Press Review (September 29, 2012) – Revue de presse (29 septembre 2012)

Bizarre, Recurrent Cancer Case May Lead to Custom Care

It’s a medical nightmare: a 24-year-old man endures 350 surgeries since childhood to remove growths that keep coming back in his throat and have spread to his lungs, threatening his life. Now doctors have found a way to help him by way of a scientific coup that holds promise for millions of cancer patients.

By Marilynn Marchionne. In TIME

http://healthland.time.com/2012/09/27/bizarre-recurrent-cancer-case-may-lead-to-custom-care/

Health Buzz: Breast Cancer Analysis Shows 4 Types of the Disease

Researchers at the University of Washington have made progress in understanding and, hopefully, treating breast cancer. In a study published Sunday in the journal Nature, researchers identified four genetically distinct forms of breast cancer.

In U.S. News & World Report

http://health.usnews.com/health-news/articles/2012/09/25/health-buzz-breast-cancer-analysis-shows-4-types-of-the-disease

Genes May Influence Impotence After Prostate Radiation

Preliminary research suggests genetic analysis might help men assess their risk.

By Steven Reinberg. In U.S. News & World Report

http://health.usnews.com/health-news/news/articles/2012/09/27/genes-may-influence-impotence-after-prostate-radiation

Doubt About Ovarian Cancer Screening

“As an advocate for women with ovarian cancer, I know that it is never easy to tell someone that screening for this disease does more harm than good (“Ovarian Cancer Screenings Have No Benefit, Panel Says, and Some Risks,” news article, Sept. 11). Yet that is what the evidence tells us and what the United States Preventive Services Task Force has confirmed”.

In The New York Times

http://www.nytimes.com/2012/09/21/opinion/doubt-about-ovarian-cancer-screening.html?_r=0

Scientists find marijuana compound fights cancer‎‎

Scientists at California Pacific Medical Center in San Francisco have discovered that cannabidiol has the ability of switching off DNA that cause some cancers to spread.

By David Joseph. In Examiner

http://www.examiner.com/article/scientists-find-marijuana-compound-fights-cancer

Study Links Another Gene Variant to Male Breast Cancer

Finding offers insight into causes of disease that kills several hundred men in US each year.

By Randy Dotinga. In U.S. News & World Report

http://health.usnews.com/health-news/news/articles/2012/09/23/study-links-another-gene-variant-to-male-breast-cancer

Prostate cancer diagnosis and surgery can lead to anxiety, depression and reduced quality of life‎

Men who undergo surgical removal of prostate cancer can experience significant levels of anxiety one year after surgery, and higher levels of anxiety appear to be linked to poor sexual satisfaction and depression, say researchers at Mayo Clinic's campus in Florida. Their recent study, published in the online edition of Psycho-Oncology, suggests that men who experience high levels of "cancer-specific anxiety" following surgery for prostate cancer could likely benefit from counseling designed to address their worries and improve their quality of life

In Medical Xpress

http://medicalxpress.com/news/2012-09-prostate-cancer-diagnosis-surgery-anxiety.html

Prévenir le cancer par l'ablation des seins et des ovaires

Anne Robert, une violoniste de 49 ans, a dû faire un choix de vie déchirant en 2010. Comme les risques de développer un cancer étaient trop grands chez elle, elle a choisi l'ablation des seins et des ovaires, à titre préventif.

Dans Canoë

http://fr.canoe.ca/artdevivre/bienetre/article1/2012/09/27/20237676-qmi.html

Traitement anti-cancer: des interactions dangereuses avec les médicaments‎‎

Une étude de l'université de Rotterdam révèle que près de la moitié des patients cancéreux qui y ont participé avalent, sans le savoir, des médicaments qui sont contre-indiqués dans le cadre d'une chimiothérapie ou d'un autre traitement anti-cancer.

Dans RTBF

http://www.rtbf.be/info/societe/detail_traitement-anti-cancer-des-interactions-dangereuses-avec-les-medicaments?id=7845724

Cancer de la prostate : les autotests de dosage du PSA interdits

Les dispositifs médicaux d’autodiagnostic par dosage du PSA (Prostate specific Antigen) sont désormais interdits en France. L’Agence nationale de Sécurité du Médicament et des Produits de Santé (ANSM) vient de l’annoncer.

Dans Destination Santé

http://www.destinationsante.com/Cancer-de-la-prostate-les-autotests-de-dosage-du-PSA-interdits.html

Cancer du sein infiltrant non métastatique, recommandations professionnelles (INCa)‎

L'Institut national du cancer (INCa) et la Société française de Sénologie et de Pathologie Mammaire (SFSPM) ont publié en juillet 2012 des recommandations professionnelles concernant la prise en charge thérapeutique du cancer du sein infiltrant non métastatique. Elles visent à compléter les recommandations nationales sur le cancer du sein in situ publiées par l'INCa en décembre 2009, et répondent à différentes questions et cas problématiques relatifs au traitement de cette forme de cancer du sein.

