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Parasite Versus Host: Pathology and Disease
Published in Eric S. Loker, Bruce V. Hofkin, Parasitology, 2023
Eric S. Loker, Bruce V. Hofkin
The esophageal cysts containing the adult worms can interfere with the ability of the dog to swallow. Such dogs eventually become emaciated. These cysts can also transform into neoplasms, resulting in malignant tumors called esophageal sarcomas (Figure 5.11). A sarcoma is a type of cancer originating in connective tissue cells. As these tumors continue to grow, they further interfere with a dog’s ability to eat. Although the exact manner in which S. lupi triggers malignant neoplasia is unknown, it has recently been shown that neoplastic nodules contain a large number of activated and rapidly dividing fibroblasts compared to non-neoplastic nodules. Cells in neoplastic nodules express high levels of fibroblast growth factor and vascular epithelial growth factor. Curiously and for reasons nobody has yet adequately explained, beagles and other hound breeds appear to be especially susceptible to S. lupi infection and esophageal sarcoma.
Neoplasia in pregnancy
Published in Hung N. Winn, Frank A. Chervenak, Roberto Romero, Clinical Maternal-Fetal Medicine Online, 2021
The majority of patients present with symptoms of localized pain or a mass. Diagnostic procedures commonly used to assess sarcomas include radiographs with abdominal shielding during pregnancy. Osteogenic sarcomas may require radio-isotope bone scanning, which is thought to be of low risk to the fetus (269). Definitive diagnosis of any type of sarcoma requires biopsy. Although pregnancy has no proven deleterious effects on the natural course of sarcomas, delayed diagnosis results in postponed treatment. These tumors present at advanced stages, which may explain isolated reports of worsened prognosis for sarcomas in pregnancy (270). The aggressive biologic behavior of pelvic sarcomas may be enhanced by hypervascularity or hormonal stimulus; however, an impaired prognosis for most sarcomas associated with pregnancy remains unsubstantiated.
Radiotherapy Physics
Published in Debbie Peet, Emma Chung, Practical Medical Physics, 2021
Andrea Wynn-Jones, Caroline Reddy, John Gittins, Philip Baker, Anna Mason, Greg Jolliffe
The increased use of imaging within the radiotherapy workflow potentially opens the door for the extraction of quantitative information from multi-modality images to incorporate into mathematical models for the prediction of treatment outcomes. Examples of suitable features could include location, texture and morphology of the delineated tumour volume. As an example, shape-based metrics based on the deviation from an ellipsoid structure was observed to have an association with survival in sarcoma patients. Further examples include the prediction of local control in lung cancer patients using PET/CT images (Oikonomou et al. 2018) and the prediction of metastatic disease in sarcoma patients using PET/MR (Vallières et al. 2015).
Bioinformatics Identification and Validation of Aging‑Related Molecular Subtype and Prognostic Signature in Sarcoma
Published in Cancer Investigation, 2023
Xu Hong, Hui Liu, Chu Chen, Tian Lai, Jingui Lin
Sarcomas were a series of heterogeneous malignancies derived from mesenchymal cells (1). Sarcomas were relatively rare, ranking about 1% of all malignancies (2). In 2020, there were an estimated of 34,270 new cases of sarcoma and 15,086 sarcoma-related deaths globally (3). No obvious difference was obtained in incidence of sarcomas between males and females (4). Though some risk factors had been identified for sarcomas, including EWSR1-ETS gene fusion (5,6), the specific mechanism involved in the oncogenesis of sarcoma had not been fully clarified. Despite surgery and chemotherapy had been used to treat sarcoma, the prognosis was still poor with a 5-year relative survival rates of 16% for metastatic patients (7). Recent studies suggested immunotherapy as one of most promising approaches for malignancies (8–10). However, sarcomas were regarded as "immune cold" tumor category and limited therapy targets had been identified for this disease (11). These data called for novel prognostic biomarkers and therapy targets for sarcomas.
The clinical utility of next-generation sequencing for bone and soft tissue sarcoma
Published in Acta Oncologica, 2022
Charles A. Gusho, Mia C. Weiss, Linus Lee, Steven Gitelis, Alan T. Blank, Dian Wang, Marta Batus
Sarcomas are a rare and heterogeneous tumor group that account for nearly 1% of adult malignancies [1]. Given that sarcomas are comprised of over 60 different histologic subtypes, obtaining an accurate diagnosis is challenging. While the divergent biology of most sarcomas has been exploited by diagnostic tools that can readily identify distinct genetic patterns, for most subtypes there are limited United States Food and Drug Administration (FDA)-approved therapies that treat specific molecular targets [2,3]. Rather, when indicated, the treatment strategy for most patients including those with metastatic sarcoma consists of cytotoxic agents and tyrosine kinase inhibitors (e.g., pazopanib). Unfortunately, the overall response rate to cytotoxic drugs is usually low, depending on the drug or combination of drugs, and the current treatment options for patients with advanced disease are generally not curative [4,5].
Avapritinib in unresectable or metastatic gastrointestinal stromal tumor with PDGFRA exon 18 mutation: safety and efficacy
Published in Expert Review of Anticancer Therapy, 2021
Miguel Henriques-Abreu, César Serrano
Sarcomas are a rare and diverse group of tumors that are derived from connective tissues. Biologically speaking, sarcomas can be classified in two broad categories: genomically-complex sarcomas, characterized by non-recurrent genetic alterations and complex karyotypes; and genomically simple sarcomas, which commonly harbor tumor-specific genetic alterations that critically drive tumor initiation and progression [1]. Gastrointestinal stromal tumor (GIST), the most common human malignant mesenchymal neoplasm, falls in this last category. Indeed, 85% to 90% of GISTs are driven by gain-of-function mutations in KIT or PDGFRA receptor tyrosine kinases (RTKs) [2]. Oncogenic activation of KIT is more common (75–80%) than PDGFRA activating events (10–15%) [3,4]. Both are mutually exclusive given that they are initiating clonal events. The remaining ~10% of GIST patients wild-type for KIT and PDGFRA constitutes a molecularly heterogeneous group with various known and yet unknown drivers [2]. The high reliance of GIST on KIT/PDGFRA oncogenic signaling has been successfully exploited in the clinic, and GIST emerged in the turn of the century as a paradigmatic model to develop targeted agents directed against driver mutations in cancer. Throughout, five tyrosine kinase inhibitors (TKIs) targeting KIT and PDGFRA have achieved regulatory approval: imatinib, sunitinib, regorafenib, and more recently, ripretinib and avapritinib [5–9].