Melanoma BRAF Inhibitors Review
46.7K views | +8 today
Follow
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.
Curated by Krishan Maggon
Your new post is loading...
Your new post is loading...
Scooped by Krishan Maggon
Scoop.it!

Metastatic Melanoma Cells: Image Details - NCI Visuals Online

Metastatic Melanoma Cells: Image Details - NCI Visuals Online | Melanoma BRAF Inhibitors Review | Scoop.it
Image information and view/download options.
more...
No comment yet.
Scooped by Krishan Maggon
Scoop.it!

Cancers | Free Full-Text | Conversion of Stem Cells to Cancer Stem Cells: Undercurrent of Cancer Initiation

Cancers | Free Full-Text | Conversion of Stem Cells to Cancer Stem Cells: Undercurrent of Cancer Initiation | Melanoma BRAF Inhibitors Review | Scoop.it
Cancer stem cells (CSCs) also known as cancer-initiating cells (CIC), are responsible for the sustained and uncontrolled growth of malignant tumors and are proposed to play significant roles in metastasis and recurrence.
more...
No comment yet.
Rescooped by Krishan Maggon from Immunology and Biotherapies
Scoop.it!

Genomic correlates of response to immune checkpoint blockade

Genomic correlates of response to immune checkpoint blockade | Melanoma BRAF Inhibitors Review | Scoop.it
Responders and non-responders to cancer immunotherapy can be identified through a range of genomic markers.

Via Gilbert C FAURE
more...
No comment yet.
Scooped by Krishan Maggon
Scoop.it!

A cell's "self-destruct" function could yield new therapies

A cell's "self-destruct" function could yield new therapies | Melanoma BRAF Inhibitors Review | Scoop.it
Scientists studying cell death are working to understand how the body protects itself from disease and use that information to form better treatments.
more...
No comment yet.
Scooped by Krishan Maggon
Scoop.it!

Evaluation of Two Dosing Regimens for Nivolumab in Combination With Ipilimumab in Patients With Advanced Melanoma: Results From the Phase IIIb/IV CheckMate 511 Trial

Evaluation of Two Dosing Regimens for Nivolumab in Combination With Ipilimumab in Patients With Advanced Melanoma: Results From the Phase IIIb/IV CheckMate 511 Trial | Melanoma BRAF Inhibitors Review | Scoop.it
PURPOSE
Nivolumab 1 mg/kg plus ipilimumab 3 mg/kg (NIVO1+IPI3) is approved for first-line treatment of patients with advanced melanoma in several countries. We conducted a phase IIIb/IV study (CheckMate 511) to determine if nivolumab 3 mg/kg plus ipilimumab 1 mg/kg (NIVO3+IPI1) improves the safety profile of the combination.

PATIENTS AND METHODS
Patients (N = 360) age 18 years or older with previously untreated, unresectable stage III or IV melanoma were randomly assigned 1:1 to NIVO3+IPI1 or NIVO1+IPI3 once every 3 weeks for four doses. After 6 weeks, all patients received NIVO 480 mg once every 4 weeks until disease progression or unacceptable toxicity. The primary end point was a comparison of the incidence of treatment-related grade 3 to 5 adverse events (AEs) between groups. Secondary end points included descriptive analyses of objective response rate, progression-free survival, and overall survival. The study was not designed to formally demonstrate noninferiority of NIVO3+IPI1 to NIVO1+IPI3 for efficacy end points.

RESULTS
At a minimum follow-up of 12 months, incidence of treatment-related grade 3 to 5
more...
No comment yet.
Scooped by Krishan Maggon
Scoop.it!

Roche - Beyond the immunity cycle

Roche - Beyond the immunity cycle | Melanoma BRAF Inhibitors Review | Scoop.it
Roche’s scientists are leading pioneers in immune biology and cancer research, which is resulting in innovative and personalised treatment options in cancer...
more...
No comment yet.
Scooped by Krishan Maggon
Scoop.it!

A sinister black finding in the stomach

A sinister black finding in the stomach | Melanoma BRAF Inhibitors Review | Scoop.it
A 68-year-old woman undergoing a routine surveillance endoscopy—part of her follow-up
for a Barrett's oesophagus—was found to have a solitary, black lesion, approximately
4 mm in diameter, in the gastric body (figure).
more...
No comment yet.
Scooped by Krishan Maggon
Scoop.it!

