Melanoma BRAF Inhibitors Review
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The Janus Face of NKT Cell Function in Autoimmunity and Infectious Diseases

The Janus Face of NKT Cell Function in Autoimmunity and Infectious Diseases | Melanoma BRAF Inhibitors Review | Scoop.it
Natural killer T cells (NKT) are a subset of T lymphocytes bridging innate and adaptive immunity. These cells recognize self and microbial glycolipids bound to non-polymorphic and highly conserved CD1d molecules. Three NKT cell subsets, type I, II, and NKT-like expressing different antigen receptors (TCR) were described and TCR activation promotes intracellular events leading to specific functional activities. NKT can exhibit different functions depending on the secretion of soluble molecules and the interaction with other cell types. NKT cells act as regulatory cells in the defense against infections but, on the other hand, their effector functions can be involved in the pathogenesis of several inflammatory disorders due to their exposure to different microbial or self-antigens, respectively. A deep understanding of the biology and functions of type I, II, and NKT-like cells as well as their interplay with cell types acting in innate (neuthrophils, innate lymphoid cells, machrophages, and dendritic cells) and adaptive immunity (CD4+,CD8+, and double negative T cells) should be important to design potential immunotherapies for infectious and autoimmune diseases.
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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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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.
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Baseline Tumor Size Is an Independent Prognostic Factor for Overall Survival in Patients with Melanoma Treated with Pembrolizumab

Baseline Tumor Size Is an Independent Prognostic Factor for Overall Survival in Patients with Melanoma Treated with Pembrolizumab | Melanoma BRAF Inhibitors Review | Scoop.it
Purpose: The purpose of this study was to assess the association of baseline tumor size (BTS) with other baseline clinical factors and outcomes in pembrolizumab-treated patients with advanced melanoma in KEYNOTE-001 ([NCT01295827][1]).
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The nephrotoxicity of immune checkpoint inhibitor–based combinations

The nephrotoxicity of immune checkpoint inhibitor–based combinations | Melanoma BRAF Inhibitors Review | Scoop.it
Immune checkpoint inhibitors (ICIs) have unveiled a new era in the treatment of cancer
with unprecedented survival data in multiple tumours [1]. However, there remain a number of patients with only mediocre responses to ICIs, which prompted the investigation of ICI-based combinations to circumvent...
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Neoadjuvant versus adjuvant ipilimumab plus nivolumab in macroscopic stage III melanoma

Neoadjuvant versus adjuvant ipilimumab plus nivolumab in macroscopic stage III melanoma | Melanoma BRAF Inhibitors Review | Scoop.it
Abstract
Adjuvant ipilimumab (anti-CTLA-4) and nivolumab (anti-PD-1) both improve relapse-free survival of stage III melanoma patients1,2. In stage IV disease, the combination of ipilimumab + nivolumab is superior to ipilimumab alone and also appears to be more effective than nivolumab monotherapy3. Preclinical work suggests that neoadjuvant application of checkpoint inhibitors may be superior to adjuvant therapy4. To address this question and to test feasibility, 20 patients with palpable stage III melanoma were 1:1 randomized to receive ipilimumab 3 mg kg−1 and nivolumab 1 mg kg−1, as either four courses after surgery (adjuvant arm) or two courses before surgery and two courses postsurgery (neoadjuvant arm). Neoadjuvant therapy was feasible, with all patients undergoing surgery at the preplanned time point. However in both arms, 9/10 patients experienced one or more grade 3/4 adverse events. Pathological responses were achieved in 7/9 (78%) patients treated in the neoadjuvant arm. None of these patients have relapsed so far (median follow-up, 25.6 months). We found that neoadjuvant ipilimumab + nivolumab expand more tumor-resident T cell clones than adjuvant application. While neoadjuvant therapy appears promising, with the current regimen it induced high toxicity rates; therefore, it needs further investigation to preserve efficacy but reduce toxicity.
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The protein kinase p38α destabilizes p63 to limit epidermal stem cell frequency and tumorigenic potential

The protein kinase p38α destabilizes p63 to limit epidermal stem cell frequency and tumorigenic potential | Melanoma BRAF Inhibitors Review | Scoop.it
Loss of p38α in mice leads to hyperplasia and tumor development in epithelial tissues. Choo et al . analyzed skin tissue and cells from normal donors, patients with premalignant keratosis or squamous cell carcinoma (SCC), and mouse models and found that p38α phosphorylated and consequently induced the degradation of the transcription factor p63, particularly that of its tumor-associated isoform ΔNp63α. Loss of p38α increased p63 abundance in the skin and thereby enhanced the expression of stem cell–associated genes, repressed the expression of a tumor-suppressive metalloprotease, and promoted stem cell outgrowth in the skin. The findings also raise the possibility that p38α inhibitors used to treat other cancers (where p38α is tumor promotive) may cause secondary SCC in patients.

