Melanoma BRAF Inhibitors Review
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Melanoma BRAF Inhibitors Review
Zelboraf (vemurafenib, Roche) and Tafinlar (dabrafenib, GSK) get FDA and EMA approval for advanced metastatic melanoma. Several follow up BRAF inhibitors are in clinical development by rival pharma companies (Novartis, BMS, J&J, Teva) to get a share of expanding melanoma market and improve complete response rates and overcome resistance. Nexavar (sorafenib, Bayer) for for liver (HCC) and renal (RCC) cancer was the first approved and marketed BRAF inhibitor.
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Vemurafenib (PLX 4032, Roche) Melanoma: FDA Review & Approval - un knol de Krishan Maggon

Vemurafenib (PLX 4032, Roche) Melanoma: FDA Review & Approval - un knol de Krishan Maggon | Melanoma BRAF Inhibitors Review | Scoop.it
Only a single new investigation drug has produced a 81% response rate and extended overall survival by 7 months (range 2-18...
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Targeting TNFR2, an immune checkpoint stimulator and oncoprotein, is a promising treatment for cancer

Targeting TNFR2, an immune checkpoint stimulator and oncoprotein, is a promising treatment for cancer | Melanoma BRAF Inhibitors Review | Scoop.it
Tumor necrosis factor receptor 2 (TNFR2) is expressed both by some cancer cells and by tumor-infiltrating immunosuppressive CD4+FoxP3+ regulatory T cells (Tregs). TNFR2 stimulates the activation and proliferation of Tregs, a major checkpoint of antitumor immune responses, and promotes cancer cell survival and tumor growth. In this issue of Science Signaling , Torrey et al . found that dominant antagonistic antibodies against human TNFR2 may be a potential therapy for ovarian cancer patients by simultaneously suppressing Treg activity and inducing the death of the cancer cells.
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Sci. Signal. 17 Jan 2017: Vol. 10, Issue 462, DOI: 10.1126/scisignal.aal2328
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Oncogene - Abstract of article: PDE4D promotes FAK-mediated cell invasion in BRAF-mutated melanoma

Oncogene - Abstract of article: PDE4D promotes FAK-mediated cell invasion in BRAF-mutated melanoma | Melanoma BRAF Inhibitors Review | Scoop.it

Oncogene


Abstract The cyclic AMP (cAMP) signaling pathway is critical in melanocyte biology for regulating differentiation. It is downregulated by phosphodiesterase (PDE) enzymes, which degrade cAMP itself. In melanoma evidence suggests that inhibition of the cAMP pathway by PDE type 4 (PDE4) favors tumor progression. For example, in melanomas harboring RAS mutations, the overexpression of PDE4 is crucial for MAPK pathway activation and proliferation induced by oncogenic RAS. Here we showed that PDE4D is overexpressed in BRAF-mutated melanoma cell lines, constitutively disrupting the cAMP pathway activation. PDE4D promoted melanoma invasion by interacting with focal adhesion kinase (FAK) through the scaffolding protein RACK1. Inhibition of PDE4 activity or inhibition of PDE4D interaction with FAK reduced invasion. PDE4D expression is increased in patients with advanced melanoma and PDE4D–FAK interaction is detectable in situ in metastatic melanoma. Our study establishes the role of PDE4D in BRAF-mutated melanoma as regulator of cell invasion, and suggests its potential as a target for preventing metastatic dissemination.

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Oncogene advance online publication 16 January 2017; doi: 10.1038/onc.2016.469
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Oncogene - Utilizing somatic mutation data from numerous studies for cancer research: proof of concept and applications

Oncogene - Utilizing somatic mutation data from numerous studies for cancer research: proof of concept and applications | Melanoma BRAF Inhibitors Review | Scoop.it

