Academic literature on the topic 'Subsequent tumours'
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Journal articles on the topic "Subsequent tumours"
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Takajo, Daiji, and Sanjeev Aggarwal. "A rhabdomyoma in the right ventricle presenting as hemodynamics of hypoplastic right heart." Cardiology in the Young 30, no. 10 (August 5, 2020): 1527–29. http://dx.doi.org/10.1017/s1047951120002358.
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AbstractRhabdomyomas are the most common paediatric cardiac tumours. The natural history of these tumours is mostly benign, and the tumour usually regresses spontaneously. Although surgical resection of these tumours is one of the considerations in patients with ventricular outflow obstruction, a palliation with Blalock–Taussig shunt is an alternative approach with the hope of regression of the tumour over time. We report a case of prenatally diagnosed rhabdomyomas in the right ventricle and its outflow presenting as hemodynamic simulating hypoplastic right ventricle in a newborn. She required prostaglandin and Blalock–Taussig shunts palliation for pulmonary flow and subsequent regression of tumours.
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Low, Shoen CS, Richard HG Lo, Te-Neng Lau, London Lucien PJ Ooi, Chee-Keong Ho, Bien-Soo Tan, Alexander YF Chung, Wen-Hsin Koo, and Pierce KH Chow. "Image-guided Radiofrequency Ablation of Liver Malignancies: Experience at Singapore General Hospital." Annals of the Academy of Medicine, Singapore 35, no. 12 (December 15, 2006): 851–57. http://dx.doi.org/10.47102/annals-acadmedsg.v35n12p851.
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Introduction: The aim of this paper was to study the efficacy, side effects and complications of radiofrequency (RF) ablation of primary and metastatic liver malignancies. Materials and Methods: We retrospectively reviewed 57 patients (39 men, 18 women; mean age, 63 years; age range, 44 to 83 years) who underwent RF ablation for liver malignancies from January 2002 to December 2004. A total of 87 tumours were ablated – 71 (81.6%) hepatocellular carcinomas and 16 (18.4%) metastases (from primaries in the colon, stomach and pancreas). RF ablation was performed either percutaneously (n = 71) under conscious sedation or intraoperatively (n = 16) under general anaesthesia. Follow-up ranged from 1 month to 41 months (mean, 15.2) and included computed tomography (CT) 1 day, 1 month and 3 months after ablation, and half-yearly thereafter. Patients were observed for local tumour progression and for the emergence of new tumours. Results: Four patients with a total of 5 tumours were lost to follow-up. Of the remaining 82 tumours treated, complete ablation was attained in 66 tumours after a single procedure, giving a primary effectiveness rate of 80.5%. Seven (8.5%) required 2 procedures to achieve complete ablation, giving a secondary effectiveness rate of 89% after 2 ablations. One tumour (1.2%) required 3 procedures to achieve complete ablation. One tumour required 4 procedures to date, with the latest follow-up CT still demonstrating incomplete ablation. Two tumours (2.4%) had an initial RF ablation and subsequent transarterial chemoembolisation (TACE). One tumour had an initial RF ablation followed by 32Phosphorus-biosilicon (BrachySil®) injection, the latter as part of a Phase IIA trial. One tumour required 2 RF ablations and a subsequent TACE. Lastly, 3 tumours received initial RF ablation but subsequent local tumour progression was not treated as the patients were deemed unfit for repeat ablation. No procedure-related deaths or major complications were encountered. Minor complications were reported in 2 patients (3.8%) – subcapsular haematoma and thermal injury to the adjacent gastric antrum, both not necessitating surgical intervention. Conclusions: RF ablation is an effective, safe and relatively simple procedure for the treatment of unresectable liver malignancies. Key words: Hepatocellular carcinoma, Liver neoplasms, Radiofrequency ablation, Therapeutic chemoembolisation
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Ishii, Norihiro, Kenichiro Araki, Takehiko Yokobori, Mariko Tsukagoshi, Takamichi Igarashi, Akira Watanabe, Norio Kubo, Keitaro Hirai, Ken Shirabe, and Hiroyuki Kuwano. "Presence of Cytokeratin 19-Expressing Cholangiocarcinoma-Like Tumour in a Liver Metastatic Lesion of Rectal Neuroendocrine Tumour." Case Reports in Gastroenterology 10, no. 2 (August 12, 2016): 431–39. http://dx.doi.org/10.1159/000446641.
