Oncology Reviews最新文献

Improvements in systemic cancer treatments have resulted in more patients surviving for prolonged periods of time on treatment. This has made treatment-related toxicity and quality of life concerns increasingly relevant. Hand-foot syndrome (HFS) is a common skin reaction to systemic therapy that should be anticipated with chemotherapeutic treatments such as pegylated liposomal doxorubicin, docetaxel, and fluoropyrimidines. In this review we discuss current knowledge of the diagnosis, incidence, pathogenesis, and management of hand-foot syndrome (HFS). Although HFS is not life threatening, it can cause significant discomfort and impairment of function, especially in elderly patients, and may seriously impact quality of life. The incidence of HFS is dependent on the chemotherapeutic drug used, the treatment schedule, and the median duration of treatment. Effective measures for prevention and treatment of HFS include systemic and topical treatments, dose reductions, and switching to other drugs in the same class that are associated with lower rates of HFS. These approaches allow patients to continue cancer treatment while reducing negative impacts on quality of life. Awareness and early recognition are important to ensure timely treatment and avoidance of dose reductions or treatment discontinuation. We provide useful recommendations to guide the management of HFS in clinical practice.

Prostate-specific antigen velocity (PSAV) is widely used to detect PC and predict its progression. In this study, we qualitatively synthesized the currently available evidence from published studies regarding the PSAV role in PC. Electronic databases were searched to find relevant articles published until January 2019. Inclusion and exclusion criteria were applied to identify related papers. Eventually, data extraction followed by evidence synthesis was conducted. Full-text screening resulted in 42 included studies. Multiple definitions and intervals were used for PSAV calculation across studies. Results from the included studies were conflicting regarding the role of PSAV in detecting PC and predicting progression in active surveillance cases. However, there is evidence that PSAV may have a predictive role in post-treated men. There is no clear-cut evidence from the published literature to support the use of PSAV in clinical practice.

Glioblastoma (GB) is an extremely pugnacious brain cancer originating from neural stem (NS) cell-like cells. Forkhead box G1 (FOXG1; previously recognized as BF-1, qin, Chicken Brain Factor 1, or XBF-1 and renamed FOXG1 for mouse and human, and FoxG1 for other chordates) is an evolutionary preserved transcription factor driven from the forkhead box group of proteins FOXG1 modulates the speed of neurogenesis by maintaining progenitor cells in a proliferative mode as well as obstructing their differentiation into neurons during the initial periods of cortical formation. FOXG1 has been implicated in the formation of central nervous system (CNS) tumors and precisely GBs. Pathophysiologically, joint actions of FOXG1 and phosphatidylinositol- 3-kinases (PI3K) intermediate in intrinsic resistance of human GB cells to transforming growth factor-beta (TGF-β) stimulation of cyclin-dependent kinase inhibitor 1(p21Cip1) as well as growth inhibition. FOXG1 and NOTCH signaling pathways may functionally interrelate at different stages to facilitate gliomagenesis. Furthermore, FoxG1 actively contributed to the formation of transcription suppression complexes with corepressors of the Groucho/transducin-like Enhancer of split (Gro/TLEs). Also, FOXG1 was stimulated by Gro/TLE1 and abridged by Grg6. FOXG1 silencing in brain tumor-initiating cells (BTICs) also resulted in diminished secretion of markers characteristic undifferentiated natural neural stem/progenitor cells (NSPC) states, such as Oligodendrocyte transcription factor (OLIG2), (sex determining region Y)-box 2. (SOX2) and B lymphoma Mo-MLV insertion region 1 homolog (BMI1). This review therefore focuses on the pathogenic and biomarker potentials of FOXG1 in GB.

Gliomas are prime brain cancers which are initiated by malignant modification of neural stem cells, progenitor cells and differentiated glial cells such as astrocyte, oligodendrocyte as well as ependymal cells. Exchange proteins directly activated by cAMP (EPACs) are crucial cyclic adenosine 3',5'-monophosphate (cAMP)-determined signaling pathways. Cyclic AMP-intermediated signaling events were utilized to transduce protein kinase A (PKA) leading to the detection of EPACs or cAMP-guanine exchange factors (cAMP-GEFs). EPACs have been detected as crucial proteins associated with the pathogenesis of neurological disorders as well as numerous human diseases. EPAC proteins have two isoforms. These isoforms are EPAC1 and EPAC2. EPAC2 also known as Rap guanine nucleotide exchange factor 4 (RAPGEF4) is generally expression in all neurites. Higher EAPC2 levels was detected in the cortex, hippocampus as well as striatum of adult mouse brain. Activation as well as over-secretion of EPAC2 triggers apoptosis in neurons and EPAC-triggered apoptosis was intermediated via the modulation of Bcl-2 interacting member protein (BIM). EPAC2 secretory levels has proven to be more in low-grade clinical glioma than high-grade clinical glioma. This review therefore explores the effects of EPAC2/RAPGEF4 on the pathogenesis of glioma instead of EPAC1 because EPAC2 and not EPAC1 is predominately expressed in the brain. Therefore, EPAC2 is most likely to modulate glioma pathogenesis rather than EPAC1.