Oncogene


Abstract Large cancer projects measure somatic mutations in thousands of samples, gradually assembling a catalog of recurring mutations in cancer. Many methods analyze these data jointly with auxiliary information with the aim of identifying subtype-specific results. Here, we show that somatic gene mutations alone can reliably and specifically predict cancer subtypes. Interpretation of the classifiers provides useful insights for several biomedical applications. We analyze the COSMIC database, which collects somatic mutations from The Cancer Genome Atlas (TCGA) as well as from many smaller scale studies. We use multi-label classification techniques and the Disease Ontology hierarchy in order to identify cancer subtype-specific biomarkers. Cancer subtype classifiers based on TCGA and the smaller studies have comparable performance, and the smaller studies add a substantial value in terms of validation, coverage of additional subtypes, and improved classification. The gene sets of the classifiers are used for threefold contribution. First, we refine the associations of genes to cancer subtypes and identify novel compelling candidate driver genes. Second, using our classifiers we successfully predict the primary site of metastatic samples. Third, we provide novel hypotheses regarding detection of subtype-specific synthetic lethality interactions. From the cancer research community perspective, our results suggest that curation efforts, such as COSMIC, have great added and complementary value even in the era of large international cancer projects. 

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Oncogene advance online publication 16 January 2017; doi: 10.1038/onc.2016.489
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Prevention of Dietary-Fat-Fueled Ketogenesis Attenuates BRAF V600E Tumor Growth

Prevention of Dietary-Fat-Fueled Ketogenesis Attenuates BRAF V600E Tumor Growth | Melanoma BRAF Inhibitors Review | Scoop.it

Summary Lifestyle factors, including diet, play an important role in the survival of cancer patients. However, the molecular mechanisms underlying pathogenic links between diet and particular oncogenic mutations in human cancers remain unclear. We recently reported that the ketone body acetoacetate selectively enhances BRAF V600E mutant-dependent MEK1 activation in human cancers. Here we show that a high-fat ketogenic diet increased serum levels of acetoacetate, leading to enhanced tumor growth potential of BRAF V600E-expressing human melanoma cells in xenograft mice. Treatment with hypolipidemic agents to lower circulating acetoacetate levels or an inhibitory homolog of acetoacetate, dehydroacetic acid, to antagonize acetoacetate-BRAF V600E binding attenuated BRAF V600E tumor growth. These findings reveal a signaling basis underlying a pathogenic role of dietary fat in BRAF V600E-expressing melanoma, providing insights into the design of conceptualized “precision diets” that may prevent or delay tumor progression based on an individual’s specific oncogenic mutation profile.

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First of its kind cancer stem cell research unlocks clues to treatment resistance

First of its kind cancer stem cell research unlocks clues to treatment resistance | Melanoma BRAF Inhibitors Review | Scoop.it
Researchers at Trinity College Dublin have made exciting new findings that could offer a means of fighting resistance to treatment for people with oesophageal cancer. Resistance to radiotherapy is a major stumbling bloc
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The top 15 best-selling cancer drugs in 2022 | FiercePharma

The top 15 best-selling cancer drugs in 2022 | FiercePharma | Melanoma BRAF Inhibitors Review | Scoop.it
If there was any doubt that the oncology market is set to reach unprecedented heights, FiercePharma's top 15 list of cancer drugs in 2022 should eliminate it.
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Biomarkers for Immunotherapy: Current Developments and Challenges | 2016 Educational Book | Meeting Library

Biomarkers for Immunotherapy: Current Developments and Challenges | 2016 Educational Book | Meeting Library | Melanoma BRAF Inhibitors Review | Scoop.it
Biomarkers for Immunotherapy: Current Developments and Challenges - Melanoma/Skin Cancers - 2016 ASCO Annual Meeting
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The impact of body composition parameters on ipilimumab toxicity and survival in patients with metastatic melanoma

The impact of body composition parameters on ipilimumab toxicity and survival in patients with metastatic melanoma | Melanoma BRAF Inhibitors Review | Scoop.it
British Journal of Cancer , (10 January 2017) | doi:10.1038/bjc.2016.431

Patients with sarcopenia and low MA are more likely to experience severe treatment-related toxicity to Ipi. Loss of muscle during treatment was predictive of worse survival. Treatments to increase muscle mass and influence outcome warrant further investigation.
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Tumour mechanopathology: Cutting the stress out