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Introduction: Tumours with adenocarcinoma and neuroendocrine components have often been reported, although the reason underlying the dual components remains unclear. Case Presentation: A 43-year-old woman with multiple liver metastatic lesions of rectal neuroendocrine tumour underwent primary tumour resection and subsequent liver transplantation. Pathological examination indicated a cholangiocarcinoma-like tumour with gland formation, adjacent to a liver metastatic lesion of the neuroendocrine tumour. This tumour comprised atypical columnar epithelium, and stained positively for neuroendocrine markers and the ductal marker cytokeratin 19, indicating amphicrine properties and a partial cholangiocarcinoma phenotype – features not observed in the primary and metastatic neuroendocrine tumours. Conclusion: The presence of adenocarcinoma only at the metastatic site indicated that neuroendocrine tumour cells acquired stemness and differentiated into adenocarcinoma through metastasis, or that the adenocarcinoma newly arose from the adjacent epithelium influenced by the neuroendocrine tumour. We propose a novel mechanism for the pathogenesis of mixed tumours in neuroendocrine tumours.
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Bryan, Richard T., Stuart I. Collins, Mark C. Daykin, Maurice P. Zeegers, KK Cheng, D. Michael A. Wallace, and Graham M. Sole. "Mechanisms of recurrence of Ta/T1 bladder cancer." Annals of The Royal College of Surgeons of England 92, no. 6 (September 2010): 519–24. http://dx.doi.org/10.1308/003588410x12664192076935.
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INTRODUCTION Bladder cancer recurrence occurs via four mechanisms - incomplete resection, tumour cell re-implantation, growth of microscopic tumours, and new tumour formation. The first two mechanisms are influenced by clinicians before and immediately after resection; the remaining mechanisms have the potential to be influenced by chemopreventive agents. However, the relative importance and timing of these mechanisms is currently unknown. Our objective was to postulate the incidence and timing of these mechanisms by investigating the location of bladder cancer recurrences over time. PATIENTS AND METHODS The topographical locations of tumours and their recurrences were analysed retrospectively for 169 patients newly-diagnosed with Ta/T1 bladder cancer, with median follow-up of 33.8 months. Tumours were assigned to one or more of six bladder sectors, and time to recurrence and location of recurrences were recorded. RESULTS Median time to first tumour recurrence was 40 months. Median times between subsequent recurrences were 6.6, 7.9, 8.0 and 6.6 months for recurrences 1 to 2, 2 to 3, 3 to 4, and 4 to 5, respectively. The risk of first tumour recurrence in any given bladder sector increased by nearly 4-fold if the primary tumour was resected from that sector (P < 0.001); this association was not significant for subsequent recurrences. The proportion of tumour recurrences in multiple bladder sectors increased from 13% for the first recurrence to 100% for recurrence seven onwards. CONCLUSIONS First tumour recurrence appears different to subsequent recurrences; incomplete resection and tumour cell re-implantation may dominate at this time-point. Only later does genuine new tumour formation appear to increase in importance. This has important implications for clinical trials, especially those involving chemopreventive agents.
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Al-Balas, Mahmoud, Antonio De Leo, Margherita Serra, Donatella Santini, and Mario Taffurelli. "Granular cell tumour of the breast: A rare presentation of a breast mass in an elderly female with a subsequent breast cancer diagnosis." SAGE Open Medical Case Reports 7 (January 2019): 2050313X1984115. http://dx.doi.org/10.1177/2050313x19841154.
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A 74-year-old female patient presented with a hard breast mass and dimpling with a clinical suspicion of a carcinoma. Histological evaluation revealed a granular cell tumour. Granular cell tumour is a rare neoplasm, mostly benign in origin that may arise in every body site, 5%–15% of cases occur in the breast. It is strongly suggested that granular cell tumours origin is Schwann cells. Clinically, granular cell tumours presentation may mimic mammary carcinoma and their similar features on mammography and ultrasound make it difficult to differentiate between them.
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Escada, Pedro, Clara Capucho, José Madeira Silva, Carlos Bentes Ruah, José Pratas Vital, and Rui Silva Penha. "Cavernous haemangioma of the facial nerve." Journal of Laryngology & Otology 111, no. 9 (September 1997): 858–61. http://dx.doi.org/10.1017/s0022215100138812.