Dans CommentCaMarche.net

http://sante-medecine.commentcamarche.net/faq/7738-cancer-du-sein-infiltrant-non-metastatique-recommandations-professionnelles-inca

Le cancer, trop mortel dans les films?

Une étude prétend que ce qui est démontré dans les films et séries en matière de cancer ne représente pas la réalité.

Dans Canoë

http://fr.canoe.ca/artdevivre/bienetre/article1/2012/09/25/20231371-bum.html

Focus : A "Twist box" Code of p53 Inactivation: Twist box:p53 Interaction Promotes p53 Degradation

Twist proteins have been shown to contribute to cancer development and progression by impinging on different regulatory pathways, but their mechanism of action is poorly defined. By investigating the role of Twist in sarcomas, we found that Twist1 acts as a mechanism alternative to TP53 mutation and MDM2 overexpression to inactivate p53 in mesenchymal tumors. We provide evidence that Twist1 binds p53 C terminus through the Twist box. This interaction hinders key posttranslational modifications of p53 and facilitates its MDM2-mediated degradation. Our study suggests the existence of a Twist box code of p53 inactivation and provides the proof of principle that targeting the Twist box:p53 interaction might offer additional avenues for cancer treatment.

Source : A "Twist box" Code of p53 Inactivation: Twist box:p53 Interaction Promotes p53 Degradation. Piccinin S, Tonin E, Sessa S, Demontis S, Rossi S, Pecciarini L, Zanatta L, Pivetta F, Grizzo A, Sonego M, Rosano C, Dei Tos AP, Doglioni C, Maestro R. Cancer Cell. 2012 Sep 11;22(3):404-15.

Free paper available at :

http://download.cell.com/cancer-cell/pdf/PIIS1535610812003510.pdf?intermediate=true

Anticancer molecules (96) – Molécules anticancéreuses (96)

CRIZOTINIB

Name: crizotinib

Commercial name: Xalkori

Pharmacological class: small tyrosine kinase inhibitor

Therapeutic class: antineoplastic

Action: crizotinib is an orally-dosed receptor tyrosine kinase inhibitor with significant activity against ALK, HGFR and RON. Across non-small cell lung carcinomas (NSCLC), some harbor an ALK fusion protein. The EML4-ALK fusion gene has been shown to affect the outcome of drug response and cells show resistance to EGFR inhibitors.

In 2011, crizotinib is approved:

● for the treatment of patients with locally advanced or metastatic non-small cell lung cancer (NSCLC) that is ALK-positive as detected by a FDA-approved test.

***

Nom: crizotinib

Nom commercial: Xalkori

Classe pharmacologique: petite molécule inhibitrice de tyrosine kinase

Classe thérapeutique: antinéoplasiques

Action: le crizotinib est un inhibiteur oral de tyrosine kinase récepteur-associée ayant une activité significative contre ALK, HGFR et RON. Parmi les carcinomes pulmonaires non à petites cellules CPNPC), certains expriment une protéine de fusion incorporant ALK. Le gène de fusion EML4-ALK s’est révélé affecter le résultat de la réaction tumorale aux médicaments et les cellules qui l’expriment présentent une résistance aux inhibiteurs de l'EGFR.

En 2011, le crizotinib est approuvé:

● pour le traitement des patients atteints de carcinome pulmonaire non à petites cellules CPNPC) localement avancé ou métastatique et qui est ALK-positif par un test de détection approuvé par la FDA.

Focus: Biomarkers: the next therapeutic hurdle in metastatic renal cell carcinoma

            Despite recent advances, metastatic renal cell carcinoma remains largely an incurable disease. Vascular endothelial growth factor and mammalian target of rapamycin inhibitors have provided improvements in clinical outcomes. High-dose interleukin 2 remains an option for highly selected patients and is associated with durable remissions in a small minority of patients. The toxicity profiles of specific agents and patient characteristics and comorbidities and costs have an important role in the current choice of therapy. Major challenges encountered in developing molecular biomarkers to guide therapy are tumour heterogeneity and standardisation of tissue collection and analysis. Although biomarkers are in their infancy of development, they should be a priority in early preclinical and clinical development in order to guide rational tailored development of emerging agents.

Source: Biomarkers: the next therapeutic hurdle in metastatic renal cell carcinoma. Sonpavde G, Choueiri TK (Toni_Choueiri@dfci.harvard.edu). Br J Cancer. 2012 Sep 4.