Tumour mechanopathology: Cutting the stress out | Melanoma BRAF Inhibitors Review | Scoop.it
Solid stress within tumours can be quantified by measuring their deformation after cutting, slicing or taking a needle biopsy of them.
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Nanotechnology Now - Press Release: New technique uses immune cells to deliver anti-cancer drugs

Nanotechnology Now - Press Release: New technique uses immune cells to deliver anti-cancer drugs | Melanoma BRAF Inhibitors Review | Scoop.it
Some researchers are working to discover new, safer ways to deliver cancer-fighting drugs to tumors without damaging healthy cells. Others are finding ways to boost the body's own immune system to attack cancer cells. Researchers at Penn State have combined the two approaches by taking biodegradable polymer nanoparticles encapsulated with cancer-fighting drugs and incorporating them into immune cells to create a smart, targeted system to attack cancers of specific types.
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Shedding mutations may let cancer evade immunotherapy - Futurity

Shedding mutations may let cancer evade immunotherapy - Futurity | Melanoma BRAF Inhibitors Review | Scoop.it
“Our findings offer evidence about how cancer cells evolve during immunotherapy,” says Victor E. Velculescu. Resistance to the drugs has been a mystery.
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Researchers reveal how cancer cells cope with genetic chaos

Researchers reveal how cancer cells cope with genetic chaos | Melanoma BRAF Inhibitors Review | Scoop.it
Scientists have uncovered how tumours are able to grow despite significant damage to the structure and number of their chromosomes - the storage units of DNA - according to two new studies published in Cancer Cell and Cance
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De novo phosphorylation and conformational opening of the tyrosine kinase Lck act in concert to initiate T cell receptor signaling

De novo phosphorylation and conformational opening of the tyrosine kinase Lck act in concert to initiate T cell receptor signaling | Melanoma BRAF Inhibitors Review | Scoop.it
The tyrosine kinase Lck is critical to T cell activation in response to stimulation of the T cell receptor (TCR). Lck activity is tightly regulated to avoid inappropriate activation of T cells and subsequent inflammation. Phosphorylation of Tyr505 causes Lck to form a closed, inhibited conformation, whereas phosphorylation of Tyr394 results in conformational opening of the kinase. To tease apart the differential effects of phosphorylation and conformational changes on Lck activity, Philipsen et al . generated different fluorescent Lck biosensors and imaged unstimulated and TCR-stimulated human T cells by fluorescence microscopy. Both the TCR-stimulated conformational opening of Lck and its subsequent phosphorylation of Tyr394 were required to stimulate T cells, and these modifications occurred primarily on Lck that was close to that TCR at the plasma membrane. These data suggest that drugs that stabilize the open conformation yet prevent the phosphorylation event could limit T cell–mediated immune responses.
Krishan Maggon 's insight:
Sci. Signal. 17 Jan 2017: Vol. 10, Issue 462, DOI: 10.1126/scisignal.aaf4736
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Reporter gene imaging of targeted T cell immunotherapy in recurrent glioma

Reporter gene imaging of targeted T cell immunotherapy in recurrent glioma | Melanoma BRAF Inhibitors Review | Scoop.it
Cytotoxic T cells engineered to kill tumor cells are becoming a mainstay of cancer immunotherapy. However, no matter how precisely they are engineered, once they are injected into a patient, they are no longer directly monitored or controlled by the researchers. As a result, if the treatment fails to work or causes toxicity, it is not clear whether the therapeutic cells are ineffective or whether they scattered through normal tissues and never reached the tumor. Keu et al . have designed a method to engineer these T cells with a reporter gene such that they can be tracked in people by positron emission tomography. The authors present a clinical trial demonstrating the feasibility and safety of this approach in glioma patients.
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Oncogene - WNT/[beta]-catenin signaling regulates mitochondrial activity to alter the oncogenic potential of melanoma in a PTEN-dependent manner