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AbstractFacial nerve haemangiomas are probably the most frequent benign tumours involving the facial nerve in its intratemporal portion. Usually facial nerve dysfunction is present when these tumours are of extremely small size, the average tumour being less than 10 mm. We present a case of a 15 mm diameter cavernous haemangioma of the geniculate region, with histological findings of nerve infiltration, without facial nerve symptoms. The atypical clinical presentation justifies the report and subsequent literature review.
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Gravius, S., O. Weber, G. Goldmann, P. Pennekamp, J. Oldenburg, G. Pagenstert, D. C. Wirtz, A. Seuser, and P. Berdel. "Pseudo tumours in haemophilia patients." Hämostaseologie 29, S 01 (2009): S74—S76. http://dx.doi.org/10.1055/s-0037-1621498.
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SummaryPseudo tumours are amongst the rare yet pathognomonic complications of haemophilia. They are old, encapsulated haematomas which due to their sometimes enormous size can cause massive complaints. These haematomas are surrounded by a thick fibrous capsule. They are attributed to persistent bleedings. The pathophysiology of pseudo tumors is not conclusively established yet. Some believe that they originate from bone material or the periosteum, while others suggest their development from soft tissue. They spread aggressively, displace the surrounding tissue, and cause secondary periosteal erosion of the bone. This results in bone resorption and destruction of surrounding muscular and soft tissue. Pseudo tumours develop slowly over many years. They occur primarily in adults and are largely unresponsive to conservative treatment. Case:A 48-year-old man with moderate hemophilia A (FVIII : C 2%) and no FVIII inhibitor. Due to recurrent bleeding into the muscle of the right thigh diagnosis of two pseudo tumours (psoas, adductor magnus). In 2004 tumour extirpation with subsequent relapse; because of high local bleeding tendency (despite permanent prophylaxis with FVIII concentrate and adjusted lifestyle) surgical revision in 02/2008. Postoperatively, no recurrent bleeding; the patient is fully fit for work three months later. Conclusion: In order to reduce the complication rate when a pseudo tumor is suspected, patients should be treated in a specially equipped interdisciplinary center with adequately trained and experienced surgeons and haemostaseologists.
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Watson, John, and Siew Yeam Chuah. "Technique for the primary culture of human breast cancer cells and measurement of their prostaglandin secretion." Clinical Science 83, no. 3 (September 1, 1992): 347–52. http://dx.doi.org/10.1042/cs0830347.
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1. A method is described for the primary culture of human breast tumour cells on feeder layers of the STO mouse embryo fibroblast cell line. 2. The secretion of the prostaglandins E2 and F2α from the cells was measured and the results indicate that the secretion of both prostaglandins was dependent on oestrogen-receptor status, with cells from oestrogen-receptor-positive tumours secreting significantly more prostaglandin than cells from oestrogen-receptor-negative tumours. 3. Postaglandin E2, but not prostaglandin F2α, secretion was also significantly greater from cells of tumours from postmenopausal women than from cells of tumours from premenopausal women. Small (< 3 cm) tumours secreted significantly more prostaglandin than large (> 3 cm) tumours, and increased levels of prostaglandin were secreted with advancing clinical stage (T1-T4). 4. Additional evidence for increased prostaglandin metabolism in oestrogen-receptor-positive tumours compared with oestrogen-receptor-negative tumours was obtained from studies on the uptake of [14C]arachidonic acid from the cultures. Significantly more labelled arachidonic acid was incorporated into cells from oestrogen-receptor-positive tumours compared with oestrogen-receptor-negative tumours, with the subsequent release of more prostaglandin in response to various stimuli.
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Nyanti, Larry E., Andy Sing Ong Tang, Adam Malik b. Ismail, Lee Ping Chew, and Tze Shin Leong. "Spontaneous tumour lysis syndrome as a rare presentation of thymoma with peripheral blood lymphocytosis." Proceedings of Singapore Healthcare 31 (April 2022): 201010582210899. http://dx.doi.org/10.1177/20101058221089989.
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Tumour lysis syndrome is common in haematological malignancies but is rarely reported in solid tumours. Peripheral blood lymphocytosis is an autoimmune feature of thymomas. We report a 63-year-old female who presented with a mediastinal mass, spontaneous tumour lysis syndrome and a leukoerythroblastic picture on peripheral blood film. Bone marrow aspiration and trephine biopsy ruled out haematological malignancy. Subsequent biopsy of the mediastinal mass confirmed thymoma. This is the first reported case of thymoma with peripheral blood lymphocytosis presenting with spontaneous tumour lysis syndrome. Clinicians are reminded that solid tumours may masquerade as haematological malignancies in the presence of peripheral blood lymphocytosis, hence careful clinical evaluation is needed to differentiate between the two diagnoses.