Free article available at:

http://www.nature.com/bjc/journal/vaop/ncurrent/pdf/bjc2012399a.pdf

Nanoparticle Gd@C82(OH)22 Interacting with Tumor-derived Matrix Metalloproteinase (MMP)

http://www.flickr.com/photos/ibm_research_zurich/7894691820/in/set-72157631322397418/

http://www.flickr.com/photos/ibm_research_zurich/7894705296/in/set-72157631322397418/

 

Focus: Molecular mechanism of pancreatic tumor metastasis inhibition by Gd@C82(OH)22 and its implication for de novo design of nanomedicine

Pancreatic adenocarcinoma is the most lethal of the solid tumors and the fourth-leading cause of cancer-related death in North America. Matrix metalloproteinases (MMPs) have long been targeted as a potential anticancer therapy because of their seminal role in angiogenesis and extracellular matrix (ECM) degradation of tumor survival and invasion. However, the inhibition specificity to MMPs and the molecular-level understanding of the inhibition mechanism remain largely unresolved. Here, we found that endohedral metallofullerenol Gd@C(82)(OH)(22) can successfully inhibit the neoplastic activity with experiments at animal, tissue, and cellular levels. Gd@C(82)(OH)(22) effectively blocks tumor growth in human pancreatic cancer xenografts in a nude mouse model. Enzyme activity assays also show Gd@C(82)(OH)(22) not only suppresses the expression of MMPs but also significantly reduces their activities. We then applied large-scale molecular-dynamics simulations to illustrate the molecular mechanism by studying the Gd@C(82)(OH)(22)-MMP-9 interactions in atomic detail. Our data demonstrated that Gd@C(82)(OH)(22) inhibits MMP-9 mainly via an exocite interaction, whereas the well-known zinc catalytic site only plays a minimal role. Steered by nonspecific electrostatic, hydrophobic, and specific hydrogen-bonding interactions, Gd@C(82)(OH)(22) exhibits specific binding modes near the ligand-specificity loop S1', thereby inhibiting MMP-9 activity. Both the suppression of MMP expression and specific binding mode make Gd@C(82)(OH)(22) a potentially more effective nanomedicine for pancreatic cancer than traditional medicines, which usually target the proteolytic sites directly but fail in selective inhibition. Our findings provide insights for de novo design of nanomedicines for fatal diseases such as pancreatic cancer.

Source: Molecular mechanism of pancreatic tumor metastasis inhibition by Gd@C82(OH)22 and its implication for de novo design of nanomedicine. Kang SG, Zhou G, Yang P, Liu Y, Sun B, Huynh T, Meng H, Zhao L, Xing G, Chen C, Zhao Y, Zhou R. Proc Natl Acad Sci U S A. 2012 Sep 4

Free paper available at:

http://www.pnas.org/content/early/2012/08/29/1204600109.long

Focus : AACR Cancer Progress Report 2012

It is a new day for cancer research and for cancer patients. Rapidly evolving technology is enabling extraordinary advances in cancer research that deepen our understanding of how cancer develops, grows and threatens the lives of millions. By exploiting this growing body of knowledge about cancer biology, we can be more strategic and innovative than ever before in the way we attack cancer. This is quickening the pace of developing new ways to prevent, detect, diagnose and treat cancer.The AACR Cancer Progress Report 2012 celebrates the many ways that we have made research count for cancer patients, particularly in the past year alone. Decades of research, in large part thanks to our Nation's long-standing investment in cancer research and biomedical science by the National Institutes of Health (NIH) and the National Cancer Institute (NCI), have provided the foundation for the progress that is helping usher in this new day for patients with many forms of cancer.Highlighted in this Report are treatment advances approved by the U.S. Food and Drug Administration (FDA) in the past 12 months alone, including: 1) a new drug for treating precancerous lesions of the skin; 2) eight new drugs for treating a variety of types of cancer, of which two are entirely new classes of drugs; 3) four new uses for previously approved cancer drugs, one of the four uses being an alternative administration to reduce side effects. The Report also presents new discoveries that are forming the foundation of tomorrow's progress.As a reminder of why it is so critical for the Nation to prioritize cancer research and biomedical science, the 2012 Report describes the exciting research progress and scientific opportunities ahead. Also, to put a face on the realities of cancer, we have chronicled the experiences and the sentiments of twelve cancer survivors, and as well as a mother and father who suffered unimaginable grief when their seven-year-old child died of neuroblastoma.

Source: AACR Cancer Progress Report 2012. AACR Cancer Progress Report Writing Committee. Clin Cancer Res. 2012 Sep 11.

Free paper available at:

http://clincancerres.aacrjournals.org/content/early/2012/09/10/1078-0432.CCR-12-2891.long

Press Review (September 22, 2012) – Revue de presse (22 septembre 2012)

Poor Pain Control for Cancer Patients

Recounting her father’s struggle with cancer was difficult for the young woman, even several years after his death. He’d endured first surgery and then chemotherapy and radiation, she told me, and the cancer had gone into remission. He was thrilled, but the aggressive treatment left him with chronic, debilitating pain. Once active, he struggled to get around in his own home. “It wasn’t the cancer that got him,” the daughter said. “It was the pain.”

By Pauline W. Chen. In The New York Times (blog)

http://well.blogs.nytimes.com/2012/09/20/poor-pain-control-for-cancer-patients/

Smoking and Drinking Linked to Earlier Pancreatic Cancer

People who smoke or drink heavily may develop pancreatic cancer at a younger age than those who don't, according to a recent study of 811 pancreatic cancer patients.