An Error-Prone Polymerase in the Fight against Cancer - ScienceDirect

An Error-Prone Polymerase in the Fight against Cancer - ScienceDirect | Melanoma BRAF Inhibitors Review | Scoop.it
Error-prone polymerases are alleged to induce mutations while replicating damaged DNA and to increase the risk of cancer. Using in vitro studies and mice models, Yoon et al. (2019) provide evidence that the error-prone Pol θ polymerase protects against ultraviolet light-induced skin cancer despite its mutagenic potential.
more...
No comment yet.
Scooped by Krishan Maggon
Scoop.it!

Comparative efficacy of combination immunotherapy and targeted therapy in the treatment of BRAF-mutant advanced melanoma: a matching-adjusted indirect comparison | Immunotherapy

Aim: Comparison of clinical outcomes of nivolumab + ipilimumab versus BRAF + MEK inhibitors (dabrafenib + trametinib or vemurafenib + cobimetinib) in BRAF-mutant advanced melanoma. Methods: Matching-adjusted indirect comparisons were conducted between nivolumab + ipilimumab (CheckMate 067/069 studies) and BRAF + MEK inhibitors (COMBI-d, COMBI-v and coBRIM studies). Overall survival (OS), progression-free survival and objective response rates were assessed. Results: After adjusting, nivolumab + ipilimumab showed improved OS versus dabrafenib + trametinib (hazard ratio [HR] = 0.64; 95% CI: 0.46–0.89) or vemurafenib + cobimetinib (HR = 0.56; 95% CI: 0.36–0.89); OS outcomes were similar at 1 year, with benefits emerging after 12 months; progression-free survival and objective response rates were similar. Grade 3/4 adverse events occurred in 54.1% with nivolumab + ipilimumab, 31.6% with dabrafenib + trametinib and 59.5% with vemurafenib + cobimetinib. Conclusion: Nivolumab + ipilimumab had significantly improved clinical outcomes versus BRAF + MEK inhibitors, with benefits increasing after longer follow-up. Ongoing randomized trials directly comparing these treatments are necessary to prospectively validate these findings.
more...
No comment yet.
Scooped by Krishan Maggon
Scoop.it!

Leucurogin and melanoma therapy - ScienceDirect

Leucurogin and melanoma therapy - ScienceDirect | Melanoma BRAF Inhibitors Review | Scoop.it
Highlights

Leucurogin is a recombinant ECD disintegrin-like cloned from Bothrops leucurus.


Leucurogin inhibits cellular processes dependent on collagen type I.


Leucurogin inhibits cellular migration, proliferation, adhesion and angiogenesis.


Leucurogin inhibits melanoma growth and metastasis in vivo.


Leucurogin can open a new approach to downstream tumor-cell signaling studies.
more...
No comment yet.
Scooped by Krishan Maggon
Scoop.it!

Alternative Splicing in Tumors — A Path to Immunogenicity? | NEJM

Alternative Splicing in Tumors — A Path to Immunogenicity? | NEJM | Melanoma BRAF Inhibitors Review | Scoop.it
Clinical Implications of Basic Research from The New England Journal of Medicine — Alternative Splicing in Tumors — A Path to Immunogenicity?
more...
No comment yet.
Scooped by Krishan Maggon
Scoop.it!

Quick Take: Association of Disease Recurrence With Survival Outcomes in Patients With Cutaneous Squamous Cell Carcinoma of the Head and Neck Treated With Multimodality Therapy

Quick Take: Association of Disease Recurrence With Survival Outcomes in Patients With Cutaneous Squamous Cell Carcinoma of the Head and Neck Treated With Multimodality Therapy | Melanoma BRAF Inhibitors Review | Scoop.it
Cutaneous squamous cell carcinoma of the head and neck (cSCC-HN) generally has a favorable prognosis, however, there is a subset of patients who experience a...
more...
No comment yet.
Scooped by Krishan Maggon
Scoop.it!

Overcoming Resistance to Dual Innate Immune and MEK Inhibition Downstream of KRAS

Overcoming Resistance to Dual Innate Immune and MEK Inhibition Downstream of KRAS | Melanoma BRAF Inhibitors Review | Scoop.it
Kitajima et al. identify BET-regulated YAP1 upregulation as a mediator of acquired
and intrinsic resistance in KRAS;LKB1 and KRAS;TP53 mutant lung cancer cells, respectively,
to combined TBK1 and MEK inhibition and show that intermittent BET inhibition overcomes
this resistance.
more...
No comment yet.
Scooped by Krishan Maggon
Scoop.it!

