleotide-based therapeutics (siRNAs, antisense RNA), aptamer therapeutics can be developed for intracellular as well as extracellular or cell-surface targets.

Technology's Essence


Aptamers are single-stranded oligonucleotides that fold into defined architectures and avidly bind to targets such as proteins, with the same effectiveness and affinity associated with mAbs. Using a novel screening technology the research team has identified a multimeric aptamer with pronounced ErbB-2/HER2 inhibitory activity. Preliminary preclinical experiments show that treatment of gastric tumor-bearing mice with trimeric aptamer resulted in reduced tumor growth that was nearly twofold stronger than that achieved with a monoclonal anti-ErbB-2/HER2 antibody.

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  • Prof. Yosef Yarden
  • Prof. Michael Sela
1601
A potent combination therapy against non-invasive breast cancer Breast cancer is the most common cancer in females. Among the different subtypes of breast cancer, ductal carcinoma in situ (DCIS) represents an intermediate step between normal breast tissue and invasive breast cancer. Currently, about 25...

A potent combination therapy against non-invasive breast cancer

Breast cancer is the most common cancer in females. Among the different subtypes of breast cancer, ductal carcinoma in situ (DCIS) represents an intermediate step between normal breast tissue and invasive breast cancer. Currently, about 25% of breast cancers that are diagnosed in the US are DCIS. DCIS is commonly treated by surgical intervention followed by adjuvant radiation therapy. However, a significant fraction of the DCIS lesions, which display HER2 gene amplification, are associated with increased relapse rate following surgery. Therefore, in cases of HER2-overexpressing DCIS a molecularly targeted therapy might be necessary for complete eradication of microscopic remnants following surgical tumor removal. The current technology presents an potential DCIS therapeutic strategy that collectively targets the functionally linked HER2 and Notch pathways.

 

Applications


  • Combination therapy for DCIS patients following surgical tumor removal.
  • Classification of DCIS patients according to HER2 Notch activation patterns to identify patients with increased risk of relapse after surgery.
  • Diagnostic antibodies to NRG4 to screen for cancer cell subtypes that express/over-express NRG4.
  • NRG4 fusion conjugates, where NRG4 acts as a vehicle to direct the conjugate to cells specifically expressing the receptor ErbB4.

 


Advantages


  • Targeted cancer therapies will give doctors a better way to tailor cancer treatment.
  • Targeted cancer therapies hold the promise of being more selective, thus harming fewer normal cells, reducing side effects, and improving the quality of life.
  • The proposed treatment strategy may prove beneficial in DCIS patients with poor prognosis.

 


Technology's Essence


The HER2/Neu oncogene, a member of the HER/ErbB signaling network, encodes a receptor-like tyrosine kinase, whose overexpression in breast cancer predicts poor prognosis and resistance to conventional therapies. Pre-invasive lesions, such as DCIS, overexpress HER2 at higher frequency than invasive ones. Another signal transduction pathway critical for breast cancer progression comprises Notch family receptors and their membrane-bound ligands. In the current technology, a team of researchers from the Weizmann Institute of Science uncovered that overexpression of HER2 in a novel experimental model of DCIS leads to transcriptional upregulation of Notch pathway components, resulting in enhanced tumor cell survival and proliferation. Combined treatment with HER2 and Notch pathway inhibitors resulted in decreased proliferative and tumorigenic potential. The current technology offers specific and combined targeting of HER2 and Notch pathways for DCIS treatment. This approach may also be tailored for DCIS patients with enhanced co-expression of HER2 and Notch.

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  • Prof. Yosef Yarden
1650
Efficient Production of natural Astaxanthin in bioengineered bacteria is a game changer for the nutraceuticals industry. The market-pull for natural Astaxanthin is much greater than the supply. Synthetic Astaxanthin is produced from petrochemical sources; it contains unwanted stereoisomers and is...

Efficient Production of natural Astaxanthin in bioengineered bacteria is a game changer for the nutraceuticals industry. The market-pull for natural Astaxanthin is much greater than the supply. Synthetic Astaxanthin is produced from petrochemical sources; it contains unwanted stereoisomers and is rejected by consumers who prefer natural Astaxanthin. Production of natural Astaxanthin in microalgae is laborious, expensive, and time-consuming.
Researchers at the Weizmann Institute used a combinatorial approach to construct bioengineered operons capable of modulating the expression levels of enzymes involved in the production of Astaxanthin. By combinatorial pairing of these genes in E. coli, they achieved natural Astaxanthin production 4-fold higher than previously reported.
The innovative method can challenge the deficiencies of natural Astaxanthin production in microalgae. Following scale-up and industrial development of the proprietary process, production of natural Astaxanthin has the potential to be considerably cheaper and competitive with the cost of synthesizing Astaxanthin.