By Jaimie Dalessio. In Huffington Post

http://www.huffingtonpost.com/2012/09/20/smoking-drinking-pancreatic-cancer-alcohol-tobacco_n_1899948.html

Least Aggressive Breast Cancer Still Poses Long-Term Risk, Study Finds

Women with common tumor types might die of disease a decade later, affecting treatment decisions.

In U.S. News & World Report

http://health.usnews.com/health-news/news/articles/2012/09/18/least-aggressive-breast-cancer-still-poses-long-term-risk-study-finds

Cancer surpasses heart disease as cause of death among Hispanics‎‎

Cancer is now the leading cause of death among Hispanics in the United States, surpassing deaths due to heart disease, researchers reported Monday.

By Michael Muskal. In Los Angeles Times

http://www.latimes.com/news/nation/nationnow/la-na-nn-cancer-heart-disease-latinos-20120917,0,4898893.story

Merck KGaA pulls second lung cancer drug filing‎

German drugmaker Merck KGaA has withdrawn its second attempt to win European approval for use of its Erbitux drug against lung cancer, capping a string of setbacks in its drug development.

In Reuters

http://www.reuters.com/article/2012/09/18/us-merck-erbitux-idUSBRE88H09420120918

Quality-of-life program may help cancer patients

A therapy program focused on improving quality of life can help people being treated for advanced cancer, researchers from the Mayo Clinic in Rochester, Minnesota, have found.

In Reuters

http://www.reuters.com/article/2012/09/14/us-cancer-idUSBRE88D1ED20120914

Cancer de la prostate : le traitement Zytiga confirme son efficacité

Une étude internationale publiée mardi indique qu'une nouvelle molécule connue sous le nom de Zytiga et composée d'acétate d'abiratérone aurait la propriété d'améliorer la qualité de vie de patients atteints de cancer avancé de la prostate.

Dans Maxisciences

http://www.maxisciences.com/cancer-de-la-prostate/cancer-de-la-prostate-le-traitement-zytiga-confirme-son-efficacite_art26641.html

Cancer du sein : les limites du dépistage‎‎

Près de 20 % de cancers pourraient survenir dans l'intervalle entre deux dépistages organisés, affirment des spécialistes.

Dans Le Point

http://www.lepoint.fr/sante/cancer-du-sein-les-limites-du-depistage-18-09-2012-1507585_40.php

Cancers : que faire si l'on vient d'une famille à risques ?‎‎

Les consultations oncogénétiques, comme celles en pré et en postnatal, s'adressent à des personnes bien ciblées.

Par Nathalie Szapiro-Manoukian. Dans Le Figaro

http://sante.lefigaro.fr/actualite/2012/09/17/19063-cancers-que-faire-si-lon-vient-dune-famille-risques

Le sel favoriserait le cancer de l'estomac‎

Limiter sa consommation de sel est bénéfique non seulement au chapitre de la pression artérielle, mais aussi du cancer de l’estomac..

Par Marie-Claude Ouellet. Dans Agence Science-Presse

http://www.sciencepresse.qc.ca/revue-presse/2012/09/20/sel-favoriserait-cancer-lestomac

Focus: TGF-beta -- an excellent servant but a bad master

ABSTRACT: The transforming growth factor (TGF-beta) family of growth factors controls an immense number of cellular responses and figures prominently in development and homeostasis of most human tissues. Work over the past decades has revealed significant insight into the TGF-beta signal transduction network, such as activation of serine/threonine receptors through ligand binding, activation of SMAD proteins through phosphorylation, regulation of target genes expression in association with DNA-binding partners and regulation of SMAD activity and degradation. Disruption of the TGF-beta pathway has been implicated in many human diseases, including solid and hematopoietic tumors. As a potent inhibitor of cell proliferation, TGF-beta acts as a tumor suppressor; however in tumor cells, TGF-beta looses anti-proliferative response and become an oncogenic factor. This article reviews current understanding of TGF-beta signaling and different mechanisms that lead to its impairment in various solid tumors and hematological malignancies.

Source: TGF-beta -- an excellent servant but a bad master. Kubiczkova L, Sedlarikova L, Hajek R, Sevcikova S (sevcik@med.muni.cz). J Transl Med. 2012 Sep 3;10(1):183.

Free paper available at:

http://www.translational-medicine.com/content/pdf/1479-5876-10-183.pdf

Focus : Comprehensive genomic characterization of squamous cell lung cancers

Lung squamous cell carcinoma is a common type of lung cancer, causing approximately 400,000 deaths per year worldwide. Genomic alterations in squamous cell lung cancers have not been comprehensively characterized, and no molecularly targeted agents have been specifically developed for its treatment. As part of The Cancer Genome Atlas, here we profile 178 lung squamous cell carcinomas to provide a comprehensive landscape of genomic and epigenomic alterations. We show that the tumour type is characterized by complex genomic alterations, with a mean of 360 exonic mutations, 165 genomic rearrangements, and 323 segments of copy number alteration per tumour. We find statistically recurrent mutations in 11 genes, including mutation of TP53 in nearly all specimens. Previously unreported loss-of-function mutations are seen in the HLA-A class I major histocompatibility gene. Significantly altered pathways included NFE2L2 and KEAP1 in 34%, squamous differentiation genes in 44%, phosphatidylinositol-3-OH kinase pathway genes in 47%, and CDKN2A and RB1 in 72% of tumours. We identified a potential therapeutic target in most tumours, offering new avenues of investigation for the treatment of squamous cell lung cancers.