Bispecific antibodies are next new thing in cancer immunotherapy

Bispecific antibodies are next new thing in cancer immunotherapy | Melanoma BRAF Inhibitors Review | Scoop.it
Though signs point to bispecifics, like other immunotherapies, eliminating cancer in a small fraction of people, there are hints they could help many more.
more...
No comment yet.
Scooped by Krishan Maggon
Scoop.it!

Local Immune‐Triggered Surface‐Modified Stem Cells for Solid Tumor Immunotherapy - Kim - - Advanced Functional Materials - Wiley Online Library

Here, described are additional treatment strategies that make use of human mesenchymal stem cell (hMSC)‐based local immunotherapeutic agents for the treatment of solid tumors. Dibenzocyclooctyne‐poly(ethylene glycol)‐pheophorbide A conjugates are engineered for cell surface conjugation by copper‐free click chemistry and are subsequently conjugated to hMSC (hMSC‐DPP). hMSC‐DPP can recognize and migrate toward cancer lesions, where they secrete pro‐inflammatory cytokines such as interleukin (IL)‐6, IL‐8, and heat shock protein 70 in pursuance of photodynamic therapy‐mediated cell death. The secreted immune factors trigger interferon gamma, IL‐2, IL‐4, IL‐12, and granulocyte‐macrophage colony‐stimulating factor, resulting in the local accumulation of T cells, B cells, natural killer cells, and antigen presenting cells at the tumor site. Treatment with hMSC‐DPP induces the accumulation of cytokines at the cancer site and minimizes systemic immune‐based side effects. This strategy is expected to increase the vulnerability of cancer cells to immune cells and cytokines, thus aiding in the development of a robust treatment platform for cancer immunotherapy.
more...
No comment yet.
Rescooped by Krishan Maggon from Immunology and Biotherapies
Scoop.it!

Paraneoplastic neurological syndromes in the era of immune-checkpoint inhibitors

Paraneoplastic neurological syndromes in the era of immune-checkpoint inhibitors | Melanoma BRAF Inhibitors Review | Scoop.it
Immunotherapy with immune-checkpoint inhibitors (ICIs) is a new pillar in the treatment of cancer but can a have range of immune-related adverse effects, including some rare neurological toxicities that constitute paraneoplastic neurological syndromes (PNSs). In this Review, the authors provide an overview of PNSs, the associations of these conditions with ICI therapy and recommendations for the prevention and management of ICI-associated PNSs.

Via Gilbert C FAURE
more...
No comment yet.
Scooped by Krishan Maggon
Scoop.it!

IJMS | Free Full-Text | Loss of SR-BI Down-Regulates MITF and Suppresses Extracellular Vesicle Release in Human Melanoma

IJMS | Free Full-Text | Loss of SR-BI Down-Regulates MITF and Suppresses Extracellular Vesicle Release in Human Melanoma | Melanoma BRAF Inhibitors Review | Scoop.it
Melanoma is a skin tumor with a high tendency for metastasis and thus is one of the deadliest cancers worldwide. Here, we investigated the expression of the scavenger receptor class B type 1 (SR-BI), a high-density lipoprotein (HDL) receptor, and tested for its role in melanoma pigmentation as well as extracellular vesicle release. We first analyzed the expression of SR-BI in patient samples and found a strong correlation with MITF expression as well as with the melanin synthesis pathway. Hence, we asked whether SR-BI could also play a role for the secretory pathway in metastatic melanoma cells. Interestingly, gain- and loss-of-function of SR-BI revealed regulation of the proto-oncogene MET. In line, SR-BI knockdown reduced expression of the small GTPase RABB22A, the ESCRT-II protein VPS25, and SNAP25, a member of the SNARE complex. Accordingly, reduced overall extracellular vesicle generation was detected upon loss of SR-BI. In summary, SR-BI expression in human melanoma enhances the formation and transport of extracellular vesicles, thereby contributing to the metastatic phenotype. Therapeutic targeting of SR-BI would not only interfere with cholesterol uptake, but also with the secretory pathway, therefore suppressing a key hallmark of the metastatic program.
more...
No comment yet.
Scooped by Krishan Maggon
Scoop.it!