Applications


  • Cost-effective Production of natural Astaxanthin for the nutraceuticals industry, animal feed industry, and others.
  • A doorway to the generation of many future products in E. coli, specifically metabolites that are produced in elaborate metabolic pathways.

Advantages


  • Full control over carotenoid accumulation profile.
  • Cheaper, straightforward generation of Astaxanthin in E. coli as opposed to generation in algae which involves high raw materials cost, land usage, air emissions etc.
  • Natural Astaxanthin as opposed to synthetic, uncontaminated with intermediate compounds and stereoisomers.

Technology's Essence


At Dr. Ron Milo’s lab researchers employed a method that uses the relatively short Ribosome Binding Site (RBS) sequence in a combinatorial manner. The methodology involves combinatorial pairing of target genes (Astaxanthin metabolic pathway enzymes) with a small set of RBS sequences and assembling them into a library of synthetic operons to explore protein expression space and to locate desired phenotypes in bacteria.
The researchers used a small set of RBS sequences to modulate in parallel the protein expression levels of multiple genes over several orders of magnitude. Using this approach, they were able to efficiently scan a large fraction of the Astaxanthin metabolic expression space with a manageable set of tested genotypes.

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  • Prof. Ron Milo
1441
New protein as a target to treat B cell-related cancer.Chronic lymphocytic leukemia (CLL), a malignant disease characterized by the accumulation of B lymphocytes in the blood, lymphoid organs, and bone marrow, is the second most common type of leukemia in adults, accounting for about 7,000 new cases of...

New protein as a target to treat B cell-related cancer.
Chronic lymphocytic leukemia (CLL), a malignant disease characterized by the accumulation of B lymphocytes in the blood, lymphoid organs, and bone marrow, is the second most common type of leukemia in adults, accounting for about 7,000 new cases of leukemia each year. Presently, there is no cure for CLL, and the overall goal of leukemia treatment is to bring about a remission. Therefore, identifying new proteins that may serve as a target for inducing cell death in the malignant cells is highly desirable. The present technology identifies a new regulator protein that is essential for the survival of CLL cells.

Applications


• Treatment of CLL, as well as other B cell-related cancers (e.g. gastric cancer and renal cell carcinoma), by blocking CD84 activity
• Diagnosis of CLL

Advantages


• Very specific to malignant B cells
• Diagnosis, and therefore treatment, can be made at early stages of the disease

 


Technology's Essence


B cells taken from CLL patients have a high level of the protein CD84. Stimulation of CD84 upregulates the survival of B-CLL. However, inhibition of CD84 activity with a blocking antibody downregulates the expression of another protein which controls B-CLL survival, thus inducing cell death. Therefore, the present invention reveals CD84 as a regulator of B-CLL survival

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  • Prof. Idit Shachar
1518
Improved immunotherapy for breast cancer. Monoclonal antibodies (mAbs) to ErbB-2/HER2 growth factor receptor, or to its sibling, the epidermal growth factor receptor (EGFR), prolong survival of cancer patients, especially when combined with cytotoxic therapies. However, low effectiveness of...

Improved immunotherapy for breast cancer.

Monoclonal antibodies (mAbs) to ErbB-2/HER2 growth factor receptor, or to its sibling, the epidermal growth factor receptor (EGFR), prolong survival of cancer patients, especially when combined with cytotoxic therapies. However, low effectiveness of therapeutic mAbs and the evolution of patient resistance call for improvements. Furthermore, the response to the clinically approved monotherapy of Herceptin (a humanized mAb directed against ErbB-2), is relatively low (~15%) and short lived (median duration, 9 months). Therefore, there is a need to improve the therapeutic treatment against this receptor. The present technology enhances the therapeutic activity of anti-ErB-2 receptor antibodies, by combining two or more epitope-distinct antibodies.

Applications


  • Improved treatment of ErbB-2-overexpressing tumors (e.g. in breast and ovary cancers).


Advantages


  • May enhance patient response and delay acquisition of resistance.
  • Enhancement of therapeutic efficacy and synergy with chemotherapy.

Technology's Essence


Optimal selection of mAbs for cancer immunotherapy may improve its therapeutic potential. The outlined technology addresses an emerging strategy, which enhances the therapeutic activity of anti-receptor antibodies by combining two mAbs engaging distinct epitopes. It was demonstrated that pairs of anti-ErbB-2 mAbs better inhibit ErbB-2-overexpressing tumors than the respective individual mAbs, both in vitro and in vivo.