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Morcavallo, Alaide, Karen Barker, Toma Adachi, Jessica K. R. Boult, Colin Kwok, Patricia Benites Goncalves da Silva, Konstantin Okonechnikov, et al. "TMOD-03. A NOVEL MB GR3 TRANSGENIC MOUSE MODEL IS GENERATED BY MYCN AND P53 DEFECTS IN VENTRICULAR ZONE PROGENITORS." Neuro-Oncology 23, Supplement_1 (June 1, 2021): i36. http://dx.doi.org/10.1093/neuonc/noab090.144.
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Abstract Medulloblastoma (MB) represents the most common embryonal tumour of the Central Nervous System in childhood. MB occurs in the cerebellum and molecular features dictate the classification into four subgroups. Although Group3 (Gr3) MB tumours are dominated by primitive progenitor-like cells, the cells of origin remain unidentified. Gr3 MB is associated with relatively common MYC family member amplification and overexpression, often combined with p53 pathway defects at relapse. Molecularly stratified treatment is not yet available, causing Gr3 MB and its subsequent relapse to often represent an unstoppable progressive disease. The limited understanding of Gr3 tumorigenesis and targeted therapy development is also due to the lack of faithful in vivo models and consequently, their use in preclinical studies. We have now developed a new germline genetically engineered mouse model (GEMM), harbouring MYCN amplification in a p53 inactive background (tamoxifen-inducible p53 activation, Trp53ERTAM). The purpose of the GEMM is to investigate the developmental significance of MYC aberration in putative Gr3 MB cells of origin and exploit it in preclinical studies. A LSL-MYCN-Luciferase strain was crossed with mice expressing Cre recombinase under the Blbp promoter and subsequently to Trp53ERTAM inducible mice. As result, the MYCN overexpression alone did not generate tumours, conversely to the combination of MYCN with p53 deregulation. Tumours arise exclusively in the hindbrain of homozygote mice, with a penetrance of 100% and a latency of ~135 days. Pathology report suggests tumours are Gr3 MB with large cell/anaplastic (LCA) histology. Preliminary transcriptional profiling data analysis reveals that tumours share molecular features with human counterparts, clustering with Gr3 MB. Ongoing analysis will explore the tumour cells of origin, followed by tumour progression alteration restoring p53 activity and blood-brain barrier integrity status. In conclusion, we have developed a MYCN/Trp53ERTAM Gr3 MB GEMM arising from ventricular zone progenitor cells and resembling human cancer characteristics.
Dissertations / Theses on the topic "Subsequent tumours"
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Charrier, Thibaud. "Study of the occurrence of multiple iatrogenic events in long-term survivors of childhood cancer." Electronic Thesis or Diss., université Paris-Saclay, 2024. http://www.theses.fr/2024UPASR030.