Tissue-specificity in cancer: The rule, not the exception

Tissue-specificity in cancer: The rule, not the exception | Melanoma BRAF Inhibitors Review | Scoop.it

We are in the midst of a renaissance in cancer genetics. Over the past several decades, candidate-based targeted sequencing efforts provided a steady stream of information on the genetic drivers for certain cancer types. However, with recent technological advances in DNA sequencing, this stream has become a torrent of unbiased genetic information revealing the frequencies and patterns of point mutations and copy number variations (CNVs) across the entire spectrum of cancers. One of the most important observations from this work is that genetic alterations in bona fide cancer drivers (those genes that, when mutated, promote tumorigenesis) show a remarkable spectrum of tissue specificity: Alterations in certain driver genes appear only in cancers derived from one or a few tissue types ([ 1 ][1]). Only a handful of cancer drivers [such as telomerase reverse transcriptase ( TERT ), TP53 , the cyclin-dependent kinase inhibitor 2A ( CDKN2A ) locus, and MYC ] show broad tissue spectrums. Here, we discuss the concept of tissue specificity of genetic alterations in cancer and provide general hypotheses to help explain this biological phenomenon.

Tissue-specific mutational frequencies of both tumor suppressor genes and oncogenes have been observed in sporadic cancers (see the figure). Similarly, individuals with classical inherited cancer predisposition syndromes only develop cancers in certain tissues. Although differences may relate to tissue-specific variation in expression and/or mutability of these genes (in sporadic cancers), it is becoming increasingly clear that the tissue-specificity of oncogenes and tumor suppressor usage is more likely rooted in the underlying biology of tissues ([ 1 ][1]). Understanding how and why distinct genetic alterations promote cancer in one tissue but not another remains an important and enigmatic question in cancer research. Nevertheless, the answer to this conundrum may also hold the key to precision medicine because unlocking the secret of what makes a particular tissue permissive to a specific cancer-causing genetic alteration may also reveal tissue-specific therapeutic vulnerabilities.

Various molecular mechanisms have been invoked to explain the tissue specificity of certain oncogenes and tumor suppressors ([ 1 ][1], [ 2 ][2]). For example, the estrogen receptor ( ESR1 ) gene is highly expressed, and its product controls proliferation and differentiation in the specific organs subject to estrogen-driven cancers, such as ovarian, endometrial, and breast cancer. Alternatively, xeroderma pigmentosum proteins (such as ERCC3 and XPC) are involved in excision repair of DNA damage, and their loss primarily leads to cancers of the skin, an organ that is uniquely exposed to ultraviolet (UV) radiation. Last, each tissue uses a specific regulatory mechanism to promote differentiation and limit stem cell expansion, which can contribute to tumorigenesis. The transcription factor GATA3 is one such example because it regulates breast cell ductal differentiation and its loss is significantly enriched in breast cancers ([ 3 ][3]).


more...
No comment yet.
Scooped by Krishan Maggon
Scoop.it!

A sinister black finding in the stomach

A 68-year-old woman undergoing a routine surveillance endoscopy—part of her follow-up
for a Barrett's oesophagus—was found to have a solitary, black lesion, approximately
4 mm in diameter, in the gastric body (figure).
more...
No comment yet.
Scooped by Krishan Maggon
Scoop.it!

VEGF in Signaling and Disease: Beyond Discovery and Development - ScienceDirect

VEGF in Signaling and Disease: Beyond Discovery and Development - ScienceDirect | Melanoma BRAF Inhibitors Review | Scoop.it
The discovery of vascular endothelial-derived growth factor (VEGF) has revolutionized our understanding of vasculogenesis and angiogenesis during development and physiological homeostasis. Over a short span of two decades, our understanding of the molecular mechanisms by which VEGF coordinates neurovascular homeostasis has become more sophisticated. The central role of VEGF in the pathogenesis of diverse cancers and blinding eye diseases has also become evident. Elucidation of the molecular regulation of VEGF and the transformative development of multiple therapeutic pathways targeting VEGF directly or indirectly is a powerful case study of how fundamental research can guide innovation and translation. It is also an elegant example of how agnostic discovery and can transform our understanding of human disease. This review will highlight critical nodal points in VEGF biology, including recent developments in immunotherapy for cancer and multitarget approaches in neovascular eye disease.

more...
No comment yet.
Scooped by Krishan Maggon
Scoop.it!

