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Diffuse Intrinsic Pontine Glioma
Published in David A. Walker, Giorgio Perilongo, Roger E. Taylor, Ian F. Pollack, Brain and Spinal Tumors of Childhood, 2020
Katherine E. Warren, Carolyn R. Freeman, Dannis G. van Vuurden
In contrast to adult high-grade gliomas43,44 and other pediatric CNS tumors such as medulloblastoma,45 the primary disease-determining aberrations in DIPG (histone mutations and their partners) appear to be spatially conserved, i.e., present in primary, contiguous, and metastatic sites of disease, and temporally preserved, present over the entire course of the disease.7,46 Tumor evolutionary studies suggest histone H3K27M mutations and their obligate partner mutations involving cell cycle or growth factor pathways arise first and remain present during tumor invasion and metastases.7 Whereas histologic-grade intratumoral heterogeneity is present and has no correlation with prognosis, genomic/molecular driver mutations are conserved, are spatially homogeneous, and do correlate with prognosis. This alleviates concerns about biopsy representation of tumor and is important when considering biopsy to determine treatment for patients. Additional oncogenic mutations may arise later and are subclonal.7
Radiation Hormesis in Cancer
Published in T. D. Luckey, Radiation Hormesis, 2020
Benign tumors keep a well-defined boundary; malignant tumors can metastasize and are called cancers. Since benign tumors may become malignant, an agent which induces either is oncogenic according to the U.S. Environmental Protection Agency.319 Tumors and cancers develop from cells which lose a factor that keeps them under host growth and contact control. The “search and destroy” mission of white blood cells is usually effective for new microscopic cancers in tissues with vigorous blood supply. The most important cells involved are T cells which mature in the thymus. Although identification is relatively easy if foreign cells invade, it can become quite difficult if host cells mutate and become cancers. The search function becomes less effective in areas which have poor blood supply, such as scar or encapsulated tissue. The destroy function is ineffective for large, well established cancers due, in part, to the attachment of host antibodies on surfaces.
Comparative Genomic Hybridization and Copy Number Abnormalities in Breast Cancer
Published in Brian Leyland-Jones, Pharmacogenetics of Breast Cancer, 2020
The progression of normal breast epithelial cells from a normal state toward one characterized by uncontrolled growth and metastatic behavior is caused by the deregulation of key cellular processes and signaling pathways. These alterations in normal cellular behavior are rooted in the accumulation of genomic and epigenomic lesions that impact hallmarks of cancer, such as the ability of the cell to control proliferation, undergo apoptosis, increase motility leading to invasion, and alter angiogenesis. A suite of technologies has now been developed to assess genomic and epigenomic aberrations that contribute to cancer progression. The application of these has shown that genome copy number abnormalities (CNAs) are among the most frequent genomic aberrations. Remarkably, these studies have revealed that 10% to 15% of the genes in a typical carcinoma tumor may be deregulated by recurrent genome CNAs and regions. Some of these genes influence disease progress and so may be assessed to facilitate prognosis. Others influence response to therapy and so may be assessed as predictive markers. Some of these enable oncogenic processes, on which tumors depend for survival, and so are candidate therapeutic targets. In most cases, array comparative genomic hybridization (CGH) is the method of choice for their discovery and may be used in some setting for clinical assessments of these abnormalities. Accordingly, we review here several of the current array CGH technologies available and the considerations needed when determining the technology most applicable to a given study.
The dark side of lipid metabolism in prostate and renal carcinoma: novel insights into molecular diagnostic and biomarker discovery
Published in Expert Review of Molecular Diagnostics, 2023
Nicola Antonio di Meo, Francesco Lasorsa, Monica Rutigliano, Martina Milella, Matteo Ferro, Michele Battaglia, Pasquale Ditonno, Giuseppe Lucarelli
The goal of this review was to advance knowledge of lipid biology in cancer and uncover fresh approaches for PCa and RCC treatment. FAs, cholesterol, and lipid metabolism all play significant roles in the pathogenetic and metabolic roots of RCC and PCa. In the past ten years, an integrated strategy utilizing lipidomic and transcriptome data has improved our understanding of these pathways. Although lipid metabolism has an effect on AR signaling, it also plays a significant role in controlling the immune system in the tumor microenvironment. Cancer development and oncogenic signaling to increase cell proliferation and survival appear to be influenced by disturbances in the regulation and changes in the characteristics of immune cells and cancer cells. Both in vitro and in vivo studies have demonstrated promising outcomes for innovative diagnostic tools in biomarker identification as well as novel treatment ways to target cancer cells’ FAs or cholesterol balance by either limiting production or uptake.
New insight into brain disease therapy: nanomedicines-crossing blood–brain barrier and extracellular space for drug delivery
Published in Expert Opinion on Drug Delivery, 2022
Ziqi Gu, Haishu Chen, Han Zhao, Wanting Yang, Yilan Song, Xiang Li, Yang Wang, Dan Du, Haikang Liao, Wenhao Pan, Xi Li, Yajuan Gao, Hongbin Han, Zhiqian Tong
For a long time, the traditional drugs for the treatment of brain tumors have high molecular weight and low histocompatibility, so it is difficult to pass through BBB and has a significant cytotoxic effect on normal cells. Compared with the BBB, although blood–tumor barrier (BTB) is leaky generally, but its penetration is not well-distributed. Furthermore, cancer cells exhibit the enhancement of oncogenic, pro-survival signaling. All of these reduce the therapeutic effect of tumor drugs. A variety of nanomedicines using the different mediation methods have developed to treat brain tumors and evaluate their effects. For example, the poly (ethylene glycol)-poly (butylene adipate)-poly (ethylene glycol) superparamagnetic iron oxide NPs loaded with temozolomide have the positive antitumor effect on C6 glioma cells in vitro [152]. The TfR-mediated peptide T12 and mannose-functionalized albumin nanoparticles can pass through BBB and be targeted and delivered into glioma [153]. A functionalized gold-iron oxide NPs containing therapeutic microRNA by intranasal administration can improve the survival time of mouse glioma model [154].
Telomerase: a good target in hepatocellular carcinoma? An overview of relevant preclinical data
Published in Expert Opinion on Therapeutic Targets, 2022
Maria Lina Tornesello, Anna Lucia Tornesello, Noemy Starita, Andrea Cerasuolo, Francesco Izzo, Luigi Buonaguro, Franco Maria Buonaguro
Silencing of TERT promoter in normal cells and its activation in stem cells are tightly regulated by numerous transcription factors, which bind to regulatory elements such as GC-motifs and E-boxes [61,62]. These factors include among others c-Myc [63], Sp1 [64], NFX1-123 [65], survivin [66], the estrogen receptor [67], NF-kB [68], Ets2 [69], p27KIP1 [70], TGFβ [71], STAT3 [72] and E2F1 [73]. The majority of these transcription factors are spatially, sequentially and temporally expressed in normal tissues during development, cell renewal and differentiation. However, many of them become abnormally expressed and associated with oncogenic processes in human cancers [74]. The enhanced expression of oncogenic transcription factors binding to TERT promoter rapidly disrupt the fine tuning of telomerase function in tumor cells [75].