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Le taux de survie à 5 ans des cancers de l'enfant atteint aujourd'hui 80 %. Les survivants à 5 ans de cancer pédiatrique (CCS) ont cependant un risque accru d'occurrence de nombreux évènements. Beaucoup d'études ont été réalisé pour comprendre les liens entre ces évènements iatrogènes et les traitements pédiatriques, et un taux élevé d'évènements iatrogènes multiples a été observé. Cependant, ce taux d'évènements iatrogènes multiples est méconnu. Ce projet de thèse avait pour objectif d'étudier les causes et conséquences de ce taux élevé.La recherche présentée dans cette thèse est basée sur les données de la French Childhood Cancer Survivors Study, une cohorte rétrospective à suivi prospectif de 7670 CCS diagnostiqués avant l'âge de 21 ans entre 1945 et 2000 en France. La cohorte contient des données détaillées sur les traitements des cancers pédiatriques, et un important travail de validation des évènements iatrogènes a été réalisé.Nous avons utilisé la méthode de landmark combiné avec des pseudo-observations, afin de pouvoir étudier les effets des seconds cancers sur l'incidence cumulée d'évènement cardiaque et les années de vie perdues des patients.Nous avons constanté une augmentation de risque instantanné (csHR: 2.1, 95% CI: 1,5-2,9) et de l'incidence cumulée d'évènement cardiaque (CD) (+3,8%, 95% CI: 0,5-7,1) après un second cancer. Nous avons aussi constaté un impact de la radiothérapie, des seconds cancers, et des CD sur l'espérance de vie des patients, avec respectivement 6, 10,5 et 7,7 années de vie perdues à 16 ans. Nous avons trouvé un effet nul de l'interaction entre second cancer et CD, mais notre analyse de simulation a montré que ce résultat est biaisé par la corrélation entre seconds cancers et CD.En conclusion, dans cette thèse nous avons démontré que le risque accru de multi-morbidité chez les CCS est partiellement attribuable à l'occurrence d'un premier évènements iatrogène. Nous avons aussi montré un fort impact des seconds cancers et évènements cardiaques sur l'espérance de vie des patients. Ces résultats nous ammènent à recommander une forte surveillance des patients dévelopant l'une de ces maladies, et de poursuivre la recherche sur la multi-morbidité chez les CCS qui apapraît complexe et forte de conséquences pour les patients5-years survival of childhood cancer exceeds 80% today. Nonetheless, 5-year childhood cancer survivors (CCS) are at increased risk of health-related late effects. Many studies have been conducted to investigate the link between those late effects and childhood cancer treatments. Furthermore, an elevated number of patients experiencing multiple iatrogenic event was observed. However, little is known about the causes of this multi-morbidity. This thesis aimed to study the causes et consequences of this elevated multi-morbidity.Research presented in this thesis is based on the French Childhood Cancer Survivors Study, a retrospective cohort with prospective follow-up, following 7,670 CCS diagnosed in France before 21 years old between 1945 and 2000. This cohort contains detailed data regarding childhood cancer treatments, and the iatrogenic event observed were validated by trained professionals.We used the landmark method combined with pseudo-observations to study the consequences of subsequent malignant neoplasm on the cumulative incidence of cardiac disease, and the life years lost by CCS.We found a subsequent malignant neoplasm (SMN) to cause a two-fold increase in the cause-specific hazard of cardiac disease (CD) and a 3.8% increase of its cumulative incidence. We found the use of radiotherapy to treat childhood cancer, the occurrence of SMN, and of CD to impact the life expectancy of CCS, with respectively 6, 10.5, and 7.7 life years lost at 16 years old. We found a nul effect of the interaction of SMN and CD on the life expectancy, although our simulation study suggested this was biased by the correlation between SMN and CD.In conclusion, we demonstrated that the increased risk of multi-morbidity among CCS is partially attributable to the occurrence of a first iatrogenic event. We also showed that subsequent malignant neoplasm and cardiac disease have a strong impact on the life expectancy of CCS. Therefore, we recommend to keep following in details the CCS developing either disease, and to pursue further research on the multi-morbidity among CCS which appears to be complex and consequentful for patients
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Trabbic, Kevin R. "Approaches to Increase the Immunogenicity of Carbohydrate Antigens Using PS A1 and Subsequent Immunotherapies." University of Toledo / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=toledo1470330973.
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Al-Shudiefat, Abd Al-Rahman. "Protective role of olive oil and its major component oleic acid in TNF-α induced remodeling subsequent to myocardial infarction in rats." Springer, 2013. http://hdl.handle.net/1993/20074.
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Oxidative stress and inflammation are important factors involved in the progression of heart failure. An important cytokine produced during myocardial infarction (MI) is tumor necrosis factor alpha (TNF-α). TNF-α may induce oxidative stress, cell damage, apoptosis and cardiac dysfunction. Considering the anti-inflammatory and anti-oxidant properties of extra-virgin olive oil and its major component (80%) oleic acid (OA), and their benefits to the cardiovascular system, we hypothesized that the negative effects of TNF-α in the pathogenesis of heart failure will be mitigated by olive oil consumption. This hypothesis was tested by examining the effects of a special diet supplemented with 10% olive oil, in coronary artery ligated animal model of MI. Corn oil (10%) supplementation was used as a control for matching caloric intake. Animals in the sham and ligated groups fed regular chow, olive oil, and corn oil were studied at 4 and 16 weeks post myocardial infarction (PMI).
