Medical Oncology 

About: Medical Oncology is an academic journal published by Springer Science+Business Media. The journal publishes majorly in the area(s): Cancer & Medicine. It has an ISSN identifier of 1357-0560. Over the lifetime, 4676 publications have been published receiving 92817 citations. The journal is also known as: MO.

Long non-coding RNA MALAT-1 overexpression predicts tumor recurrence of hepatocellular carcinoma after liver transplantation

Abstract: Metastasis-associated lung adenocarcinoma transcript 1(MALAT1), a long non-coding RNA (lncRNA), is up-regulated in many solid tumors and associated with cancer metastasis and recurrence. However, its role in hepatocellular carcinoma (HCC) remains poorly understood. In the present study, we evaluated the expression of MALAT1 by quantitative real-time PCR in 9 liver cancer cell lines and 112 HCC cases including 60 cases who received liver transplantation (LT) with complete follow-up data. Moreover, small interfering RNA (siRNA) was used to inhibit MALAT1 expression to investigate its biological role in tumor progression. We found that MALAT1 was up-regulated in both cell lines and clinical tissue samples. Patients with high expression level of MALAT1 had a significantly increased risk of tumor recurrence after LT, particularly in patients who exceeded the Milan criteria. On multivariate analysis, MALAT1 was an independent prognostic factor for predicting HCC recurrence (hazard ratio, 3.280, P = 0.003).In addition, inhibition of MALAT1 in HepG2 cells could effectively reduce cell viability, motility, invasiveness, and increase the sensitivity to apoptosis. Our data suggest that lncRNA MALAT1 play an important role in tumor progression and could be a novel biomarker for predicting tumor recurrence after LT and serve as a promising therapeutic target.

Physical activity and survival after breast cancer diagnosis: meta-analysis of published studies

Abstract: Published data have shown that physical activity (PA) has a positive role on the primary prevention of breast cancer risk However, the role of PA on breast cancer outcome has been controversial with inconsistent data The lack of a meta-analysis that addresses that issue prompted the current report A comprehensive literature search identified eight studies, of which two studies were excluded The remaining six studies (12,108 patients with breast cancer) were included in this meta-analysis Pre-diagnosis PA reduced all causes mortality by 18% but had no effect on breast cancer deaths Post-diagnosis PA reduced breast cancer deaths by 34% (HR = 066, 95% CI, 057–077, P < 000001), all causes mortality by 41% (HR = 059, 95% CI, 053–065, P < 000001), and disease recurrence by 24% (HR = 076, 95% CI, 066–087, P = 000001) Breast cancer mortality was reduced by pre-diagnosis PA in women with body mass index (BMI) < 25 kg/m2, while post-diagnosis PA reduced that risk among those with BMI ≥ 25 kg/m2 On the other hand, post-diagnosis PA reduced all causes mortality regardless of the BMI The analysis showed that post-diagnosis PA reduced breast cancer deaths (HR = 050, 95% CI, 034–074, P = 00005), and all causes mortality (HR = 036, 95% CI, 012–103, P = 006) among patients with estrogen receptor (ER)-positive tumor, while women with ER-negative disease showed no gain The current meta-analysis provides evidence for an inverse relationship between PA and mortality in patients with breast cancer and supports the notion that appropriate PA should be embraced by breast cancer survivors

High expression of PD-L1 in lung cancer may contribute to poor prognosis and tumor cells immune escape through suppressing tumor infiltrating dendritic cells maturation

Abstract: The immunohistochemical analysis was used to evaluate the expression of PD-L1 in 109 non-small cell lung cancer (NSCLC) tissues and para-tumor tissues. Associations between expressed PD-L1 and tumor histological types, degree of differentiation, and lymph node metastasis were calculated, and overall survival was assessed. Meanwhile, immunohistochemistry and immunofluorescence double labeling technique were performed to detect the expressions of PD-L1, CD1α, and CD83 on TIDC of 20 lung cancer tissues, and the expression of PD-L1 in CD1α+DCs and CD83+DCs and their significances were also explored. We found that the expression rate of PD-L1 in NSCLC was associated with histological types and overall survival. Patients with either adenocarcinoma or survival time after surgery less than 3 years showed higher expression rate of PD-L1. Furthermore, Cox model analysis indicated that PD-L1 might be regarded as a poor prognostic factor. PD-L1 could be also detected in CD1α+ immature DC in NSCLC, indicating that as a class of key anti-tumor immunocyte in tumor microenvironment, DC expressing PD-L1 itself might play an important role in keeping its immature status and contributing to tumor cells immune escape and disease progression.

Treatment resistance of solid tumors: role of hypoxia and anemia.

Abstract: Hypoxia is a characteristic property of locally advanced solid tumors, resulting from an imbalance between the supply and consumption of oxygen. Major pathogenetic mechanisms for the development of hypoxia are (1) structural and functional abnormalities of the tumor microvasculature, (2) increased diffusion distances, and (3) tumor-associated and therapy-induced anemia. The oxygenation status is independent of clinical tumor size, stage, grade, and histopathological type, but is affected by the hemoglobin level. Hypoxia is intensified in anemic patients, especially in tumors with low perfusion rates. Hypoxia and anemia (most probably via worsening of tumor hypoxia) can lead to therapeutic problems, as they make solid tumors resistant to sparsely ionizing radiation and some forms of chemotherapy. In addition to more direct mechanisms involved in the development of therapeutic resistance, there are also indirect machineries that can cause barriers to therapies. These include hypoxia-driven proteome and genome changes and clonal selection. These, in turn, can drive subsequent events that are known to further increase resistance to therapy (in addition to critically affecting long-term prognosis). Treatment resistance in anemic patients can be, at least partially, prevented or overcome by anemia correction, resulting in better locoregional tumor control and overall survival of patients.

Metformin and cancer: new applications for an old drug

Abstract: Metformin, one of most widely prescribed oral hypoglycemic agents, has recently received increased attention because of its potential antitumorigenic effects that are thought to be independent of its hypoglycemic effects. Several potential mechanisms have been suggested for the ability of metformin to suppress cancer growth in vitro and vivo: (1) activation of LKB1/AMPK pathway, (2) induction of cell cycle arrest and/or apoptosis, (3) inhibition of protein synthesis, (4) reduction in circulating insulin levels, (5) inhibition of the unfolded protein response (UPR), (6) activation of the immune system, and (7) eradication of cancer stem cells. There is also a growing number of evidence, mostly in the form of retrospective clinical studies that suggest that metformin may be associated with a decreased risk of developing cancer and with a better response to chemotherapy. There are currently several ongoing randomized clinical trials that incorporate metformin as an adjuvant to classic chemotherapy and aim to evaluate its potential benefits in this setting. This review highlights basic aspects of the molecular biology of metformin and summarizes new advances in basic science as well as intriguing results from recent clinical studies.