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Le cancer du sein touche une partie importante de la population féminine. Bien que ce cancer ait un bon pronostic, le cancer du sein triple négatif est d'une tout autre mesure, beaucoup plus agressif. En effet, ce cancer est caractérisé par l'absence d'expression des récepteurs aux œstrogènes et à la progestérone, ainsi que par l'absence de surexpression du récepteur Her-2. Par conséquent, il ne répond pas aux traitements habituels, ciblant ces récepteurs. Des altérations dans les gènes codant pour les protéines BRCA I et BRCA2 ont été associées à ce type de cancer et offrent des pistes nouvelles de compréhension de la maladie. Des mutations au sein de ces gènes amènent de nombreux dommages à l'ADN. BRCAI et BRCA2 forment en effet des complexes distincts nécessaires à la recombinaison homologue. BRCA1 possède également des rôles supplémentaires : il permet l'arrêt du cycle cellulaire menant à la réparation ou à l'apoptose de la cellule et contrôle l'amplification des centrosomes permettant d'éviter la formation de cellules aneuploïdiques. Il n'existe pas de traitements efficaces pour ce cancer très agressif; ces dernières années, seuls les inhibiteurs de PARP ont montré une certaine activité thérapeutique. Ces derniers sont, cependant, sujets à des phénomènes de résistance. Actuellement, seul le dépistage précoce en particulier chez les patients à risque permet de maximiser les chances de traitement curatif. La mastectomie préventive permet par ailleurs de prendre les devants sur l'apparition du cancer. Breast cancer affects a significant proportion of the women population. Although this cancer has usually a good prognosis, the so-called triple negative breast cancer is much more aggressive. Indeed, this cancer is characterized by the absence of the expression of estrogen and progesterone receptors as well as by the lack of Her-2 receptor overexpression. Therefore, this cancer does not respond to conventional treatment targeting these receptors. Alterations in the genes that encode the BRCA1 and BRCA2 proteins are now associated with this type of cancer and offer new avenues for understanding the disease. Mutations in these genes lead to many DNA damages. Indeed, BRCA1 and BRCA2 form distinct complexes that are necessary for homologous recombination. BRCA1 gas also additional roles: it allows cell cycle arrest to facilitate DNA repair or instead promotes cell apoptosis, and controls centrosome amplification to avoid aneuploidy. There are no highly efficient treatments for this aggressive cancer besides PARP inhibitors that show some therapeutic activity in the last years. Those are, however, subject to resistance phenomena. Currently, only early diagnosis in particular for patients at risk allows to maximize the chances of curative treatments. Preventive mastectomy can also be proposed to anticipate cancer development.

Triple Negative Breast Neoplasms --- BRCA1 Protein --- BRCA2 Protein

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Breast Neoplasms --- Genetic Counseling --- Genes, BRCA1 --- Genes, BRCA2 --- Logistic Models --- Risk Assessment --- etiology --- methods --- genetics

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Despite the efficiency of current cancer treatments, cancer is still a deadly disease for too many. In 2008, 7.6 million people died of cancer; with the current development, it is estimated that the annual cancer death number will grow to 13 million by 2030. There is clearly a need for not only more research but also more innovative and out of the mainstream scientific ideas to discover and develop even better cancer treatments. This book presents the collective works published in the recent Special Issue entitled “Killing Cancer: Discovery and Selection of New Target Molecules”. These articles comprise a selection of studies, ideas, and opinions that aim to facilitate knowledge, thoughts, and discussion about which biological and molecular mechanisms in cancer we should target and how we should target them.

Research & information: general --- Biology, life sciences --- ferlin --- myoferlin --- dysferlin --- otoferlin --- C2 domain --- plasma membrane --- sulconazole --- NF-κB --- IL-8 --- mammosphere --- breast cancer stem cells --- AF1Q --- MLLT11 --- WNT --- STAT --- esophageal cancer --- prognosis --- mTORC1 --- mTORC2 --- metabolism --- rapalogs --- mTOR inhibitors --- cancer metabolism --- mTOR in immunotherapy --- nutrient metabolism --- kinase inhibitors --- mTOR signaling --- MAPK kinase --- ERK1 --- ERK2 --- CD domain --- Rolled --- SCH772984 --- VRT-11E --- sevenmaker --- cancer therapy --- EMT --- lysosome --- lysosome-mediated invasion --- MZF1 --- phosphorylation --- PAK4 --- SUMOylation --- transcription factor --- zinc finger --- glucocorticoids --- 3D growth --- nuclear factor kappa-light-chain-enhancer of activated B-cells (NF-κB) --- epithelial-mesenchymal transition --- anoikis --- proliferation --- targeted cancer therapy --- disulfiram --- NPL4 --- replication stress --- DNA damage --- BRCA1 --- BRCA2 --- ATR pathway --- PDAC --- TCIRG1 --- ATP6V0a3 --- invasion --- migration --- matrix degradation --- pH-regulation --- autophagy --- multidrug resistance in cancer --- drug efflux pumps --- ATP-binding cassette transporter --- breast cancer resistance protein (BCRP) --- ABCG2 --- pyrazolo-pyrimidine derivative --- SCO-201 --- colorectal cancer --- immunotherapy --- inflammation --- microsatellite instability --- oncofetal chondroitin sulfate --- chondroitin sulfate --- cancer --- solid tumors --- target --- pediatric cancer --- VAR2 --- dexamethasone --- thyroid cancer --- microgravity --- space environment --- ferlin --- myoferlin --- dysferlin --- otoferlin --- C2 domain --- plasma membrane --- sulconazole --- NF-κB --- IL-8 --- mammosphere --- breast cancer stem cells --- AF1Q --- MLLT11 --- WNT --- STAT --- esophageal cancer --- prognosis --- mTORC1 --- mTORC2 --- metabolism --- rapalogs --- mTOR inhibitors --- cancer metabolism --- mTOR in immunotherapy --- nutrient metabolism --- kinase inhibitors --- mTOR signaling --- MAPK kinase --- ERK1 --- ERK2 --- CD domain --- Rolled --- SCH772984 --- VRT-11E --- sevenmaker --- cancer therapy --- EMT --- lysosome --- lysosome-mediated invasion --- MZF1 --- phosphorylation --- PAK4 --- SUMOylation --- transcription factor --- zinc finger --- glucocorticoids --- 3D growth --- nuclear factor kappa-light-chain-enhancer of activated B-cells (NF-κB) --- epithelial-mesenchymal transition --- anoikis --- proliferation --- targeted cancer therapy --- disulfiram --- NPL4 --- replication stress --- DNA damage --- BRCA1 --- BRCA2 --- ATR pathway --- PDAC --- TCIRG1 --- ATP6V0a3 --- invasion --- migration --- matrix degradation --- pH-regulation --- autophagy --- multidrug resistance in cancer --- drug efflux pumps --- ATP-binding cassette transporter --- breast cancer resistance protein (BCRP) --- ABCG2 --- pyrazolo-pyrimidine derivative --- SCO-201 --- colorectal cancer --- immunotherapy --- inflammation --- microsatellite instability --- oncofetal chondroitin sulfate --- chondroitin sulfate --- cancer --- solid tumors --- target --- pediatric cancer --- VAR2 --- dexamethasone --- thyroid cancer --- microgravity --- space environment