Cancer is primarily a disease of the elderly, with the incidence of older patients with cancer expected to increase in the coming years. Despite remarkable advances during the last decade, lung cancer remains a leading cause of mortality worldwide, non-small cell lung cancer (NSCLC) being the dominant (85-90%) subtype. At diagnosis, 50% of NSCLC patients are ≥70 years and 15%, over 80 years of age. Due to their under-representation in clinical trials, current treatment decisions for older patients with cancer are based on a low level of scientific evidence. The little evidence that exists suggests that chemotherapy is effective in elderly NSCLC patients, but also indicates that they are at more risk of chemotherapy toxicity than younger adults. However, if carefully selected and monitored, elderly patients can benefit from standard chemotherapy regimens. The Comprehensive Geriatric Assessment (CGA) has historically been adopted to identify elderly patients who are unfit for chemotherapy, yet in clinical practice this is often not feasible as it is too time-consuming. Two promising new tools have emerged - the CRASH and CARG scores - to assign patients to varying intensities of chemotherapy based on a pre-therapy risk assessment. The strengths and shortcomings of each tool were discussed by a group of six advisors with expertise in the treatment of NSCLC. Based on a literature review and on their personal experience, CRASH and CARG were considered feasible toxicity prediction tools, appropriate for implementation in routine clinical practice, with a potentially high impact in optimizing therapy selection for elderly patients with cancer.

Background: accurate prognostic tools are relevant for decision-making in cancer care. Objective measures, such as bioelectrical impedance (BI), have the potential to improve prognostic accuracy for these patients. This cross-sectional study aimed to investigate whether phase angle (PhA) derived from the electrical properties of the body tissues is a predictor of muscular strength in breast cancer survivors (BCS). Methods: a total of 41 BCS (age 54.6 ± 9.2 years) were evaluated. PhA, obtained at frequency 50 kHz, was assessed with BI spectroscopy, and muscular strength with a handgrip dynamometer. Moderate-to-vigorous physical activity (MVPA) was assessed using the International Physical Activity Questionnaire (IPAQ). Measurements were performed in the morning after an overnight fast. Results: linear regression analysis showed that PhA accounted for 22% (r² = 0.22) of muscular strength variance. PhA remained a borderline predictor of muscular strength variance independently of age and MVPA. Conclusions: the findings of this study suggest that PhA is a significant predictor of maximal forearm isometric strength and a potential indicator of disease-related functionality in BCS.

Bone disease is a frequent event in cancer patients, both due to cancer spread to bone and to cancer therapies. Bone is the organ most frequently affected by metastatic disease when considering the two most frequent cancers in the Western world (breast and prostate cancers). Bone metastases can have a substantial detrimental effect on patients' quality of life, as well as significant morbidity due to complications collectively known as skeletal‐related events (SREs), which include hypercalcaemia, pathological fractures, spinal cord compression, and need of radiotherapy or surgery to the bone. These have been successfully mitigated with the development of bone‐targeted agents (BTAs; bisphosphonates and denosumab), focused on inhibiting osteoclast activity. The potential direct antitumour effect of bisphosphonates, as well as the impact of osteoclast inhibition with subsequent decrease in bone metabolism, have also propelled investigation on the role of BTAs in preventing cancer relapse in bone. In this review, the authors aimed to discuss the role of BTAs in the treatment and prevention of bone metastases, as well as their potential value in preventing cancer treatment‐induced bone loss (CTIBL). The review will focus on breast and prostate cancers, with the aim of providing the most relevant clinical data emerging from bench to bedside translational research in the field of cancer‐induced bone disease.

To investigate mutations selected in viruses from HIV-2-infected patients failing a highly active antiretroviral treatment (HAART) regimen including atazanavir/ritonavir. Twenty-eight HIV-2-infected patients previously exposed to atazanavir/ritonavir and failing therapy were studied. The protease (PR) gene was amplified and sequenced, and mutations emerging under atazanavir/ritonavir selective pressure were reported. The I50L mutation emerged in 4 out of 28 HIV-2-infected patients failing a HAART regimen including atazanavir/ritonavir. Besides I50L, four PR mutations previously associated with protease inhibitor resistance (I54L, I64V, V71I and I82F) and six PR mutations of unknown impact (V10I, E37D, S43T, K45R, I75V and F85L) in HIV-2 were also identified in this small group of patients. Several mutations were associated with virological failure of a regimen including atazanavir/ritonavir in HIV-2-infected patients, including I50L for the first time. It should be included in HIV-2 algorithms for interpretation of genotypic resistance data, and taken into account when making therapeutic decisions for HIV-2-infected patients.

To characterize the HIV-2 integrase gene polymorphisms and the pathways to resistance of HIV-2 patients failing a raltegravir-containing regimen, we studied 63 integrase strand transfer inhibitors (INSTI)-naïve patients, and 10 heavily pretreated patients exhibiting virological failure while receiving a salvage raltegravir-containing regimen. All patients were infected by HIV-2 group A. 61.4% of the integrase residues were conserved, including the catalytic motif residues. No INSTI-major resistance mutations were detected in the virus population from naïve patients, but two amino acids that are secondary resistance mutations to INSTIs in HIV-1 were observed. The 10 raltegravir-experienced patients exhibited resistance mutations via three main genetic pathways: N155H, Q148R, and eventually E92Q - T97A. The 155 pathway was preferentially used (7/10 patients). Other mutations associated to raltegravir resistance in HIV-1 were also observed in our HIV-2 population (V151I and D232N), along with several novel mutations previously unreported. Data retrieved from this study should help build a more robust HIV-2-specific algorithm for the genotypic interpretation of raltegravir resistance, and contribute to improve the clinical monitoring of HIV-2-infected patients.

Advanced ovarian cancer remains a leading cause of death from gynecologic malignancy. Surgery and, in most cases, platinum-based chemotherapy with or without maintenance with bevacizumab and/or poly-ADP ribose polymerase inhibitors (PARPi) represent the mainstay of treatment, but the disease typically recurs. The treatment of these patients represents a clinical challenge because sequential chemotherapy regimens are often used, with suboptimal outcomes and cumulative toxicity. Chemotherapy-free regimens, based on combinations of PARPi, vascular endothelial growth factor receptor inhibitors, anti-programmed cell death protein-1/programmed death-ligand 1, and anti-cytotoxic T-lymphocyte-associated protein-4 antibodies, among others, represent a valid option, with manageable toxicity profile and ease of administration. This review addresses this new strategy in the management of recurrent ovarian cancer and discusses its feasibility in the treatment landscape of the disease.