Oncogene - WNT/[beta]-catenin signaling regulates mitochondrial activity to alter the oncogenic potential of melanoma in a PTEN-dependent manner | Melanoma BRAF Inhibitors Review | Scoop.it

Oncogene 


Abstract Aberrant regulation of WNT/β-catenin signaling has a crucial role in the onset and progression of cancers, where the effects are not always predictable depending on tumor context. In melanoma, for example, models of the disease predict differing effects of the WNT/β-catenin pathway on metastatic progression. Understanding the processes that underpin the highly context-dependent nature of WNT/β-catenin signaling in tumors is essential to achieve maximal therapeutic benefit from WNT inhibitory compounds. In this study, we have found that expression of the tumor suppressor, phosphatase and tensin homolog deleted on chromosome 10 (PTEN), alters the invasive potential of melanoma cells in response to WNT/β-catenin signaling, correlating with differing metabolic profiles. This alters the bioenergetic potential and mitochondrial activity of melanoma cells, triggered through regulation of pro-survival autophagy. Thus, WNT/β-catenin signaling is a regulator of catabolic processes in cancer cells, which varies depending on the metabolic requirements of tumors.

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Oncogene advance online publication 16 January 2017; doi: 10.1038/onc.2016.450
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Cancer reproducibility project releases first results

Cancer reproducibility project releases first results | Melanoma BRAF Inhibitors Review | Scoop.it
An open-science effort to replicate dozens of cancer-biology studies is off to a confusing start.
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SATB1 Expression Governs Epigenetic Repression of PD-1 in Tumor-Reactive T Cells

SATB1 Expression Governs Epigenetic Repression of PD-1 in Tumor-Reactive T Cells | Melanoma BRAF Inhibitors Review | Scoop.it

Summary Despite the importance of programmed cell death-1 (PD-1) in inhibiting T cell effector activity, the mechanisms regulating its expression remain poorly defined. We found that the chromatin organizer special AT-rich sequence-binding protein-1 (Satb1) restrains PD-1 expression induced upon T cell activation by recruiting a nucleosome remodeling deacetylase (NuRD) complex to Pdcd1 regulatory regions. Satb1 deficienct T cells exhibited a 40-fold increase in PD-1 expression. Tumor-derived transforming growth factor β (Tgf-β) decreased Satb1 expression through binding of Smad proteins to the Satb1 promoter. Smad proteins also competed with the Satb1-NuRD complex for binding to Pdcd1 enhancers, releasing Pdcd1 expression from Satb1-mediated repression, Satb1-deficient tumor-reactive T cells lost effector activity more rapidly than wild-type lymphocytes at tumor beds expressing PD-1 ligand (CD274), and these differences were abrogated by sustained CD274 blockade. Our findings suggest that Satb1 functions to prevent premature T cell exhaustion by regulating Pdcd1 expression upon T cell activation. Dysregulation of this pathway in tumor-infiltrating T cells results in diminished anti-tumor immunity.

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Tumor suppressor key in maintaining stem cell status in muscle

Tumor suppressor key in maintaining stem cell status in muscle | Melanoma BRAF Inhibitors Review | Scoop.it
A gene known to suppress tumor formation in a broad range of tissues plays a key role in keeping stem cells in muscles dormant until needed, a finding that may have implications for both human health and animal production
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Tissue Phenomics® | Definiens

Tissue Phenomics® | Definiens | Melanoma BRAF Inhibitors Review | Scoop.it

Definiens is the Tissue Phenomics leader for diagnostics development in oncology.