The molecular circuitry directing tissue development and homeostasis is hardwired by genetic programs but may also be subject to fine-tuning or major modification by environmental conditions. It remains unclear whether such malleability is at work—particularly in tissues directly in contact with the environment—and contributes to their optimal maintenance and resilience. The protein kinase p38α is activated by physiological cues that signal tissue damage and neoplastic transformation. Here, we found that p38α phosphorylated and thereby destabilized p63, a transcription factor essential for epidermal development. Through this regulatory mechanism, p38α limited the frequency of keratinocytes with stem cell properties and tumorigenic potential. Correspondingly, epidermal loss of p38α expression or activity promoted or correlated with carcinogenesis in mouse and human skin, respectively. Genetic mouse models revealed a tumorigenic mechanism from p38α loss through p63-mediated suppression of the matrix metalloprotease MMP13. These findings illustrate a previously uncharacterized epidermal tumor–suppressive mechanism in which stress-activated signaling induces the contraction of stem cell–like keratinocyte pools.
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Cancer patients with rare deadly brain infection treated successfully with off-the-shelf adoptive T-cell therapy

Cancer patients with rare deadly brain infection treated successfully with off-the-shelf adoptive T-cell therapy | Melanoma BRAF Inhibitors Review | Scoop.it
An emerging treatment known as adoptive T-cell therapy has proven effective in a Phase II clinical trial for treating progressive multifocal leukoencephalopathy (PML), a rare and often fatal brain infection sometimes observed ...
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Reprogramming normal human epithelial tissues to a common, lethal neuroendocrine cancer lineage

Reprogramming normal human epithelial tissues to a common, lethal neuroendocrine cancer lineage | Melanoma BRAF Inhibitors Review | Scoop.it
Epithelial cancers develop resistance to targeted therapies in a number of different ways. Several cancer types do so by undergoing phenotypic conversion to a highly aggressive cancer called small cell neuroendocrine carcinoma (SCNC). Whether distinct cancer types accomplish this “reprogramming” through the same mechanism has been unclear. Park et al. show that the same set of oncogenic factors transforms both normal lung and normal prostate epithelial cells into SCNCs that resemble clinical samples (see the Perspective by Kareta and Sage). This convergence of molecular pathways could potentially simplify the development of new therapies for SCNC, which is currently untreatable.

Science , this issue p. [91][1]; see also p. [30][2]

The use of potent therapies inhibiting critical oncogenic pathways active in epithelial cancers has led to multiple resistance mechanisms, including the development of highly aggressive, small cell neuroendocrine carcinoma (SCNC). SCNC patients have a dismal prognosis due in part to a limited understanding of the molecular mechanisms driving this malignancy and the lack of effective treatments. Here, we demonstrate that a common set of defined oncogenic drivers reproducibly reprograms normal human prostate and lung epithelial cells to small cell prostate cancer (SCPC) and small cell lung cancer (SCLC), respectively. We identify shared active transcription factor binding regions in the reprogrammed prostate and lung SCNCs by integrative analyses of epigenetic and transcriptional landscapes. These results suggest that neuroendocrine cancers arising from distinct epithelial tissues may share common vulnerabilities that could be exploited for the development of drugs targeting SCNCs.