Source : Comprehensive genomic characterization of squamous cell lung cancers. The Cancer Genome Atlas Research Network; (Participants are arranged by area of contribution and then by institution.); Genome sequencing centres: Broad Institute, Hammerman PS, Lawrence MS, Voet D, Jing R, Cibulskis K, Sivachenko A, Stojanov P, McKenna A, Lander ES, Gabriel S, Getz G, Sougnez C, Imielinski M, Helman E, Hernandez B, Pho NH, Meyerson M; Genome characterization centres: BC Cancer Agency, Chu A, Chun HJ, Mungall AJ, Pleasance E, Gordon Robertson A, Sipahimalani P, Stoll D, Balasundaram M, Birol I, Butterfield YS, Chuah E, Coope RJ, Corbett R, Dhalla N, Guin R, He A, Hirst C, Hirst M, Holt RA, Lee D, Li HI, Mayo M, Moore RA, Mungall K, Ming Nip K, Olshen A, Schein JE, Slobodan JR, Tam A, Thiessen N, Varhol R, Zeng T, Zhao Y, Jones SJ, Marra MA; Broad Institute, Saksena G, Cherniack AD, Schumacher SE, Tabak B, Carter SL, Pho NH, Nguyen H, Onofrio RC, Crenshaw A, Ardlie K, Beroukhim R, Winckler W, Hammerman PS, Getz G, Meyerson M; Brigham & Women’s Hospital/Harvard Medical School, Protopopov A, Zhang J, Hadjipanayis A, Lee S, Xi R, Yang L, Ren X, Zhang H, Shukla S, Chen PC, Haseley P, Lee E, Chin L, Park PJ, Kucherlapati R; Memorial Sloan-Kettering Cancer Center (TCGA pilot phase only), Socci ND, Liang Y, Schultz N, Borsu L, Lash AE, Viale A, Sander C, Ladanyi M; University of North Carolina at Chapel Hill, Todd Auman J, Hoadley KA, Wilkerson MD, Shi Y, Liquori C, Meng S, Li L, Turman YJ, Topal MD, Tan D, Waring S, Buda E, Walsh J, Jones CD, Mieczkowski PA, Singh D, Wu J, Gulabani A, Dolina P, Bodenheimer T, Hoyle AP, Simons JV, Soloway MG, Mose LE, Jefferys SR, Balu S, O'Connor BD, Prins JF, Liu J, Chiang DY, Neil Hayes D, Perou CM; University of Southern California/Johns Hopkins, Cope L, Danilova L, Weisenberger DJ, Maglinte DT, Pan F, Van Den Berg DJ, Triche Jr T, Herman JG, Baylin SB, Laird PW; Genome data analysis centres: Broad Institute, Getz G, Noble M, Voet D, Saksena G, Gehlenborg N, Dicara D, Zhang J, Zhang H, Wu CJ, Yingchun Liu S, Lawrence MS, Zou L, Sivachenko A, Lin P, Stojanov P, Jing R, Cho J, Nazaire MD, Robinson J, Thorvaldsdottir H, Mesirov J, Park PJ, Chin L; Memorial Sloan-Kettering Cancer Center, Schultz N, Sinha R, Ciriello G, Cerami E, Gross B, Jacobsen A, Gao J, Arman Aksoy B, Weinhold N, Ramirez R, Taylor BS, Antipin Y, Reva B, Shen R, Mo Q, Seshan V, Paik PK, Ladanyi M, Sander C; The University of Texas MD Anderson Cancer Center, Akbani R, Zhang N, Broom BM, Casasent T, Unruh A, Wakefield C, Craig Cason R, Baggerly KA, Weinstein JN; University of California Santa Cruz/Buck Institute, Haussler D, Benz CC, Stuart JM, Zhu J, Szeto C, Scott GK, Yau C, Ng S, Goldstein T, Waltman P, Sokolov A, Ellrott K, Collisson EA, Zerbino D, Wilks C, Ma S, Craft B; University of North Carolina at Chapel Hill, Wilkerson MD, Todd