Unique tissue signatures that accelerate cancer breakthroughs


Tissue Phenomics Literature Scientific Literature: Systematic Analysis of Breast Cancer Morphology Uncovers Stromal Features Associated with Survival In-silico insights on the prognostic potential of immune cell infiltration patterns in the breast lobular epithelium Area of poorly differentiated clusters in a tissue quantified by image analysis improves staging of CRC Collateral Downloads: An Introduction to Immunotherapy and the Promise of Tissue Phenomics

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Angiogenesis Inhibitors

Angiogenesis Inhibitors | Melanoma BRAF Inhibitors Review | Scoop.it
A fact sheet that describes the process of eliminating the blood supply to tumors. Lists the cancers in which this approach is being tested.
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Cell Research - Regulatory T cells in cancer immunotherapy

Cell Research - Regulatory T cells in cancer immunotherapy | Melanoma BRAF Inhibitors Review | Scoop.it

Cell Research (2017) 27:109–118. doi:10.1038/cr.2016.151; published online 20 December 2016 Regulatory T cells in cancer immunotherapy Atsushi Tanaka1,2 and Shimon Sakaguchi1 


Abstract FOXP3-expressing regulatory T (Treg) cells, which suppress aberrant immune response against self-antigens, also suppress anti-tumor immune response. Infiltration of a large number of Treg cells into tumor tissues is often associated with poor prognosis. There is accumulating evidence that the removal of Treg cells is able to evoke and enhance anti-tumor immune response. However, systemic depletion of Treg cells may concurrently elicit deleterious autoimmunity. One strategy for evoking effective tumor immunity without autoimmunity is to specifically target terminally differentiated effector Treg cells rather than all FOXP3+ T cells, because effector Treg cells are the predominant cell type in tumor tissues. Various cell surface molecules, including chemokine receptors such as CCR4, that are specifically expressed by effector Treg cells can be the candidates for depleting effector Treg cells by specific cell-depleting monoclonal antibodies. In addition, other immunological characteristics of effector Treg cells, such as their high expression of CTLA-4, active proliferation, and apoptosis-prone tendency, can be exploited to control specifically their functions. For example, anti-CTLA-4 antibody may kill effector Treg cells or attenuate their suppressive activity. It is hoped that combination of Treg-cell targeting (e.g., by reducing Treg cells or attenuating their suppressive activity in tumor tissues) with the activation of tumor-specific effector T cells (e.g., by cancer vaccine or immune checkpoint blockade) will make the current cancer immunotherapy more effective. 


 Keywords: Treg; CTLA-4; cancer; immunotherapy

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A biosensor is able to detect tumors at early stages | Scienmag: Latest Science and Health News