[1]: /lookup/volpage/362/91?iss=6410
[2]: /lookup/doi/10.1126/science.aav1044
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Cancer immunotherapy pioneers win 2018 Nobel Prize in Physiology or Medicine

Cancer immunotherapy pioneers win 2018 Nobel Prize in Physiology or Medicine | Melanoma BRAF Inhibitors Review | Scoop.it
The 2018 Nobel Prize in Physiology or Medicine has been awarded to two researchers whose discoveries opened up a new field of cancer therapy based on unleashing the immune system to attack tumors....
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Allison Reflects on a Career in Immunology, Nobel Prize

Allison Reflects on a Career in Immunology, Nobel Prize | Melanoma BRAF Inhibitors Review | Scoop.it
James P. Allison, PhD, reflects on his research in immunology, the impact it has had on patients with cancer, and where the field is headed.
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Are Personalized Vaccines Part of a New Combination Approach to Treating Melanoma?

Are Personalized Vaccines Part of a New Combination Approach to Treating Melanoma? | Melanoma BRAF Inhibitors Review | Scoop.it
Bracing for cold weather and the threat of runny noses and sore throats, millions of Americans are vaccinated for the flu each year. By priming the immune system, the vaccine reduces the risk of catching the flu and, if not successful at preventing it altogether, reduces both the severity and...
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Age-related changes in skin structure and lymphatic system promote melanoma metastasis

Age-related changes in skin structure and lymphatic system promote melanoma metastasis | Melanoma BRAF Inhibitors Review | Scoop.it
Changes in the structure of the skin and the lymphatic system that occur with the natural aging process create permissive conditions for melanoma metastasis, according to two studies by The Wistar Institute.
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Checkpoint inhibition in practice and in public. Checkpoint inhibition in practice and in public. Oncology videos for healthcare professionals - ecancer

Dr Christy Ralph - St. James's Institute of Oncology, Leeds, UK Dr Ralph speaks with ecancer at the ACP immunotherapy workshop about the implementation of checkpoint inhibitor therapy for cancer patients. She notes successes for checkpoint therapy in different disease indications, and considers how clinical data from these may inform development for other diseases where checkpoint inhibitors have yet to improve outcomes. Dr Ralph also considers the challenges facing the UK approvals agency NICE in managing availability and suitability of expensive drugs for sometimes rare disease or patient subtypes, and the role of doctors in communicating with, and on behalf of, patients when incomplete science enters public awareness.
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FDA Approves Libtayo® (cemiplimab-rwlc, Sanofi, Regeneron) as First and Only Treatment for Advanced Cutaneous Squamous Cell Carcinoma

FDA Approves Libtayo® (cemiplimab-rwlc, Sanofi, Regeneron) as First and Only Treatment for Advanced Cutaneous Squamous Cell Carcinoma | Melanoma BRAF Inhibitors Review | Scoop.it

Regeneron Pharmaceuticals, Inc. (NASDAQ: REGN) and Sanofi today announced that the U.S. Food and Drug Administration (FDA) has approved Libtayo® (cemiplimab-rwlc) for the treatment of patients with metastatic cutaneous squamous cell carcinoma (CSCC) or locally advanced CSCC who are not candidates for curative surgery or curative radiation. Libtayo is a fully-human monoclonal antibody targeting the immune checkpoint receptor PD-1 (programmed cell death protein-1) and is the first and only treatment specifically approved and available for advanced CSCC in the U.S.

 

CSCC is the second most common form of skin cancer and is responsible for an estimated 7,000 deaths each year in the U.S. It currently accounts for approximately 20% of all skin cancers in the U.S., with the number of newly diagnosed cases expected to rise annually. When CSCC invades deeper layers of the skin or adjacent tissues, it is categorized as locally advanced. Once it spreads to other distant parts of the body, it is considered metastatic.

 

In addition to advanced CSCC, cemiplimab-rwlc is being investigated in trials in non-small cell lung cancer, basal cell carcinoma, and cervical cancer along with trials in squamous cell carcinoma of the head and neck, melanoma, colorectal cancer, prostate cancer, multiple myeloma, Hodgkin lymphoma and non-Hodgkin lymphoma. These potential uses are investigational, and their safety and efficacy have not been evaluated by any regulatory authority.

 

 

Krishan Maggon 's insight:

Libtayo was evaluated by the FDA under Priority Review, which is reserved for medicines that represent significant improvements in safety or efficacy in treating serious conditions, and in 2017 was granted Breakthrough Therapy Designation status for advanced CSCC. 

