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

Slides:



Advertisements
Similar presentations
Advances in the Management of Skeletal Related Events/Bone Metastases in Prostate Cancer Robert Dreicer, M.D., M.S., FACP, FASCO Chair Dept of Solid Tumor.
Advertisements

Optimization of personalized therapies for anticancer treatment Alexei Vazquez The Cancer Institute of New Jersey.
New developments in Prostate Cancer Dr Jo Bowen Consultant Oncologist Worcestershire Royal Hospital.
AR-V7 Splice Variant in Prostate Cancer : Taking Centre Stage
Figure 1 Food, nutrition, obesity, physical activity, and the cellular processes linked to cancer Figure 1 | Food, nutrition, obesity, physical activity,
Nat. Rev. Clin. Oncol. doi: /nrclinonc
Figure 2 Underreporting by physicians of specific treatment-associated symptoms by physicians in the TORCH trial Figure 2 | Underreporting by physicians.
Figure 2 Response after initial increase in total tumour burden
Nat. Rev. Clin. Oncol. doi: /nrclinonc
Expanding Horizons in the Clinical Care of ER-Positive, HER2-Negative Metastatic Breast Cancer.
Role of Chemotherapy in the Current Treatment Paradigm for Men With CRPC.
Figure 1 Concept of the therapeutic index
Figure 2 Multiscale modelling in oncology
Figure 3 Risk-adapted and response-adapted
Figure 5 Schematic illustration of different clinical trial designs
Nat. Rev. Clin. Oncol. doi: /nrclinonc
Figure 3 Monitoring clonal evolution using liquid biopsies
Figure 1 Key time points in the discovery and development of imatinib for the treatment of chronic myeloid leukaemia (CML) and gastrointestinal stromal.
Nat. Rev. Clin. Oncol. doi: /nrclinonc
Nat. Rev. Clin. Oncol. doi: /nrclinonc
Figure 5 Identification of mucinous carcinoma
Figure 1 Classical and non-classical models of the cell cycle in RB1-proficient cells Figure 1 | Classical and non-classical models of the cell cycle in.
Figure 3 The cell cycle and the role of CDK4/6 inhibition
Figure 1 Underreporting of treatment-related toxicities by physicians, relative to patients with either advanced-stage lung cancer, or early-stage breast.
Figure 4 Possible combination therapies CDK4/6 inhibitors
Figure 2 Therapeutic targeting of the PI3K/AKT/mTOR pathway
Figure 1 Proposed treatment algorithm for advanced gastroesophageal cancer based on publish recommendations Figure 1 | Proposed treatment algorithm for.
Nat. Rev. Clin. Oncol. doi: /nrclinonc
Nat. Rev. Clin. Oncol. doi: /nrclinonc
Figure 1 CAR-T-cell design
Figure 1 Treatment-induced resistance and evolution to lineage crisis
Figure 2 The association between CD8+ T‑cell density of the tumour
Figure 4 Macrophage-targeting antitumour treatment approaches
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
therapy and to block androgen action
Figure 2 Differences between MC and AC
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
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 Nonmalignant tissue can be spared from radiation
Figure 3 Summary of overall survival by Kaplan–Meier
Figure 3 Clinical trial design in charged-particle therapy (CPT)
Figure 3 The yin and yang of tumour-associated
Figure 2 Median monthly launch price of a new anticancer drug,
Figure 5 The mechanism underlying epithelial-to-mesenchymal
Figure 2 The patterns of epithelial-to-mesenchymal
Figure 2 Host immune responses, not the radiosensitivity
Figure 2 Approaches to improve CAR-T-cell therapy
Nat. Rev. Clin. Oncol. doi: /nrclinonc
Nat. Rev. Clin. Oncol. doi: /nrclinonc
Figure 2 Dominance of the cell-extrinsic effects of autophagy
Figure 2 Frequency and overlap of alterations
Figure 2 Variations between planned and delivered doses of radiation
Figure 3 Tumours secrete factors that cause systemic immunosuppression
Targeting the Androgen Pathway: Current Best Practice and Future Directions.
Figure 2 Effect of chromosomal instability tolerance
Nat. Rev. Clin. Oncol. doi: /nrclinonc
Nat. Rev. Clin. Oncol. doi: /nrclinonc
Nat. Rev. Urol. doi: /nrurol
Nat. Rev. Urol. doi: /nrurol
Figure 3 Determination of the primary site
Evaluating the Totality of Evidence
Figure 4 Molecular signalling and immunological
Nat. Rev. Clin. Oncol. doi: /nrclinonc
Uncovering the Right Sequence
Presentation transcript:

Nat. Rev. Clin. Oncol. doi:10.1038/nrclinonc.2016.181 Figure 2 Treatment cycling to prevent progression to treatment-induced mCRPC Figure 2 | Treatment cycling to prevent progression to treatment-induced mCRPC. a | Prostate tumours are heterogeneous (left) but are often treated with drugs targeting a single oncogenic mechanism, until a clinical response is no longer obtainable. This approach can lead to toxicity, loss of drug sensitivity, and the accumulation of multidrug-resistant cancer cells. b | Rapid cycling of agents that target cancer cells might enable sustained drug sensitivity through different resistance mechanisms while, at the same time, controlling prostate cancer progression through the suppression of oncogenic signalling. Thus, the use of this approach can maintain drug sensitivity and continued growth inhibition. c | In the Prostate Cancer Intensive Non-crossreactive Therapy (PRINT) clinical trial23, men with metastatic castration-resistant prostate cancer (mCRPC) will receive different specific treatments in cyclical modules, each for 12 weeks. Module one is comprised of androgen receptor (AR)-targeted therapy (abiraterone) and α radiation (223Ra), module two consists of cytotoxic agents (cabazitaxel and/or carboplatin), and module three consists of androgen receptor (AR)- targeted therapy (enzalutamide) and α radiation (223Ra). Progression will be assessed after completion of modules one to three, with the option of performing additional cycles. Roubaud, G. et al. (2016) Strategies to avoid treatment-induced lineage crisis in advanced prostate cancer Nat. Rev. Clin. Oncol. doi:10.1038/nrclinonc.2016.181