Mortality, diet consumption, weight gain and conduction system abnormalities were comparable among all ligated groups. Echocardiography showed that MI deteriorated cardiac function, and olive oil restored the function. At 16 weeks PMI, only corn oil fed groups showed significant increase in both total cholesterol and HDL. Corn oil was not able to offer protection to the heart, suggesting that the beneficial effects of olive oil are not due to increased caloric intake or increased HDL. MI increased myocardial TNF-α, oxidative stress, lipid peroxidation, pro-apoptotic protein expression (Bax, cleaved Caspase 3, cleaved PARP, TGFβ, Bnip3), cytochrome C release, MAP kinase activation (p38, JNK) and decreased anti-apoptotic protein Bcl-xL expression at both 4 and 16 weeks PMI, and these changes were modulated by olive oil.
In order to further test the central role of TNF-α PMI, we examined the possible miti-gation of TNF-α induced changes by OA in isolated adult rat cardiomyocytes. TNF-α in-creased oxidative stress, cell damage, cell death, and apoptosis, while OA treatment miti-gated these TNF-α induced effects.
We concluded that TNF-α is implicated in the progression of heart failure subsequent to MI and that OA in olive oil may prevent this progression, through its anti-oxidant, anti-inflammatory, anti-hypertensive, and inotropic effects.
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Lampel, Netanya. "Screening of the human tumor necrosis factor (TNF) gene and its receptor 1 (TNFR1) gene for DNA alterations and the subsequent investigation of these and an IL12p40 polymorphism for an association with paediatric tuberculosis." Master's thesis, University of Cape Town, 2004. http://hdl.handle.net/11427/8628.
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Includes bibliographical references (leaves 85-96).Infection with Mycobacterium tuberculosis is characterised by diverse outcomes; the majority of infected individuals remain well and yet others develop disease ranging from limited pulmonary tuberculosis to severe disseminated disease. The reasons for this diverse outcome are poorly understood, but host factors are thought to play an important role. In particular, a genetic component to susceptibility to tuberculosis has been proposed. An important clue was the description of a group of Maltese children with an unusual susceptibility to progressive non-tuberculous mycobacterial infections. These patients showed defective tumor necrosis factor (TNF) production in response to endotoxin and a failure to upregulate TNF production in response to interferon gamma as well as diminished interferon gamma production during T-cell proliferation. They were found to lack expression of the interferon gamma receptor ligand-binding chain (IFN-yR1) on their cell surfaces due to a single point substitution resulting in a truncated protein. Since then other defects in the type 1 cytokine pathway leading to susceptibility to non-tuberculous mycobacteria, as well as to tuberculosis, have been described in rare isolated cases. From these findings, the hypothesis arose that less severe mutations in such pathways might individually, or in combination, lead to increased susceptibility to tuberculosis in the general population. The following study forms part of a larger multi-centre collaboration, which aims to better understand the genetic basis of susceptibility to mycobacterial infection by addressing this hypothesis. The approach taken has been the recruitment and immuno-phenotyping of a large group of children with tuberculosis as well as control subjects. Candidate genes, of the type 1 cytokine pathways being investigated, include interferon gamma, interleukin12 and their receptors and TNF. The focus of the study described in this thesis has been the screening of a sub-cohort of patients and control subjects for DNA sequence alterations in the TNF and TNFR1 genes. The individuals in this cohort were selected on the basis of their whole blood stimulation assays, where either high or low levels of TNF in response to non-specific stimulatory factors, were the determining criteria. It was assumed that these two phenotypic groupings would be enriched for gene variants contributing to the TNF responses recorded in the stimulation assays. Once identified, these polymorphisms would be screened for frequencies in the broader patient and control groupings and assessed for any association with susceptibility to tuberculosis. This study was considered important in attempting to explain which genes and their polymorphisms are involved in determining the high prevalence of tuberculosis in African populations.
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PILLAI, Vinoshene. "Intravital two photon clcium imaging of glioblastoma mouse models." Doctoral thesis, Scuola Normale Superiore, 2021. http://hdl.handle.net/11384/109211.
Full textBooks on the topic "Subsequent tumours"
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Archer, Nick, and Nicky Manning. Cardiac tumours. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199230709.003.0018.
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Introduction 252Echogenic foci 254Rhabdomyoma 258Teratoma 260Fibroma 262Haemangioma 262Myxoma 262• Cardiac tumours are rare.• Identification requires subsequent monitoring for:• Fetal well-being.• Growth of the tumour.• Planning management of delivery and neonatal period.• It is important to consider the possibility of non-cardiac problems....