Basal cell carcinoma (BCC) as a non-melanoma skin cancer type is the most common malignant tumor throughout the world. The incidence is higher in age over 60. The intense of exposure to ultraviolet radiation is one of the known risk factors. Over 50% of BCC of the periocular region initially occur on the lower lid and inner angle. Literature review of treatment options for basal cell carcinoma, which consist of surgery, or combined techniques plus vismodegib, radiotherapy and imiquimod. The first consideration for treatment of periocular BCC is radical surgical excision using Mohs micrographic technique. Functional and esthetic outcome in patients are important after clear excisions and reconstruction should be carefully considered. Radical exenteration is considered in the case of orbital invasion of high-risk aggressive BCC.

Gingival tissues are attacked by oral pathogens which can induce inflammatory reactions. The immune-inflammatory responses play essential roles in the patient susceptibility to periodontal diseases. There is a wealth of evidence indicating a link between chronic inflammation and risk of malignant transformation of the affected oral epithelium. Periodontitis is associated with an increased risk of developing chronic systemic conditions including autoimmune diseases and different types of cancers. Besides, some risk factors such as smoking, alcohol consumption and human papilloma virus have been found to be associated with both periodontitis and oral cancer. This review article aimed to study the current concepts in pathogenesis of chronic periodontitis and oral cancer by reviewing the related articles.

Surgical resection followed by concurrent radiation therapy and temozolomide (TMZ) chemotherapy is the current standard treatment for glioblastoma multiforme (GBM). The present metaanalysis investigated the impact of prolonged TMZ maintenance therapy (more than 6 cycles) in comparison with standard TMZ maintenance therapy (exactly six cycles) on overall survival (OS) and progression-free survival (PFS) of patients with GBM. A meta-analysis of the literature was conducted using Medline, PubMed, EMBASE and the Cochrane Library in accordance with PRISMA guidelines. Seven articles involving 1018 patients were included. The overall survival was higher in the case group (>6 cycles TMZ) compared to the control group (6 cycles TMZ) (Z=2.375, P=0.018). The lower and upper limits were between 1.002-10.467 months. The case group had higher progression-free survival compared with the control group (Z=3.84; P<0.001). The lower and upper limits were between 2.559-7.894 months. Evidence from this meta-analysis suggests that prolonged TMZ therapy compared to the standard 6-cycle TMZ therapy was associated with higher survival in patients with glioblastoma.

The main role of amniotic membrane (AM), or amnion, is to protect the fetus from drying out and create an appropriate environment for its growth. AM is also a suitable candidate for the treatment of various diseases due to its unique characteristics. In recent years, a new line of research has focused on the anticancer properties of amnion and its potential use in cancer treatment. The in vitro and in vivo studies indicate the anti-proliferative and proapoptotic activities, as well as the angioregulatory and immunomodulatory properties of the amniotic membrane. However, the exact mechanism and molecular basis of these anticancer effects of AM are not fully elucidated. This paper presents an overview of the latest findings and knowledge about the anticancer effects of AM and its underlying molecular mechanisms, which is crucial for the application of amnion in cancer therapy.

Hepatocellular carcinoma represents one of the most aggressive cancers with high recurrence rates. The high recurrence is a major problem in the management of this disease. Cancer stem cells (CSCs) are often regarded as the basis of cancer recurrence. The anti-proliferative therapy kills the proliferating cells but induces mitotic quiescence in CSCs which remain as residual dormant CSCs. Later on, withdrawal of treatment reactivates the residual CSCs from dormancy to produce new cancer cells. The proliferation of these newly formed cancer cells initiates new tumor formation in the liver leading to tumor recurrence. HCC cells evade the immune surveillance via modulating the key immune cells by alpha feto-protein (AFP) secreted from CSCs or hepatic progenitor cells. This AFP mediated immune evasion assists in establishing new tumors by cancer cells in the liver. In this review, we will summarise the CSC mechanisms of recurrence, mitotic quiescence, dormancy and reactivation of CSCs, metastasis and immune evasion of hepatocellular carcinoma.