4b Tumor biology

2004 ◽  
pp. 95-107
Keyword(s):  
Tumor Biology

Tumor biology driven treatment selection in primary ovarian cancer

2014 ◽  
Vol 74 (S 01) ◽  
Author(s):  
F Arnold ◽  
D Margraf ◽  
O Hoffmann ◽  
K von Dehn-Rotfelser ◽  
I Funke ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Tumor Biology ◽  
Treatment Selection ◽  
Primary Ovarian Cancer

Role of TWEAK and Fn14 in tumor biology

10.2741/2270 ◽  
2007 ◽  
Vol 12 (1) ◽  
pp. 2761 ◽  
Author(s):  
Jeffrey, A. Winkles
Keyword(s):  
Tumor Biology

Opiophobia in Cancer Biology- Justified? - The Role of Perioperative Use of Opioids in Cancer Recurrence

2019 ◽  
Vol 25 (28) ◽  
pp. 3020-3027 ◽  
Author(s):  
Mir W. Sekandarzad ◽  
Chris Doornebal ◽  
Markus W. Hollmann
Keyword(s):  
Pain Management ◽  
Cancer Biology ◽  
Tumor Biology ◽  
Cancer Recurrence ◽  
Standard Of Care ◽  
Cancer Surgery ◽  
Perioperative Pain Management ◽  
Tumor Growth And Metastasis

: Opioids remain the standard of care in the provision of analgesia in the patient undergoing cancer surgery preoperatively. : The effects of opioids on tumor growth and metastasis have been discussed for many years. In recent years their use as part of the perioperative pain management bundle in the patients undergoing cancer surgery has been thought to promote cancer recurrence and metastasis. : This narrative review highlights earlier and more recent in vitro, in vivo and human retrospective studies that yield conflicting results as to the immune-modulatory effects of morphine on tumor biology. The article examines and explains the discrepancies with regards to the seemingly opposite results of morphine in the tumor milieu. The results of both, earlier studies that demonstrated procarcinogenic effects versus the data of more recent refined rodent studies that yielded neutral or even anti-carcinogenic effects are presented here. : Until the results of prospective randomized controlled trials are available to clarify this important question, it is currently not warranted to support opiophobia and opioids continue to constitute a pivotal role in the pain management of cancer patients.

Molecular Mechanisms Underlying the Functions of Cellular Markers Associated with the Phenotype of Cancer Stem Cells

2019 ◽  
Vol 14 (5) ◽  
pp. 405-420 ◽  
Author(s):  
Eduardo Alvarado-Ortiz ◽  
Miguel Á. Sarabia-Sánchez ◽  
Alejandro García-Carrancá
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Molecular Mechanisms ◽  
Tumor Biology ◽  
Molecular Tools ◽  
Recent Past ◽  
Functional Roles ◽  
Cellular Population ◽  
Cellular Markers ◽  
A Minor

Cancer Stem Cells (CSC) generally constitute a minor cellular population within tumors that exhibits some capacities of normal Stem Cells (SC). The existence of CSC, able to self-renew and differentiate, influences central aspects of tumor biology, in part because they can continue tumor growth, give rise to metastasis, and acquire drug and radioresistance, which open new avenues for therapeutics. It is well known that SC constantly interacts with their niche, which includes mesenchymal cells, extracellular ligands, and the Extra Cellular Matrix (ECM). These interactions regularly lead to homeostasis and maintenance of SC characteristics. However, the exact participation of each of these components for CSC maintenance is not clear, as they appear to be context- or cell-specific. In the recent past, surface cellular markers have been fundamental molecular tools for identifying CSC and distinguishing them from other tumor cells. Importantly, some of these cellular markers have been shown to possess functional roles that affect central aspects of CSC. Likewise, some of these markers can participate in regulating the interaction of CSC with their niche, particularly the ECM. We focused this review on the molecular mechanisms of surface cellular markers commonly employed to identify CSC, highlighting the signaling pathways and mechanisms involved in CSC-ECM interactions, through each of the cellular markers commonly used in the study of CSC, such as CD44, CD133, CD49f, CD24, CXCR4, and LGR5. Their presence does not necessarily implicate them in CSC biology.

scholarly journals Gender Differences in Treatment Allocation and Survival of Advanced Gastroesophageal Cancer: a Population-Based Study