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PhRMA: List of 2018 Medicines in Development                 48 for melanoma, 69 skin cancer and 300 for Skin Disease  

PhRMA: List of 2018 Medicines in Development                 48 for melanoma, 69 skin cancer and 300 for Skin Disease   | Melanoma BRAF Inhibitors Review | Scoop.it
More than 300 medicines to treat skin diseases are in development
by biopharmaceutical research companies to help more than 100 million Americans affected by a broad range of skin conditions.

 

48 new drugs in development for melanoma and metastatic refractory melanoma.

69 drugs in development for skin cancer and over 300 for skin diseases

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Thyroiditis and immune check point inhibitors: the post‐marketing experience using the French National Pharmacovigilance database - Garon‐Czmil - - Fundamental & Clinical Pharmacology - Wiley O...

Abstract
Immunotherapy with immune checkpoint inhibitors (ICIs) for cancer has become increasingly prescribed in recent years. Indeed, it is used to treat both solid and hematological malignancies due to their considerable potential in treating melanoma, non‐small cell lung and other cancers. Immune‐mediated related adverse endocrine toxicity, and especially thyroiditis, are seen as a growing problem needing specific screening and management. This study aims at describing thyroid dysfunctions induced by the ICIs marketed in France, which are registered in the French Pharmacovigilance database. This database was queried for nivolumab, pembrolizumab and ipilimumab‐induced adverse drug reactions reported before 30 April 2017. Both a pharmacologist and an endocrinologist have reviewed each case to select only those of peripheral thyroiditis (thyrotoxicosis and hypothyroidism). During this period, 110 thyroiditis following ICI therapy were reported. Sex/ratio was around one. Most of the cases (47·2%) were asymptomatic. Although some thyrotoxicosis cases were severe, no orbitopathy was reported. Hypothyroidism and thyrotoxicosis were equally described. Antithyroid antibodies were positive in only 16% patients. The ultrasonography was informative in 19% patients. Levothyroxine supplementation was necessary in 57% patients, leading to 19% recovery. With a dedicated optimized management, most of the cases did not require immunotherapy discontinuation. Finally, immune‐mediated related thyroiditis are increasing due to a wider prescription of ICI therapy in various cancer conditions and systematic screening. Often asymptomatic, they lead to a local activation accompanied by hormonal deficiency in the long run. It is necessary to carry out an early and sustained multidisciplinary screening to allow immunotherapy continuation.
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Predictive and on-treatment monitoring biomarkers in advanced melanoma: Moving toward personalized medicine - ScienceDirect

Predictive and on-treatment monitoring biomarkers in advanced melanoma: Moving toward personalized medicine - ScienceDirect | Melanoma BRAF Inhibitors Review | Scoop.it
Highlights

Validated biomarkers predictive for response to therapy are needed in melanoma.


Baseline immune biomarkers are emerging to personalize therapeutic decisions.


On-treatment ctDNA analysis may provide early evidence of response and progression.
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Immune-mediated neuropathies

Immune-mediated neuropathies | Melanoma BRAF Inhibitors Review | Scoop.it
Abstract
Since the discovery of an acute monophasic paralysis, later coined Guillain–Barré syndrome, almost 100 years ago, and the discovery of chronic, steroid-responsive polyneuropathy 50 years ago, the spectrum of immune-mediated polyneuropathies has broadened, with various subtypes continuing to be identified, including chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) and multifocal motor neuropathy (MMN). In general, these disorders are speculated to be caused by autoimmunity to proteins located at the node of Ranvier or components of myelin of peripheral nerves, although disease-associated autoantibodies have not been identified for all disorders. Owing to the numerous subtypes of the immune-mediated neuropathies, making the right diagnosis in daily clinical practice is complicated. Moreover, treating these disorders, particularly their chronic variants, such as CIDP and MMN, poses a challenge. In general, management of these disorders includes immunotherapies, such as corticosteroids, intravenous immunoglobulin or plasma exchange. Improvements in clinical criteria and the emergence of more disease-specific immunotherapies should broaden the therapeutic options for these disabling diseases.
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Biomarkers, Novel Combinations Key to Improving Response to Immunotherapy

Biomarkers, Novel Combinations Key to Improving Response to Immunotherapy | Melanoma BRAF Inhibitors Review | Scoop.it
In a roundtable discussion at the 2018 International Cancer Immunotherapy Conference, Nobel Prize Winner James P. Allison, MD, and other experts discussed the research that is still necessary to bring immunotherapy response rates to 100%.
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Neoadjuvant combination checkpoint blockade trial yields high response rates for patients with stage 3 melanoma

