Searched over 200M research papers for "neoplasm cancer"
10 papers analyzed
These studies suggest that neoplasms and cancer progression are influenced by factors such as intratumoural heterogeneity, radiation exposure, and genetic variability, with childhood cancer survivors at increased risk for subsequent neoplasms, and emphasize the need for personalized interventions and improved screening strategies.
20 papers analyzed
Neoplasms, or abnormal growths of tissue, evolve through genetic and epigenetic changes. These changes are influenced by the microenvironment of the neoplastic cells, which determines the adaptive benefits of these alterations. A proposed framework classifies tumors based on intratumoral heterogeneity and the ecological factors affecting neoplastic cell survival. This classification, involving an evolutionary index (Evo-index) and an ecological index (Eco-index), aims to help clinicians personalize cancer treatments by understanding how tumors evolve and respond to interventions.
Childhood cancer survivors face a significant risk of developing subsequent neoplasms (SNs) as they age. Studies show that 5-year survivors of childhood cancer have a cumulative incidence of 20.5% for all subsequent neoplasms 30 years post-diagnosis. Factors such as female sex, older age at diagnosis, and radiation therapy increase this risk. Hodgkin lymphoma survivors are particularly vulnerable, with the highest standardized incidence ratios (SIRs) for subsequent neoplasms .
Survivors of childhood cancer who received cranial radiation therapy are at an increased risk of developing subsequent central nervous system (CNS) neoplasms. The risk is significantly higher compared to the general population, with a dose-response relationship observed between radiation exposure and the development of CNS tumors. The survival rates for subsequent high-grade gliomas and meningiomas are similar to those for primary tumors of the same histology, indicating the severity of these secondary neoplasms .
The progression of neoplasms to cancer is driven by genetic instability, leading to cellular diversity and clonal expansions. Studies indicate that clonal diversity, rather than genetic homogenization, is a predictor of progression to cancer. This principle is evident in conditions like Barrett's esophagus, where clonal diversity measures can predict the progression to esophageal adenocarcinoma, even when controlling for established genetic risk factors .
The increasing number of cancer survivors has led to a rise in second malignant neoplasms (SMNs), which are influenced by treatment-related factors, genetic susceptibility, and environmental exposures. Strategies for risk reduction include understanding the etiologic factors and implementing targeted preventive measures. Health care providers need to be aware of the elevated risks to offer appropriate counseling and follow-up for survivors .
Neoplasm cancer research highlights the importance of understanding the evolutionary and ecological dynamics of tumors, the significant risks faced by childhood cancer survivors, and the role of genetic diversity in neoplastic progression. Personalized treatment strategies and targeted preventive measures are crucial for managing the long-term health of cancer survivors. Continued research is essential to refine these approaches and improve outcomes for patients.
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