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  • Prof. Yosef Yarden
1245

Applications


The novel DNA Aptamer is a promising candidate for therapeutic as well as diagnostic uses: Therapeutic: A novel therapy for Influenza Diagnostics: Detection of Influenza infection in vertebrates such as avian, swine and human

Technology's Essence


Scientists at the Weizmann Institute of Science describe a novel oligonucleotide, also known as an Aptamer, which has been designed to complement the receptor-binding region of the influenza haemagglutinin molecule. It was constructed by screening a DNA library and processing by the SELEX procedure. This DNA Aptamer comprises of a polynucleotide sequence that can bind to a polypeptide within the binding region of the influenza virus to the host cell. The proposed mode of action of this Aptamer is by blocking the binding of influenza virus to target cell receptors and consequently preventing the virus invasion into the host cells. Aptamer is capable of inhibiting the haemagglutinin capacity of the virus and the viral infectivity in vitro. Furthermore, it was shown in an animal model to inhibit viral infection by different influenza strains, as manifested by up to 99% reduction of virus burden in the lungs of treated mice.

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  • Prof. Ruth Arnon
1397
A novel antibody which can be used, for the first time, to recognize ubiquitinated histone 2B. This technology is novel in its ability to recognize proteins and their destinations, and may serve in diagnostics and immunoprecipitation processes.

A novel antibody which can be used, for the first time, to recognize ubiquitinated histone 2B. This technology is novel in its ability to recognize proteins and their destinations, and may serve in diagnostics and immunoprecipitation processes.

Applications


Primary applications in research. Use as a detection tool in western blotting, immunoprecipitation and chromatin immunoprecipitation. Might be used for monitoring processes associated with modulations of ubiquitinated-H2B levels.

Technology's Essence


The invention involves the generation of antibodies specific to ubiquitinated-H2B which selectively recognize H2B when it is ubiquitinated but not H2B in its unmodified state, or ubiquitin unconjugated to H2B.

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  • Prof. Moshe Oren
1499
Bladder cancer is a common malignancy; it is the 4th most common cancer in males and the 9th in females.  The presenting symptom is usually blood in the urine, and diagnosis is currently based on cystoscopy, which is invasive, costly, painful and time consuming.  To date, no biomarker has been...

Bladder cancer is a common malignancy; it is the 4th most common cancer in males and the 9th in females.  The presenting symptom is usually blood in the urine, and diagnosis is currently based on cystoscopy, which is invasive, costly, painful and time consuming.  To date, no biomarker has been identified in the urine that might be used for screening, staging, prognosis and monitoring treatment.  We now report that the amount of the 60 kDa heat shock protein (HSP60) in a subject’s urine is a biomarker for muscle invasion in patients with bladder cancer – stage T2 and higher.  Moreover, subjects with stage T1 disease can be stratified by their urine levels of HSP60 into a sub-group likely to progress into stage T2 or into a sub-group more likely to respond to conservative treatment with BCG, which does not require removal of the bladder.  The distinction between these two sub-groups of T1 bladder cancer can identify earlier subjects in need of cystectomy, while sparing others unnecessary major surgery.

Applications


  • Screening subjects with overt hematuria, or at risk of developing bladder cancer (such as heavy smokers)
  • tratifying bladder cancer subjects
  • Prognosis
  • Determining treatment program
  • Monitoring response to therapy.

Advantages


  • Non-invasive
  • Easy to apply
  • Relatively inexpensive
  • Prognositic.

Technology's Essence


Quantitative measurement of HSP60 levels in a subject’s urine by ELISA, radio-immunoassay or other simple assays.

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  • Prof. Irun R. Cohen
1033
A novel diagnostic test to identify individuals with increased risk of lung cancer. Lung cancer is the number one killer among cancers, with 160,000 deaths/year in the USA and 1.6 million/year worldwide. Early detection of lung cancer increases 5-year survival rate from 4% to 54%. Moreover, the...

A novel diagnostic test to identify individuals with increased risk of lung cancer.

Lung cancer is the number one killer among cancers, with 160,000 deaths/year in the USA and 1.6 million/year worldwide. Early detection of lung cancer increases 5-year survival rate from 4% to 54%. Moreover, the National Lung Cancer Trial (NLST) showed that early detection of lung cancer by low-dose CT reduces mortality by at least 20%. Despite recommendations for low-dose CT screening for heavy smokers fulfilling the NLST criteria, compliance is low. In addition, 80 million smokers and ex-smokers in the US who do not fulfil NLST risk criteria have no recommended solution.

The MyRepair test fulfils this unmet medical need by providing a quantitative prediction of lung cancer risk using a simple blood test. The test is based on a personalized measurement of the patient’s DNA repair capacity, a mechanism which is highly connected to the onset of cancer. Therefore, the MyRepair technology can potentially increase early detection of lung cancer and thus save lives.

 

Applications


A novel diagnostic test to identify individuals with increased risk of lung cancer


Advantages


·         Simplicity – MyRepair is based on a simple, cost-effective blood test.

·         Accessibility – Compared to low-dose CT which requires specific equipment, the MyRepair test can be easily integrated in general diagnostic labs and therefore may be more accessible to a larger portion of the population.

