Nat. Rev. Clin. Oncol. doi: /nrclinonc

Slides:

Advertisements

Similar presentations

by Rogelio Zamilpa, and Merry L. Lindsey

Advertisements

Targeting the DNA Damage Response in Cancer

Nat. Rev. Clin. Oncol. doi: /nrclinonc

Nat. Rev. Clin. Oncol. doi: /nrclinonc

Figure 1 CTLA-4 and PD-1–PD-L1 immune checkpoints

Figure 1 Concept of the therapeutic index

Nat. Rev. Clin. Oncol. doi: /nrclinonc

Figure 2 Multiscale modelling in oncology

Figure 1 Radiation-induced effects on tumour cells

Figure 5 Schematic illustration of different clinical trial designs

Figure 3 The contribution of the tumour microenvironment

Figure 4 Simplified T cell and antigen presenting

Figure 2 Signalling pathways and physiological domains that are

Figure 1 Four nodes to target when inducing anti-tumour immunity

Nat. Rev. Clin. Oncol. doi: /nrclinonc

Figure 1 Key time points in the discovery and development of imatinib for the treatment of chronic myeloid leukaemia (CML) and gastrointestinal stromal.

Figure 1 Current treatments for PNETs

Nat. Rev. Clin. Oncol. doi: /nrclinonc

Nat. Rev. Clin. Oncol. doi: /nrclinonc

Figure 7 Clinical options for HCC therapy

Nat. Rev. Clin. Oncol. doi: /nrclinonc

Nat. Rev. Clin. Oncol. doi: /nrclinonc

Figure 4 Possible combination therapies CDK4/6 inhibitors

Figure 2 Therapeutic targeting of the PI3K/AKT/mTOR pathway

Nat. Rev. Clin. Oncol. doi: /nrclinonc

Figure 1 CAR-T-cell design

Figure 3 Defects in the T cell receptor signalling pathway

Figure 6 Combination therapy for HCC

Figure 1 Putative anticancer mechanisms of action of PARP inhibitors

Nat. Rev. Urol. doi: /nrurol

Nat. Rev. Clin. Oncol. doi: /nrclinonc

Nat. Rev. Clin. Oncol. doi: /nrclinonc

Nat. Rev. Clin. Oncol. doi: /nrclinonc

Figure 1 Therapeutic targeting of the B-cell receptor (BCR)

Figure 3 Drug cycling with collateral sensitivity

Nat. Rev. Clin. Oncol. doi: /nrclinonc

Figure 3 Possible modalities for reconciliation of patient's and physician's report of symptomatic treatment-associated toxicities Figure 3 | Possible.

Nat. Rev. Clin. Oncol. doi: /nrclinonc

Figure 1 The dynamic nature of resistance mechanisms can be

Figure 1 Critical signalling pathways involved in PDAC pathogenesis

Figure 2 Metabolic heterogeneity in tumours

Figure 3 Clinical trial design in charged-particle therapy (CPT)

Nat. Rev. Clin. Oncol. doi: /nrclinonc

Figure 3 The yin and yang of tumour-associated

Figure 5 The mechanism underlying epithelial-to-mesenchymal

Figure 1 Simplified representation of the physiological

Nat. Rev. Clin. Oncol. doi: /nrclinonc

Nat. Rev. Clin. Oncol. doi: /nrclinonc

Figure 2 Approaches to improve CAR-T-cell therapy

Nat. Rev. Clin. Oncol. doi: /nrclinonc

Inhibition of mammalian target of rapamycin: Two goals with one shot?

Figure 3 Inflammatory mechanisms in tendinopathy

Figure 2 Frequency and overlap of alterations

Nat. Rev. Clin. Oncol. doi: /nrclinonc

Nat. Rev. Endocrinol. doi: /nrendo

Translating Germline Cancer Risk into Precision Prevention

Nat. Rev. Clin. Oncol. doi: /nrclinonc

Figure 1 Mechanisms of action of immunotherapy modalities

Figure 5 Schematic overview of a clinical decision-support

Nat. Rev. Clin. Oncol. doi: /nrclinonc

Figure 3 Bile acid-induced hepatic inflammation and carcinogenesis

Nat. Rev. Clin. Oncol. doi: /nrclinonc

Figure 4 Radiogenomics analysis can reveal relationships

Figure 1 Overview of the imaging biomarker roadmap

Figure 3 Determination of the primary site

Distribution of immune checkpoint in tumor cells and immune microenvironment. CTLA-4, cytotoxic T lymphocyte antigen-4; MHC, major histocompatibility complex;

Signalling pathways and involved entities that are unravelling experimental therapeutic targets for TNBC. Depicted molecular landscape of TNBC confers.

Figure 4 Molecular signalling and immunological

Schematic representation of signaling by HTLV-1 Tax.

Connections between insulin/insulin-like growth factor 1 signaling and metabolic pathways in tumor cells. Connections between insulin/insulin-like growth.

Presentation transcript:

Nat. Rev. Clin. Oncol. doi:10.1038/nrclinonc.2016.79 Figure 2 Combination strategies to augment the biological effects of radiotherapy Figure 2 | Combination strategies to augment the biological effects of radiotherapy. Irradiation of the tumour causes a variety of biological consequences, which can be exploited by combining radiotherapy with novel agents that target the relevant pathways123. ATR, ataxia telangiectasia and Rad3-related protein; CA9, carbonic anhydrase 9; Chk1, checkpoint kinase 1; CTLA-4, cytotoxic T-lymphocyte-associated protein 4; DDR, DNA damage response; DNA-PK, DNA-dependent protein kinase; HIF-1-α, hypoxia-inducible factor 1-alpha; MCT 1, monocarboxylate transporter 1; MCT 4, monocarboxylate transporter 4; mTOR, mechanistic target of rapamycin ; PARP, poly(ADP-ribose) polymerase; PD-1, programmed cell death protein 1; PI3K, phosphoinositide 3-kinase; NF-κB, nuclear factor-kappa-B; UPR, unfolded protein response. Sharma, R. A. et. al. (2016) Clinical development of new drug–radiotherapy combinations Nat. Rev. Clin. Oncol. doi:10.1038/nrclinonc.2016.79