Auman J, Hoadley KA, Du Y, Cabanski C, Walter V, Singh D, Wu J, Gulabani A, Bodenheimer T, Hoyle AP, Simons JV, Soloway MG, Mose LE, Jefferys SR, Balu S, Marron JS, Liu Y, Wang K, Liu J, Prins JF, Neil Hayes D, Perou CM; Baylor College of Medicine, Creighton CJ, Zhang Y; Pathology committee, Travis WD, Rekhtman N, Yi J, Aubry MC, Cheney R, Dacic S, Flieder D, Funkhouser W, Illei P, Myers J, Tsao MS; Biospecimen core resources: International Genomics Consortium, Penny R, Mallery D, Shelton T, Hatfield M, Morris S, Yena P, Shelton C, Sherman M, Paulauskis J; Disease working group, Meyerson M, Baylin SB, Govindan R, Akbani R, Azodo I, Beer D, Bose R, Byers LA, Carbone D, Chang LW, Chiang D, Chu A, Chun E, Collisson E, Cope L, Creighton CJ, Danilova L, Ding L, Getz G, Hammerman PS, Neil Hayes D, Hernandez B, Herman JG, Heymach J, Ida C, Imielinski M, Johnson B, Jurisica I, Kaufman J, Kosari F, Kucherlapati R, Kwiatkowski D, Ladanyi M, Lawrence MS, Maher CA, Mungall A, Ng S, Pao W, Peifer M, Penny R, Robertson G, Rusch V, Sander C, Schultz N, Shen R, Siegfried J, Sinha R, Sivachenko A, Sougnez C, Stoll D, Stuart J, Thomas RK, Tomaszek S, Tsao MS, Travis WD, Vaske C, Weinstein JN, Weisenberger D, Wigle DA, Wilkerson MD, Wilks C, Yang P, John Zhang J; Data coordination centre, Jensen MA, Sfeir R, Kahn AB, Chu AL, Kothiyal P, Wang Z, Snyder EE, Pontius J, Pihl TD, Ayala B, Backus M, Walton J, Baboud J, Berton DL, Nicholls MC, Srinivasan D, Raman R, Girshik S, Kigonya PA, Alonso S, Sanbhadti RN, Barletta SP, Greene JM, Pot DA; Tissue source sites, Tsao MS, Bandarchi-Chamkhaleh B, Boyd J, Weaver J, Wigle DA, Azodo IA, Tomaszek SC, Christine Aubry M, Ida CM, Yang P, Kosari F, Brock MV, Rogers K, Rutledge M, Brown T, Lee B, Shin J, Trusty D, Dhir R, Siegfried JM, Potapova O, Fedosenko KV, Nemirovich-Danchenko E, Rusch V, Zakowski M, Iacocca MV, Brown J, Rabeno B, Czerwinski C, Petrelli N, Fan Z, Todaro N, Eckman J, Myers J, Kimryn Rathmell W, Thorne LB, Huang M, Boice L, Hill A, Penny R, Mallery D, Curley E, Shelton C, Yena P, Morrison C, Gaudioso C, Bartlett JM, Kodeeswaran S, Zanke B, Sekhon H, David K, Juhl H, Van Le X, Kohl B, Thorp R, Viet Tien N, Van Bang N, Sussman H, Duc Phu B, Hajek R, Phi Hung N, Khan KZ, Muley T; Project team: National Cancer Institute, Mills Shaw KR, Sheth M, Yang L, Buetow K, Davidsen T, Demchok JA, Eley G, Ferguson M, Dillon LA, Schaefer C; National Human Genome Research Institute, Guyer MS, Ozenberger BA, Palchik JD, Peterson J, Sofia HJ, Thomson E; Writing committee, Hammerman PS, Neil Hayes D, Wilkerson MD, Schultz N, Bose R, Chu A, Collisson EA, Cope L, Creighton CJ, Getz G, Herman JG, Johnson BE, Kucherlapati R, Ladanyi M, Maher CA, Robertson G, Sander C, Shen R, Sinha R, Sivachenko A, Thomas RK, Travis WD, Tsao MS, Weinstein JN, Wigle DA, Baylin SB, Govindan R, Meyerson M. Nature. 2012 Sep 9.