A Human Ribonuclease Variant and ERK-Pathway Inhibitors Exhibit Highly Synergistic Toxicity for Cancer Cells

A Human Ribonuclease Variant and ERK-Pathway Inhibitors Exhibit Highly Synergistic Toxicity for Cancer Cells | Melanoma BRAF Inhibitors Review | Scoop.it
Abstract
Pancreatic-type ribonucleases (ptRNases) are prevalent secretory enzymes that catalyze the cleavage of RNA. Ribonuclease inhibitor (RI) is a cytosolic protein that has femtomolar affinity for ptRNases, affording protection from the toxic catalytic activity of ptRNases, which can invade human cells. A human ptRNase variant that is resistant to inhibition by RI is a cytotoxin that is undergoing a clinical trial as a cancer chemotherapeutic agent. We find that the ptRNase and protein kinases in the ERK pathway exhibit strongly synergistic toxicity toward lung cancer cells (including a KRASG12C variant) and melanoma cells (including BRAFV600E variants). The synergism arises from inhibiting the phosphorylation of RI and thereby diminishing its affinity for the ptRNase. These findings link seemingly unrelated cellular processes, and suggest that the use of a kinase inhibitor to unleash a cytotoxic enzyme could lead to beneficial manifestations in the clinic.
more...
No comment yet.
Scooped by Krishan Maggon
Scoop.it!

Non-invasive biomarkers derived from the extracellular matrix associate with response to immune checkpoint blockade (anti-CTLA-4) in metastatic melanoma patients - Nordic Bioscience

Non-invasive biomarkers derived from the extracellular matrix associate with response to immune checkpoint blockade (anti-CTLA-4) in metastatic melanoma patients - Nordic Bioscience | Melanoma BRAF Inhibitors Review | Scoop.it
BACKGROUND: Excessive extracellular matrix (ECM) remodeling and a reactive stroma can affect T-cell infiltration and T-cell activity in the tumor and hereby influence response to immune checkpoint inhibitors (ICI). In the pursuit of finding biomarkers that predict treatment response, we evaluated the association between serum biomarkers of collagen and vimentin turnover and outcomes in metastatic melanoma patients treated with the anti-CTLA-4 antibody ipilimumab (IPI). METHODS: Type III collagen formation (PRO-C3), MMP-degraded type I, type III and type IV collagens (C1M, C3M and C4M), and citrullinated and MMP-degraded vimentin (VICM) were measured with ELISAs in serum from metastatic melanoma patients before (n = 66) and 3 weeks after (n = 52) initiation of IPI treatment. Biomarker levels were associated with Disease Control Rate (DCR) and survival outcomes. RESULTS: We found that baseline levels of PRO-C3 (p = 0.011), C1M (p = 0.003), C3M (p = 0.013) and C4M (p = 0.027) were significantly elevated in patients with progressive disease (PD). Univariate Cox regression analysis identified high PRO-C3 (p = 0.021) and C4M (p = 0.008) as predictors of poor overall survival (OS) and the biomarkers remained significant when evaluated with other covariates (PRO-C3 (p = 0.049) and C4M (p = 0.046)). Multivariate analysis identified VICM as a predictor of longer OS (p = 0.026). Similarly, a high C3M/PRO-C3 ratio predicted for increased OS (p = 0.034). Only C3M (p = 0.003) and VICM (p < 0.0001) increased 3 weeks after treatment. CONCLUSIONS: ECM and tissue remodeling quantified in pre-treatment serum were associated with response and survival outcomes in metastatic melanoma patients treated with IPI. This highlights the importance of addressing the ECM and stromal component non-invasively in future ICI studies. Go to full publication
more...
No comment yet.
Scooped by Krishan Maggon
Scoop.it!

Clinical spectrum of cutaneous melanoma morphology - ScienceDirect

Clinical spectrum of cutaneous melanoma morphology - ScienceDirect | Melanoma BRAF Inhibitors Review | Scoop.it
Background
Melanoma can mimic other cutaneous lesions, but the full spectrum and prevalence of these morphologic variants remain largely unknown.

Objective
To classify nonacral cutaneous melanomas into distinct morphologic clusters and characterize clusters’ clinicopathologic features.

Methods
All pathologic melanoma diagnoses (occurring during 2011-2016) were reviewed for routine prebiopsy digital photographs (n = 400). Six dermatologists independently assigned lesions into 1 of 14 diagnostic classes on the basis of morphology. Image consensus clusters were generated by K-means; clinicopathologic features were compared with analysis of variance and χ2.

