The role of bevacizumab in breast cancer

AbstractNeoangiogenesis and expression of the main angiogenic factor Vascular endothelial growth factor (VEGF) are critical steps already present at an early stage of breast cancer development. As tumor growth progresses other pro-angiogenic factors, including bFGF, TGFa and IL-8, are overexpressed and act in addition to VEGF. VEGF expression has been associated to poor prognosis and therapy outcome in breast cancer. Moreover, several studies have documented that HER-2 overexpression induces VEGF expression/secretion and neovascularization and that VEGF expression increases when tumors become resistant to treatment. On these bases the anti-VEGF drug Bevacizumab has been evaluated in the clinical setting in breast cancer patients. Recently, phase III studies have demonstrated that Bevacizumab in combination with taxanes produces a high rate of responses and increases the Progression Free survival of breast cancer patients. A large array of studies is currently ongoing with Bevacizumab in combination with chemotherapy and hormone-therapy in the metastatic, neoadjuvant and adjuvant setting

Panitumumab: the evidence of its therapeutic potential in metastatic colorectal cancer care

Colorectal cancer is the fourth most common malignant disease. Of newly diagnosed patients, 40% have metastatic disease at diagnosis, and approximately 25% of patients with localized disease at diagnosis will ultimately develop metastatic disease. The benefits of systemic chemotherapy in the treatment of metastatic colorectal cancer over best supportive care have been established. Panitumumab (ABX-EGF) is the first fully human monoclonal antibody developed for use in colorectal cancer that targets the extracellular domains of epidermal growth factor receptor

Re: Ian D. Davis, Wanling Xie, Carmel Pezaro, et al. Efficacy of Second-line Targeted Therapy for Renal Cell Carcinoma According to Change from Baseline in International Metastatic Renal Cell Carcinoma Database Consortium Prognostic Category. Eur Urol 2017;71:970-8: The Change in Baseline IMDC Prognostic Category: From the Past, Implications for the Future

No abstract availabl

Acquired hemophagocytic syndrome: comment to the case report

No abstract availabl

KRAS-Dependency in Pancreatic Ductal Adenocarcinoma: Mechanisms of Escaping in Resistance to KRAS Inhibitors and Perspectives of Therapy

Pancreatic ductal adenocarcinoma (PDAC) is still one of the deadliest cancers in oncology because of its increasing incidence and poor survival rate. More than 90% of PDAC patients are KRAS mutated (KRASmu), with KRASG12D and KRASG12V being the most common mutations. Despite this critical role, its characteristics have made direct targeting of the RAS protein extremely difficult. KRAS regulates development, cell growth, epigenetically dysregulated differentiation, and survival in PDAC through activation of key downstream pathways, such as MAPK-ERK and PI3K-AKT-mammalian target of rapamycin (mTOR) signaling, in a KRAS-dependent manner. KRASmu induces the occurrence of acinar-to-ductal metaplasia (ADM) and pancreatic intraepithelial neoplasia (PanIN) and leads to an immunosuppressive tumor microenvironment (TME). In this context, the oncogenic mutation of KRAS induces an epigenetic program that leads to the initiation of PDAC. Several studies have identified multiple direct and indirect inhibitors of KRAS signaling. Therefore, KRAS dependency is so essential in KRASmu PDAC that cancer cells have secured several compensatory escape mechanisms to counteract the efficacy of KRAS inhibitors, such as activation of MEK/ERK signaling or YAP1 upregulation. This review will provide insights into KRAS dependency in PDAC and analyze recent data on inhibitors of KRAS signaling, focusing on how cancer cells establish compensatory escape mechanisms

Immunogenic Cell Death: An Emerging Target in Gastrointestinal Cancers

Immunogenic cell death (ICD) is a regulated form of cell death that induces the activation of both innate and adaptive immune responses through the release of damage-associated molecular patterns (DAMPs) and their subsequent recognition by pattern-recognition receptors (PRRs), generating specific CD8+ T lymphocytes. Thus, ICD inducers (such as certain chemotherapeutic agents, targeted therapies, radiation, and oncolytic viruses) could become a potential cancer treatment by providing antitumour immunity and cancer vaccination. Moreover, their combination with immunotherapy, especially with immune checkpoint inhibitors, could overcome the immunosuppressive tumour microenvironment that characterises certain cancers, including gastrointestinal cancers. This review will provide insights into the role of ICD induction in colorectal, gastric, pancreatic, and hepatocellular carcinomas. Specifically, we will discuss the main mechanisms involved in ICD, their potential application in gastrointestinal cancer treatment, and the latest clinical trial updates

The role of EGFR inhibitors in nonsmall cell lung cancer

The epidermal growth factor receptor is a cell membrane receptor that plays a key role in cancer development and progression. Ligand-activated epidermal growth factor receptor-dependent signaling is involved in cell proliferation, apoptosis, angiogenesis, invasion, and metastasis. Targeting the epidermal growth factor receptor represents a promising molecular approach in cancer treatment. Several antiepidermal growth factor receptor agents are in clinical development. This review focuses on the available clinical data on epidermal growth factor receptor-targeting drugs in the treatment of nonsmall cell lung cancer

Adherence to dietary guidelines (DG) and body weight change (BWC) in early-stage breast cancer (EBC): A prospective trial in patients submitted to nutrition evidence-based educational intervention

n/