Free paper available at:

http://www.nature.com/nature/journal/vaop/ncurrent/pdf/nature11404.pdf

FDA approves production of imaging agent that helps detect prostate cancer

The U.S. Food and Drug Administration recently approved the production and use of Choline C 11 Injection, a Positron Emission Tomography (PET) imaging agent used to help detect recurrent prostate cancer.

Choline C 11 Injection is administered intravenously to produce an image that helps to locate specific body sites for follow-up tissue sampling and testing in men with recurrent prostate cancer.

PET imaging with Choline C 11 Injection is performed in patients whose blood prostate specific antigen (PSA) levels are increasing after earlier treatment for prostate cancer. An elevated PSA result suggests that prostate cancer may have returned, even though conventional imaging tests, such as computerized tomography (CT), have not shown any signs of cancer. PET imaging is not a replacement for tissue sampling and testing.

Focus: Causes, consequences, and remedies for growth-induced solid stress in murine and human tumors

The presence of growth-induced solid stresses in tumors has been suspected for some time, but these stresses were largely estimated using mathematical models. Solid stresses can deform the surrounding tissues and compress intratumoral lymphatic and blood vessels. Compression of lymphatic vessels elevates interstitial fluid pressure, whereas compression of blood vessels reduces blood flow. Reduced blood flow, in turn, leads to hypoxia, which promotes tumor progression, immunosuppression, inflammation, invasion, and metastasis and lowers the efficacy of chemo-, radio-, and immunotherapies. Thus, strategies designed to alleviate solid stress have the potential to improve cancer treatment. However, a lack of methods for measuring solid stress has hindered the development of solid stress-alleviating drugs. Here, we present a simple technique to estimate the growth-induced solid stress accumulated within animal and human tumors, and we show that this stress can be reduced by depleting cancer cells, fibroblasts, collagen, and/or hyaluronan, resulting in improved tumor perfusion. Furthermore, we show that therapeutic depletion of carcinoma-associated fibroblasts with an inhibitor of the sonic hedgehog pathway reduces solid stress, decompresses blood and lymphatic vessels, and increases perfusion. In addition to providing insights into the mechanopathology of tumors, our approach can serve as a rapid screen for stress-reducing and perfusion-enhancing drugs.

Source: Causes, consequences, and remedies for growth-induced solid stress in murine and human tumors. Stylianopoulos T, Martin JD, Chauhan VP, Jain SR, Diop-Frimpong B, Bardeesy N, Smith BL, Ferrone CR, Hornicek FJ, Boucher Y, Munn LL, Jain RK (jain@steele.mgh.harvard.edu). Proc Natl Acad Sci U S A. 2012 Aug 29.

Free paper available at:

http://www.pnas.org/content/early/2012/08/28/1213353109.long

Recently adopted names for antitumoral compounds (September 2012) - Noms d’antitumoraux adoptés récemment (septembre 2012)

Name (nom)	Code name	Type	Target(s)
Aldoxorubicin hydrochloride	INNO-206	An albumin-binding doxorubicin prodrug	DNA intercalator
Entilomod	CBLB502	Protein	Radiation countermeasure drug
Nelipepimut-S (NeuVax)	E75 peptide	Peptide (vaccine)	HER2/neu
Pimasertib	MSC1936369A; AS703026; EMD 1036239	Synthetic small molecule inhibitor	MEK1
Ramucirumab	IMC-1121B	Monoclonal antibody	VEGFR-2
Rebastinib tosylate	DP-1919.TO, DCC-2036	Synthetic small molecule inhibitor	Multiple tyrosine kinases

Press Review (September 15, 2012) – Revue de presse (15 septembre 2012)

Ovarian Cancer Screenings Are Not Effective, Panel Says

Tests commonly recommended to screen healthy women for ovarian cancer do more harm than good and should not be performed, a panel of medical experts said on Monday.

By Denise Grady. In The New York Times

http://www.nytimes.com/2012/09/11/health/research/ovarian-cancer-tests-are-ineffective-medical-panel-says.html

Cancer Study Points to Tighter Pairing of Drugs and Patients

The first large and comprehensive study of the genetics of a common lung cancer has found that more than half the tumors from that cancer have mutations that might be treated by new drugs that are already in the pipeline or that could be easily developed.

By Gina Kolata. In The New York Times

http://www.nytimes.com/2012/09/10/health/research/for-a-lung-cancer-drug-treatment-may-be-within-reach.html

Pancreatic Cancer May Soon Be the Second-Deadliest Cancer

Pancreatic cancer is the fourth leading cause of cancer death in the United States, but it could move up to the second as early as 2015, according to a new report from the Pancreatic Cancer Action Network, a national organization for pancreatic cancer research and advocacy.

By Allison Takeda. In Huffington Post

http://www.huffingtonpost.com/2012/09/12/pancreatic-cancer-deadly-_n_1877380.html

Pregnancy exposures determine risk of breast cancer in multiple generations of offspring ‎‎

Researchers from Georgetown Lombardi Comprehensive Cancer Center demonstrate, in animals, that maternal exposure to a high-fat diet or excess estrogen during pregnancy can increase breast cancer risk in multiple generations of female offspring — daughters, granddaughters and even great-granddaughters.

In Science Codex

http://www.sciencecodex.com/pregnancy_exposures_determine_risk_of_breast_cancer_in_multiple_generations_of_offspring-98216

The Trials of Cancer Trials ‎

I spent last week trying to hope for the recurrence of a malignancy, a tumor of at least 1.5 centimeters (a bit more than half an inch) that would be visible on a CT scan. Am I crazy? Maybe, yet without such evidence of cancer’s return, I won’t be eligible for a trial that can offer me an experimental drug not yet approved by the Food and Drug Administration but potentially useful at keeping my cancer at bay for a bit longer.

By Susan Gubar. In The New York Times

http://well.blogs.nytimes.com/2012/09/13/the-trials-of-cancer-trials/

False Promises on Ovarian Cancer

New evidence that women are more likely to be harmed than helped by screening tests for ovarian cancer is disturbing. The tests do nothing to prevent healthy women from dying from the usually fatal disease. Yet they often lead doctors to perform needless surgeries that cause serious complications in many patients.