Neoadjuvant combination checkpoint blockade trial yields high response rates for patients with stage 3 melanoma | Melanoma BRAF Inhibitors Review | Scoop.it
Combination checkpoint blockade before surgery (neoadjuvant therapy) produced a high response rate among patients with high-risk stage 3 melanoma, with nearly half having no sign of disease at surgery, but a high incidence ...
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Bill Nemitz: Two miracle workers win Nobel and save my life - Portland

Bill Nemitz: Two miracle workers win Nobel and save my life - Portland | Melanoma BRAF Inhibitors Review | Scoop.it
James P. Allison and Tasuku Honjo laid the groundwork for a new generation of immunotherapy drugs that offer hope to cancer patients who previously had none.
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The biology and treatment of Merkel cell carcinoma: current understanding and research priorities

The biology and treatment of Merkel cell carcinoma: current understanding and research priorities | Melanoma BRAF Inhibitors Review | Scoop.it
Merkel cell carcinoma (MCC) is a rare and aggressive form of nonmelanoma skin cancer. The availability of immune checkpoint inhibition has improved the outcomes of a subset of patients with MCC, although many unmet needs continue to exist.
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CAR‐T cell therapy in melanoma: a future success story? - Simon - - Experimental Dermatology - Wiley Online Library

Chimeric antigen receptor (CAR)‐T cells are one of the impressive recent success stories of anti‐cancer immunotherapy. Especially in hematological malignancies this treatment strategy has shown promising results leading to the recent approval of two CAR‐T cell constructs targeting CD19 in the United States and the European Union. After the huge success in hematological cancers, the next step will be the evaluation of its efficacy in different solid tumors, which is currently investigated in preclinical as well as clinical settings. A commonly examined tumor model in the context of immunotherapy is melanoma, since it is known for its immunogenic features. However, first results of CAR‐T cell therapy in solid tumors did not reveal the same impressive outcomes that were observed in hematological malignancies, as engineered cells need to cope with several challenges. Obstacles include the lack of migration of CAR‐T cells from blood vessels to the tumor site as well as the immunosuppressive tumor microenvironment within solid tumors. Another hurdle is posed by the identification of an ideal target antigen to avoid on‐target/off‐tumor toxicities. Regarding immune escape mechanisms, which can be developed by tumor cells to by‐pass immune recognition, the observation of antigen loss should also be considered. This article gives an overview of the challenges displayed in CAR‐T cell therapy for the use in solid tumors and discusses different new strategies and approaches that deal with these problems in order to improve CAR‐T cell therapy, particularly for its use in melanoma. This article is protected by copyright. All rights reserved.
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The immuno man