·         Additional applications – Since the test is based on measuring personalized DNA repair mechanism, it can be adopted in the future for the diagnosis of additional cancer types and DNA repair related diseases.


Technology's Essence


Based on the strong and well documented connection between impaired capacity for DNA repair and onset of cancer, the Livneh lab invented the MyRepair Test, a method for predicting lung cancer risk, based on measuring activity of 3 DNA repair enzymes.

Combining enzyme activities with experimental risk estimates generated MyRepair Score, which measures personalized DNA repair capacity of tested subjects.

An epidemiological/clinical study performed in Israel, further validated in an independent UK study, demonstrated that lung cancer patients have lower MyRepair Score than healthy people. In addition, subjects who test MyRepair-positive have an 85-fold higher risk to develop lung cancer compared to the general population.

Low MyRepair Score is a risk factor independent of smoking, and of comparable magnitude, indicating that it can be a prognostic tool for smokers, ex-smokers, and non-smokers.

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  • Prof. Zvi Livneh
1270
Monoclonal antibodies to IgE Description: Rat monoclonal anti-IgE antibodies that was generated by fusion of plasmacytoma (84.1C) or myeloma (EM953) cells with splenocytes of rat immunized with purified murine IgE mAb. The antibodies react with various IgE mAb of different specificities and not with...

Monoclonal antibodies to IgE

Description: Rat monoclonal anti-IgE antibodies that was generated by fusion of plasmacytoma (84.1C) or myeloma (EM953) cells with splenocytes of rat immunized with purified murine IgE mAb. The antibodies react with various IgE mAb of different specificities and not with immunoglobulins of other classes, and recognize an epitope on the murine Fc epsilon region.

Were shown to block IgE-Fc?R interactions and inhibit passive cutaneous anaphylaxis. 

Clone 84.1c recognizes a site on IgE, which is identical or very close to the Fc?R binding site. May be used for detection and manipulation of the IgE response in mice.

Reference:  Schwarzbaum S, Nissim A, Alkalay I, Ghozi MC, Schindler DG, Bergman Y, Eshhar Z. 1989. Mapping of murine IgE epitopes involved in IgE-Fc epsilon receptor interactions. Eur J Immunol 19(6):1015-23.

 

M182, M185, M186

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  • Prof. Zelig Eshhar
1655
Cellular senescence is a permanent cell cycle arrest induced by damage or stress applied on proliferating cells. In a cell autonomous manner, senescence is a potent barrier to tumorgenesis and contributes to the cytotoxicity of some anti-cancer drugs. However, with age senescence cells accumulate and...

Cellular senescence is a permanent cell cycle arrest induced by damage or stress applied on proliferating cells. In a cell autonomous manner, senescence is a potent barrier to tumorgenesis and contributes to the cytotoxicity of some anti-cancer drugs. However, with age senescence cells accumulate and promote a number of pathological conditions. Therefore the elimination of senescent cells is desired in order to prevent tumor- and inflammation- related pathologies and also to inhibit tissue ageing.
Today, our understanding of the mechanisms regulating the viability of senescent cells is limited. It has been suggested that senescent cells are resistant to apoptosis. Therefore, senescent cells elimination may be achieved by modifying the resistance to apoptosis of these cells.
Here the researches demonstrate the first feasible therapeutic approach that leads to eradication of senescent cells. Combination of direct induction of apoptosis in senescent cells with induction of cell death by pro-inflammatory repose induce by p21 knockdown will lead to reduction of viable senescent cells.

Applications


  • A therapeutic impact on inflammatory and fibrotic disease
  • Therapy for age-related disease such as type 2 diabetes, Alzheimer’s disease, Atherosclerosis, cataracts, Chronic obstructive pulmonary disease (COPD), and Osteoporosis

Advantages


  • Effective elimination of senescent cells- removal of senescent cells can prevent or delay tissue dysfunction and extend health span
  • Does not damage normal cells even at high concentrations

Technology's Essence


Researches demonstrated that the anti-apoptotic proteins Bcl-xL and Bcl-w level were elevated in senescence cells of both human and mouse origin. A subsequent study, in which Bcl-xL and Bcl-w were knocked down by siRNA, revealed that a combined knock down of Bcl-xL and Bcl-w had synergic effect, resulting in reduction of 50% in cell viability. Thus the increased level of anti-apoptotic proteins Bcl-xL and Bcl-w may account for the apoptotic resistance of senescent cells. p21 knockdown induced pro-inflammatory response and cell death in senescent cells.
Overall, the researchers show that combined inhibition of the anti-apoptotic proteins Bcl-xL and Bcl-w allows specific elimination of senescent cells and might be used to treat diseases where senescent cells are present. The researchers also found that the same effect might be achieved by reducing the expression of p21 in senescent cells. Integrating both approaches propose a more effective therapy.

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  • Prof. Valery Krizhanovsky

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