In The New York Times

http://www.nytimes.com/2012/09/12/opinion/false-promises-on-ovarian-cancer.html

Cancer: les métastases cérébrales, encore peu connues, enjeu d'un congrès

Longtemps négligées car considérées comme intervenantà l'ultime stade du cancer, les métastases cérébrales font l'objet jusqu'à dimanche à Marseille, d'une conférence internationale pour mieux cerner leur origine et définir un traitement plus adapté.

Dans RTBF

http://www.rtbf.be/info/societe/detail_cancer-les-metastases-cerebrales-encore-peu-connues-enjeu-d-un-congres?id=7835232

Dépistage du cancer du sein : plus de bénéfice que de risque ‎‎

Les critiques portent sur les surdiagnostics. Une enquête fait un bilan complet.

Par Martine Perez. Dans Le Figaro

http://sante.lefigaro.fr/actualite/2012/09/12/19026-depistage-cancer-sein-plus-benefice-que-risque

Cancer du col de l’utérus: 50.000 filles seront vaccinées en Côte d'Ivoire ‎‎

50.000 filles seront vaccinées contre le cancer du col de l’utérus en Côte d'Ivoire - Le gouvernement ivoirien a adopté mercredi une communication du ministère de la Santé et de la Lutte contre le sida relative à la vaccination de 50.000 jeunes filles contre le papilloma virus humain, cause du cancer du col de l’utérus chez la femme.

Dans Afrique en ligne

http://www.afriquejet.com/cancer-du-col-de-luterus-50000-filles-seront-vaccinees-en-cote-divoire-2012091344968.html

Cannabis : deux fois plus de risques d'avoir un cancer des testicules‎

C’est une nouvelle découverte sur les effets néfastes du cannabis qu’a révélé une récente étude américaine. Les fumeurs de cannabis réguliers auraient deux fois plus de risques d’avoir un cancer des testicules.

Dans LaDépêche.fr

http://www.ladepeche.fr/article/2012/09/10/1436306-cannabis-deux-fois-plus-de-risques-d-avoir-un-cancer-des-testicules.html

Découverte d'une nouvelle molécule anticancer‎‎‎‎

Des équipes de l'Institut Curie et du Centre national de la recherche scientifique ont découvert une nouvelle molécule qui agit sur les cellules résistantes à la chimiothérapie traditionnelle, et ce, grâce à un mécanisme encore inconnu.

Dans Canoë

http://fr.canoe.ca/sante/archives/2012/09/20120907-162925.html

Focus: Tamoxifen for the management of breast events induced by non-steroidal antiandrogens in patients with prostate cancer: A systematic review

BACKGROUND:

Tamoxifen has emerged as a potential management option for gynecomastia and breast pain due to non-steroidal antiandrogens, and it is considered an alternative to surgery or radiotherapy. The objective of this systematic review was to assess the benefits and harms of tamoxifen, in comparison to other treatment options, for either the prophylaxis or treatment of breast events induced by non-steroidal antiandrogens in prostate cancer patients.

METHODS:

We searched CENTRAL, MEDLINE, EMBASE, reference lists, the abstracts of three major conferences and three trial registers to identify ongoing randomized controlled trials (RCTs). Two authors independently screened the articles identified, assessed the trial quality and extracted data. The protocol was prospectively registered (CRD42011001320; http://www.crd.york.ac.uk/PROSPERO).

RESULTS:

Four studies were identified. Tamoxifen significantly reduced the risk of suffering from gynecomastia (RR 0.10, 95% CI 0.05-0.22) or breast pain (RR 0.06, 95% CI 0.02-0.17) at 6 months compared to untreated controls. Tamoxifen also showed a significant benefit for the prevention of gynecomastia (RR 0.22, 95%CI 0.08-0.58) and breast pain (RR 0.25, 95% CI 0.10-0.64) when compared to anastrozole after a median of 12 months. One study showed a significant benefit of tamoxifen for the prevention of gynecomastia (RR 0.24, 95%CI 0.09-0.65) and breast pain (RR 0.20, 95% CI 0.06-0.65) when compared with radiotherapy at 6 months. Radiotherapy increased the risk of suffering from nipple erythema and skin irritation, but there were no significant differences for any other adverse events (all p>0.05).

CONCLUSIONS:

The currently available evidence suggests good efficacy of tamoxifen for the prevention and treatment of breast events induced by non-steroidal antiandrogens. The impact of tamoxifen therapy on long-term adverse events, disease progression and survival remains unclear. Further large, well-designed RCTs, including long-term follow-ups, are warranted. Also, the optimal dose needs to be clarified.

Source: Tamoxifen for the management of breast events induced by non-steroidal antiandrogens in patients with prostate cancer: A systematic review. Kunath F (frank.kunath@uk-erlangen.de), Keck B, Antes G, Wullich B, Meerpohl JJ. BMC Med. 2012 Aug 28;10(1):96.

Free paper available at:

http://www.biomedcentral.com/content/pdf/1741-7015-10-96.pdf