The immuno man | Melanoma BRAF Inhibitors Review | Scoop.it
A blues-loving scientist from a small town in South Texas shook off the immunotherapy naysayers and made believers out of everyone Back in 1977, James Allison arrived at MD Anderson's Science Park in Smithville, Texas, with an itch to discover something new. It was the music-loving, harmonica-playing scientist's first faculty position, and he was happy to be near Austin, his favorite city. There was no way of knowing then, but Allison's initial research on the immune system at MD Anderson laid the groundwork for his return in 2012 as the father of immune checkpoint blockade — an entirely new way of treating cancer that’s yielding unprecedented results. Thanks to his clinical collaborators, he's been fortunate enough to meet some of those saved by his drug, ipilimumab (Yervoy®), the first ever to improve survival for patients with advanced melanoma. According to American Cancer Society predictions, the disease will kill more than 9,700 people in the U.S. in 2014. One of the most dramatic stories belongs to an original phase I clinical trial patient in Los Angeles. "The patient just wanted to live long enough to see her teenage sons graduate from high school," says Allison, chair of Immunology. "That was 14 years ago. She's lived to see them go to college, go to graduate school, start their own families and get established in their careers …" His voice trails off and his eyes mist. "I get emotional talking about them. That's what it’s all about." The basic science behind success   The journey from Allison's laboratory research at MD Anderson to Food and Drug Administration approval of ipilimumab for metastatic melanoma in 2011 was arduous and often frustrating. It included stops at other prestigious research institutions such as the Cancer Research Laboratory at the University of California, Berkeley, and Memorial Sloan Kettering Cancer Center, the travails of drug development and the quirks of pharmaceutical companies and clinical trials. "Jim has great scientific intuition and he's stubborn — or maybe persistent is a better word. He tells you exactly what he thinks," Patrick Hwu, M.D., says of Allison, who goes by Jim. "He had the vision to see the research through to a paradigm changing treatment strategy," adds Hwu, chair of Melanoma Medical Oncology, who's both a scientific and musical collaborator of Allison. "I truly appreciate what he's done for my patients." Follow-up studies show an unprecedented 22% of late-stage melanoma patients treated in ipilimumab clinical trials survived for at least four years. Meanwhile, checkpoint blockade is being extended to treat other cancers, and the journal Science named cancer immunotherapy its 2013 Breakthrough of the Year. Allison lost his mother to lymphoma when he was 11 years old and a brother later on to prostate cancer, a disease he himself has survived. "My family has suffered greatly from the ravages of cancer, so cancer treatment has always been in the back of my mind," he says. "But I didn't set out to develop a cancer treatment. If I had, I probably would have missed something important because the target we found isn’t on tumors, it's on T cells," Allison says. "Checkpoint blockade emerged as a cancer therapy only because we first uncovered the basic science and biology of T cells, the immune system's primary attack cells. It's a classic example of how understanding basic science can lead to new disease treatments." Allison's return to MD Anderson in November of 2012 came with a $10 million recruitment grant from the Cancer Prevention and Research Institute of Texas and an MD Anderson commitment of $30 million to develop an immunotherapy program that Allison says is unmatched in its scientific and clinical capabilities. "Immunotherapy is the most exciting and promising area of cancer research today, and its potential is just beginning to be realized," says MD Anderson President Ron DePinho, M.D. "We’re proud to have Jim leading our efforts to expand and hone this approach as executive director of MD Anderson's Moon Shots Program immunotherapy platform." Allison, who's encountered a lot of immunotherapy naysayers over the years, acknowledges DePinho's commitment to advancing the treatment. "Ron is the first cancer center leader to say 'we're really getting into this big,'" he says. "I wouldn’t be here without him."
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Dual Src and MEK Inhibition Decreases Ovarian Cancer Growth and Targets Tumor Initiating Stem-Like Cells

Dual Src and MEK Inhibition Decreases Ovarian Cancer Growth and Targets Tumor Initiating Stem-Like Cells | Melanoma BRAF Inhibitors Review | Scoop.it
Purpose: Rational targeted therapies are needed for treatment of ovarian cancers. Signaling kinases Src and MAPK are activated in high-grade serous ovarian cancer (HGSOC). Here, we tested the frequency of activation of both kinases in HGSOC and the therapeutic potential of dual kinase inhibition.
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Cancer immunologists scoop medicine Nobel prize

Cancer immunologists scoop medicine Nobel prize | Melanoma BRAF Inhibitors Review | Scoop.it
James Allison and Tasuku Honjo pioneered treatments that unleash the body’s own immune system to attack cancer cells.
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Pathologists meet their match in tumour-spotting algorithm : Research Highlights

Pathologists meet their match in tumour-spotting algorithm : Research Highlights | Melanoma BRAF Inhibitors Review | Scoop.it
Artificial-intelligence technology that examines images of lung tissue can identify two common lung cancers just as well as pathologists do.

A team led by Narges Razavian and Aristotelis Tsirigos at the New York University School of Medicine trained and tested a convolutional neural network — a deep-learning algorithm that is adept at processing images — on 1,634 images of cancerous and healthy lung tissue. The algorithm identified healthy cases and distinguished as accurately as three pathologists between two common types of lung cancer: adenocarcinoma and squamous-cell carcinoma.

The researchers also trained the network on adenocarcinoma images that had been labelled with the mutations underlying the cancer. After this training, the algorithm was able to accurately predict the mutations associated with some unlabelled images.

If the algorithm were trained on further labelled images, it might be able to identify adenocarcinomas’ mutations with greater accuracy, the researchers say. That could improve this tumour’s treatment, which is often tailored to the underlying mutation.

Nature Med. (2018)
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