2021 ◽  
Author(s):  
Willemieke P M Dijksterhuis ◽  
Marianne C Kalff ◽  
Anna D Wagner ◽  
Rob H A Verhoeven ◽  
Valery E P P Lemmens ◽  
...  
Keyword(s):  
Gender Differences ◽  
Systemic Treatment ◽  
Statistical Tests ◽  
Tumor Biology ◽  
Rank Test ◽  
Lower Probability ◽  
Gastroesophageal Cancer ◽  
Treatment Allocation ◽  
Netherlands Cancer Registry ◽  
Treatment Administration

Abstract Background Biological sex and gender have been reported to impact incidence and overall survival (OS) of curatively treated gastroesophageal cancer. The aim of this study was to compare palliative treatment allocation and OS between women and men with advanced gastroesophageal cancer. Methods Patients with an unresectable (cT4b) or metastatic (cM1) esophageal (including cardia) adenocarcinoma (EAC) or squamous cell carcinoma (ESCC), or gastric adenocarcinoma (GAC) diagnosed in 2015-2018 were identified in the Netherlands Cancer Registry. Treatment allocation was compared using chi-squared tests and multivariable logistic regression analyses, and OS using the Kaplan-Meier method with log-rank test and Cox proportional hazard analysis. All statistical tests were 2-sided. Results Of patients with EAC (n = 3,077), ESCC (n = 794) and GAC (n = 1,836), 18.0%, 39.4% and 39.1% were women, respectively. Women received less often systemic treatment compared to men in EAC (42.7% vs. 47.4%, P = 0.045) and GAC (33.8% vs. 38.8%, P = 0.03), but not in ESCC (33.2% vs. 39.5%, P = 0.07). Women had a lower probability of receiving systemic treatment in GAC in multivariable analyses (odds ratio [OR] = 0.79, 95% confidence interval [CI] = 0.62-1.00), but not in EAC (OR = 0.86, 95%CI = 0.69-1.06) and ESCC (OR = 0.81, 95%CI = 0.57-1.14). Median OS was lower in women with EAC (4.4 vs. 5.2 months, P = 0.04), but did not differ after adjustment for patient and tumor characteristics and systemic treatment administration. Conclusion We observed statistically significant and clinically relevant gender differences in systemic treatment administration and OS in advanced gastroesophageal cancer. Causes of these disparities may be sex-based, i.e. related to tumor biology, as well as gender-based, e.g. related to differences in treatment choices.

scholarly journals A Comprehensive Bioinformatics Analysis of Notch Pathways in Bladder Cancer

Cancers ◽  
2021 ◽  
Vol 13 (12) ◽  
pp. 3089
Author(s):  
Chuan Zhang ◽  
Mandy Berndt-Paetz ◽  
Jochen Neuhaus
Keyword(s):  
Cell Cycle ◽  
Bladder Cancer ◽  
Notch Signaling ◽  
Epithelial Mesenchymal Transition ◽  
Tumor Biology ◽  
Disease Free Survival ◽  
Mesenchymal Transition ◽  
Expression Levels ◽  
Notch Receptors ◽  
Notch Pathways

Background: A hallmark of Notch signaling is its variable role in tumor biology, ranging from tumor-suppressive to oncogenic effects. Until now, the mechanisms and functions of Notch pathways in bladder cancer (BCa) are still unclear. Methods: We used publicly available data from the GTEx and TCGA-BLCA databases to explore the role of the canonical Notch pathways in BCa on the basis of the RNA expression levels of Notch receptors, ligands, and downstream genes. For statistical analyses of cancer and non-cancerous samples, we used R software packages and public databases/webservers. Results: We found differential expression between control and BCa samples for all Notch receptors (NOTCH1, 2, 3, 4), the delta-like Notch ligands (DLL1, 3, 4), and the typical downstream gene hairy and enhancer of split 1 (HES1). NOTCH2/3 and DLL4 can significantly differentiate non-cancerous samples from cancers and were broadly altered in subgroups. High expression levels of NOTCH2/3 receptors correlated with worse overall survival (OS) and shorter disease-free survival (DFS). However, at long-term (>8 years) follow-up, NOTCH2 expression was associated with a better OS and DFS. Furthermore, the cases with the high levels of DLL4 were associated with worse OS but improved DFS. Pathway network analysis revealed that NOTCH2/3 in particular correlated with cell cycle, epithelial–mesenchymal transition (EMT), numbers of lymphocyte subtypes, and modulation of the immune system. Conclusions: NOTCH2/3 and DLL4 are potential drivers of Notch signaling in BCa, indicating that Notch and associated pathways play an essential role in the progression and prognosis of BCa through directly modulating immune cells or through interaction with cell cycle and EMT.

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