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Winter, Christian, and Peter Albers. Testicular cancer. Edited by James W. F. Catto. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199659579.003.0090.
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Testicular germ cell tumours (GCTs) represent the most common solid malignancy of young men aged 15–40 years. The disease is rising in incidence. Germ cell tumours are best divided into those with pure seminoma and non-seminoma (NSGCT) histology. While cryptorchidism is clearly established as a risk factor, the pathogenesis of testicular cancer remains unknown. Familial studies and molecular analyses suggest an association to genetic alterations. Most testicular cancer patients present a primary tumour in the testis. Diagnostic examinations include testis palpation and ultrasound, and measurement of serum tumour markers (AFP, ß-HCG, and LDH). Surgical exploration is obligatory for suspected tumours and radical orchidectomy should be performed if a tumour is found. Prognosis and subsequent treatment depends upon the clinical stage and the IGCCCG classification (in case of advanced GCT disease).
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Kennish, Steven. Interventional radiology. Edited by Michael Weston. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199659579.003.0135.
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Advances in imaging technology allow ever more complex yet minimally invasive diagnostic and therapeutic interventions to take place in the genitourinary tract. Imaging provides precise targeting for tissue biopsy to facilitate rapid and accurate diagnosis—the basis of all subsequent treatment regimes. Percutaneous renal intervention is invaluable in the treatment of complex stone disease and for renal preservation in the patient with malignant or benign urinary tract obstruction. Antegrade ureteric procedures allow strictures, stones, and tumours to be tackled, often with much greater ease than an alternative retrograde approach. Although interventional radiological procedures are generally safe, they do come with risks such as bleeding and sepsis, as well as the longer-term complications related to indwelling drains, catheters, and stents. It is important for the urological surgeon to be familiar with interventional uroradiological techniques so as to appropriately counsel and care for patients who require these procedures.
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Bagrodia, Aditya, and Yair Lotan. Low and intermediate risk non-muscle-invasive bladder cancer. Edited by James W. F. Catto. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199659579.003.0076.
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Bladder cancer is a common disease that affects more males than females. Most bladder tumours are histologically typed as urothelial cell carcinoma, and these are best divided into cancers invading the muscularis propria and non-invasive malignancies confined to the bladder. The latter are the majority of cancers and include low risk, indolent cancers that may recur within the bladder but not progress to invasion or metastases, and a proportion that subsequently progress to muscle invasion. The risk of intravesical recurrence or progression to invasion from a non-invasive bladder cancer can be stratified as low, intermediate, and high using various pathological factors (such as tumour grade, stage, size, multiplicity, and the presence of carcinoma in situ). In this chapter, we will give an overview of bladder cancer and focus upon tumours at low or intermediate risk of developing future progression to invasion.
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Grant, Warren, and Martin Scott-Brown. Principles of oncogenesis. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0322.
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It is obvious that the process of developing cancer—oncogenesis—is a multistep process. We know that smoking, obesity, and a family history are strong independent predictors of developing malignancy; yet, in clinics, we often see that some heavy smokers live into their nineties and that some people with close relatives affected by cancer spend many years worrying about a disease that, in the end, they never contract. For many centuries scientists have struggled to understand the process that make cancer cells different from normal cells. There were those in ancient times who believed that tumours were attributable to acts of the gods. Hippocrates suggested that cancer resulted from an imbalance between the black humour that came from the spleen, and the other three humours: blood, phlegm, and bile. It is only in the last 100 years that biologists have been able to characterize some of the pathways that lead to the uncontrolled replication seen in cancer, and subsequently examine exactly how these pathways evolve. The rampant nature by which cancer invades local and distant tissues, as well its apparent ability to spread between related individuals led some, such as Peyton Rous in 1910, to suggest that cancer was an infectious condition. He was awarded a Nobel Prize in 1966 for the 50 years of work into investigating a link between sarcoma in chickens and a retrovirus that became known as Rous sarcoma virus. He had shown how retroviruses are able to integrate sequences of DNA coding for errors in cellular replication control (oncogenes) by introducing into the human cell viral RNA together with a reverse transcriptase. Viruses are now implicated in many cancers, and in countries where viruses such as HIV and EBV are endemic, the high incidence of