Results
Five morphologic clusters were identified: typical (n = 136), nevus-like (n = 81), amelanotic/nonmelanoma skin cancer (NMSC)–like (n = 70), seborrheic keratosis (SK)–like (n = 68), and lentigo/lentigo maligna (LM)–like (n = 45) melanomas. Nevus-like melanomas were found in younger patients. Nevus-like and lentigo/LM-like melanomas tended to be thinner and more likely identified on routine dermatologic examinations. NMSC-like melanomas were tender, thicker, more mitotically active, and associated with prior NMSC. Typical and SK-like melanomas had similar clinicopathologic features.

Limitations
Cluster subdivision yielded diminished sample sizes. Visual assignment was performed without clinical context.

Conclusion
When primary cutaneous melanomas were assigned into diagnostic groups and subjected to novel consensus clustering, recurrent morphologic patterns emerged. The spectrum of these morphologies was unexpectedly diverse, which might have implications for visual training and possibly clinical diagnosis.
more...
No comment yet.
Scooped by Krishan Maggon
Scoop.it!

Structure-based design of small-molecule inhibitors of EBNA1 DNA binding blocks Epstein-Barr virus latent infection and tumor growth

Structure-based design of small-molecule inhibitors of EBNA1 DNA binding blocks Epstein-Barr virus latent infection and tumor growth | Melanoma BRAF Inhibitors Review | Scoop.it
Persistent latent infection with Epstein-Barr virus contributes to tumorigenesis in a variety of cancer types. The only viral protein that is consistently expressed in these tumors is Epstein-Barr nuclear antigen 1, which performs a variety of biological functions. To target this antigen, Messick et al. designed a series of chemical inhibitors and then tested them in vitro and in multiple mouse models of Epstein-Barr virus–associated cancer. The authors characterized the inhibitors using a variety of assays, examined the mechanism by which they work, and demonstrated preclinical effectiveness and suitable pharmacological properties, paving the way for further therapeutic development.

Epstein-Barr virus (EBV) is a DNA tumor virus responsible for 1 to 2% of human cancers including subtypes of Burkitt’s lymphoma, Hodgkin’s lymphoma, gastric carcinoma, and nasopharyngeal carcinoma (NPC). Persistent latent infection drives EBV-associated tumorigenesis. Epstein-Barr nuclear antigen 1 (EBNA1) is the only viral protein consistently expressed in all EBV-associated tumors and is therefore an attractive target for therapeutic intervention. It is a multifunctional DNA binding protein critical for viral replication, genome maintenance, viral gene expression, and host cell survival. Using a fragment-based approach and x-ray crystallography, we identify a 2,3-disubstituted benzoic acid series that selectively inhibits the DNA binding activity of EBNA1. We characterize these inhibitors biochemically and in cell-based assays, including chromatin immunoprecipitation and DNA replication assays. In addition, we demonstrate the potency of EBNA1 inhibitors to suppress tumor growth in several EBV-dependent xenograft models, including patient-derived xenografts for NPC. These inhibitors selectively block EBV gene transcription and alter the cellular transforming growth factor–β (TGF-β) signaling pathway in NPC tumor xenografts. These EBNA1-specific inhibitors show favorable pharmacological properties and have the potential to be further developed for the treatment of EBV-associated malignancies.
more...
No comment yet.
Scooped by Krishan Maggon
Scoop.it!

A new paradigm in vaccines and cancer treatments N4 Pharma

A new paradigm in vaccines and cancer treatments N4 Pharma | Melanoma BRAF Inhibitors Review | Scoop.it
Specialist pharmaceutical company N4 Pharma is developing Nuvec, a unique non-viral adjuvant delivery system for vaccines and cancer treatments. This silica nanoparticle has the potential to help commercialise cancer immunotherapy drugs and improve the effectiveness of viral vaccines.

 

Nuvec® is an engineered silica nanoparticle, which has been designed for the intracellular delivery of large nucleic acids such as pDNA and mRNA and is in the advanced research phase.

more...
No comment yet.
Scooped by Krishan Maggon
Scoop.it!

Primitive Cancer Cell States: A Target for Drug Screening?

At present, most drug screening efforts employ bulk cancer cell populations, which
may lead to selection of the more drug-resistant cancer stem cells (CSCs). However,
drug screening using CSCs has been limited, mainly owing to the difficulty of their
isolation. This article discusses how methods of reprogramming cancer cells to primitive
cancer cell states, such as transcription factor reprogramming, epithelial–mesenchymal
transition (EMT), conditional reprogramming, and hypoxia, may approach the CSC state
and thus be relevant for drug screening purposes.
more...
No comment yet.