A biosensor is able to detect tumors at early stages | Scienmag: Latest Science and Health News | Melanoma BRAF Inhibitors Review | Scoop.it
Credit: Cho, Y., Gorina, S., Jeffrey, P.D., Pavletich, N.P.; Astrojan. Before a malignant tumor is developed, the immune system tries to fight against proteins that are altered during their formation, producing certain cancer antibodies. A biosensor developed by scientists from the Complutense University of Madrid has been able to detect these defensive units in serum samples of patients with colorectal and ovarian cancer. The developed method is faster and more accurate than traditional methods. When healthy cells are transformed into tumors, the expression of some proteins is being altered. As a defense, the immune system produces certain antibodies against them. The production of these autoantibodies start several months or even years before the disease is completely developed and detected by the clinicians. "Our immune system produces these cancer autoantibodies even three years before the first symptoms appear", explains Susana Campuzano, Associate Researcher at the Department of Analytical Chemistry at the Complutense University of Madrid (UCM). In collaboration with different hospitals and the Instituto de Investigaciones Biomédicas "Alberto Sols" (Madrid), scientists at the UCM have designed a biosensor capable of detecting these antibodies in serum samples from both cancer patients and patients at high risk of suffer from cancer in the future. To verify their effectiveness, the researchers applied the developed biosensor to the analysis of serum samples from four patients with colorectal cancer and two with ovarian cancer and treated at Puerta de Hierro and La Paz Hospitals (Madrid). In addition, they also used the biosensor to analyze the sera from twenty-four patients treated at Hospital Universitario Clínico San Carlos (Madrid) with high probability of developing malignant colorectal tumors due to a familial history of cancer. With the biosensor, the scientists at UCM detected the autoantibody content generated by the patients against the p53 protein. "This protein is known as the guardian of the genome because it repairs DNA mutations, avoiding alterations in the cell cycle and the appearance of tumors", says José Manuel Pingarrón, Professor of Analytical Chemistry at UCM and co-author of the work, recently published in Analytical Chemistry. When p53 is aberrantly mutated and multiplies without control, the immune system of between 10% and 40% of all cancer patients -depending on the cancer type they suffer- produces autoantibodies against p53, alerting of a possible malignant transformation. "The presence of antibodies against p53 could be indicative of the existence of a neoplastic disease already initiated or of the risk of developing cancer in the near future", says Rodrigo Barderas, Ramón y Cajal fellow at the Biochemistry and Molecular Biology I Department of the Chemistry Faculty of the UCM and co-author of the work. Management of the disease Compared with other methods that also detect autoantibodies against p53, the biosensor demonstrated a 440-fold higher sensitivity and a better discrimination between positive and negative serum samples to p53 autoantibodies. Another advantage of the developed biosensor is its handling simplicity and speed. In less than six hours the complete test is performed including the expression and purification of p53, in contrast to the weeks or months necessary to develop the traditional methods (in which the protein is produced and purified separately from the assay). "Its simplicity of handling, portability and time to complete the full procedure make it suitable for application in clinical routine", says Campuzano. In addition to be used as an early diagnostic method in liquid biopsies, the biosensor can be used to monitor the course of the disease in patients with autoantibodies to p53. It has been demonstrated that when the tumor burden disappears, the levels of these antibodies to p53 decreases until normal values. The patients who participated in the study with high probability of developing colorectal malignant tumors are currently undergoing exhaustive follow-up by clinicians at the Hospital Universitario Clínico San Carlos (Madrid). ###**Reference: María Garranzo-Asensio, Ana Guzmán-Aránguez, Carmen Povés, María Jesús Fernández Aceñero, Rebeca M. Torrente-Rodríguez, Víctor Ruiz-Valdepeñas Montiel, Gemma Domínguez, Luis San Frutos, Nuria Rodríguez, Mayte Villalba, José; M. Pingarrón, Susana Campuzano y Rodrigo Barderas. "Towards liquid biopsy: Rapid Determination of the Humoral Immune Response in Cancer Patients using HaloTag Fusion protein-Modified Electrochemical Bioplatforms", Analytical Chemistry. November 16, 2016. DOI: 10.1021/acs.analchem.6b03526. Media Contact Susana Campuzanosusanacr@quim.ucm.es34-913-944-368http://www.ucm.es | Science news and articles on health, environment, global warming, stem cells, bird flu, autism, nanotechnology, dinosaurs, evolution -- the latest discoveries in astronomy, anthropology, biology, chemistry, climate & bioengineering, computers, engineering ; medicine, math, physics, psychology, technology, and more from the world's leading research centers universities.
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Lilly and Merck Expand Immuno-Oncology Collaboration

Lilly and Merck Expand Immuno-Oncology Collaboration | Melanoma BRAF Inhibitors Review | Scoop.it
INDIANAPOLIS, Jan. 11, 2017 /PRNewswire/ -- Lilly and Merck Expand Immuno-Oncology Collaboration. New Study to Evaluate Combination o
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New Findings on Tumor Cell Migration May Improve Cancer Therapy | GEN Genetic Engineering & Biotechnology News - Biotech from Bench to Business | GEN

New Findings on Tumor Cell Migration May Improve Cancer Therapy | GEN Genetic Engineering & Biotechnology News - Biotech from Bench to Business | GEN | Melanoma BRAF Inhibitors Review | Scoop.it
Researchers discover that tumor cells move differently than normal ones
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Limbic encephalitis following immunotherapy against metastatic malignant melanoma. - PubMed - NCBI

Limbic encephalitis following immunotherapy against metastatic malignant melanoma. - PubMed - NCBI | Melanoma BRAF Inhibitors Review | Scoop.it
BMJ Case Rep. 2016 Mar 23;2016. pii: bcr2016215012. doi: 10.1136/bcr-2016-215012. Case Reports
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