malignancies such as Kaposi’s sarcoma and Burkitt’s lymphoma is likely to be directly related. There are several families of viruses associated with cancer, broadly classed into DNA viruses, which mutate human genes using their own DNA, and retroviruses, like Rous sarcoma virus, which insert viral RNA into the cell, where it is then transcribed into genes. This link with viruses has not only led to an understanding that cancer originates from genetic mutations, but has also become a key focus in the design of new anticancer therapies. Traditional chemotherapies either alter DNA structure (as with cisplatin) or inhibit production of its component parts (as with 5-fluorouracil.) These broad-spectrum agents have many and varied side effects, largely due to their non-specific activity on replicating DNA throughout the body, not just in tumour cells. New vaccine therapies utilizing gene-coding viruses aim to restore deficient biological pathways or inhibit mutated ones specific to tumour cells. The hope is that these gene therapies will be effective and easily tolerated by patients, but development is currently progressing with caution. In a trial in France of ten children suffering from X-linked severe combined immunodeficiency and who were injected with a vector that coded for the gene product they lacked, two of the children subsequently died from leukaemia. Further analysis confirmed that the DNA from the viral vector had become integrated into an existing, but normally inactive, proto-oncogene, LM02, triggering its conversion into an active oncogene, and the development of life-threatening malignancy. To understand how a tiny change in genetic structure could lead to such tragic consequences, we need to understand the molecular biology of the cell and, in particular, to pay attention to the pathways of growth regulation that are necessary in all mammalian cell populations. Errors in six key regulatory pathways are known as the ‘hallmarks of cancer’ and will be discussed in the rest of this chapter.
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Rogler, Gerhard. Gastrointestinal system. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0021.
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Rheumatic diseases and diseases of the gastrointestinal (GI) tract are connected in two ways. The extraintestinal manifestations of inflammatory GI diseases such as inflammatory bowel disease affect joints in up to one-third of patients. On the other hand, several rheumatic diseases such as vasculitis or systemic lupus erythematosus (SLE) induce a wide spectrum of gastrointestinal manifestations. The GI tract constitutes a huge area in contact with the environment. It is exposed to billions of food antigens, commensal bacteria, and potential pathogens. Some of those antigens are thought to play a role in the pathogenesis of rheumatic diseases. The intestinal barrier function and the gut immune system are tightly regulated, as on one hand tolerance for food antigens and the resident commensal flora needs to be maintained, and on the other hand pathogens need to be rapidly and effectively eliminated. Non-infectious, chronic inflammatory diseases of the small and large intestine with rheumatic manifestations have been well known for decades. Among the susceptibility genes for Crohn's disease and ulcerative colitis are some that also cause susceptibility to rheumatoid arthritis or SLE, indicating a shared susceptibility and overlapping pathological mechanisms. Subsequently, similar therapeutic principles have successfully been applied in autoimmune GI and rheumatological diseases such as steroids, immunosuppressants, and anti-TNF (tumour necrosis factor) antibodies.
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McGregor, Laura, Monica N. Gupta, and Max Field. Septic arthritis in adults. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0098.
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Septic arthritis (SA) is a medical emergency with mortality of around 15%. Presentation is usually monoarticular but in more than 10% SA affects two or more joints. Symptoms include rapid-onset joint inflammation with systemic inflammatory responses but fever and leucocytosis may be absent at presentation. Treatment according to British Society of Rheumatology/British Orthopaedic Association (BSR/BOA) guidelines should be commenced if there is a suspicion of SA. At-risk patients include those with primary joint disease, previous SA, recent intra-articular surgery, exogenous sources of infection (leg ulceration, respiratory and urinary tract), and immunosupression because of medical disorders, intravenous drug use or therapy including tumour necrosis factor (TNF) inhibitors. Synovial fluid should be examined for organisms and crystals with repeat aspiration as required. Most SA results from haematogenous spread-sources of infection should be sought and blood and appropriate cultures taken prior to antibiotic treatment. Causative organisms include staphylococcus (including meticillin-resistant Staphylococcus aureus, MRSA), streptococcus, and Gram-negative organisms (in elderly patients), but no organism is identified in 43%, often after antibiotic use before diagnosis. Antibiotics should be prescribed according to local protocols, but BSR/BOA guidelines suggest initial intravenous and subsequent oral therapy. Medical treatment may be as effective as surgical in uncomplicated native SA, and can be cost-effective, but orthopaedic advice should be sought if necessary and always in cases of infected joint prostheses. In addition to high mortality, around 40% of survivors following SA develop limitation of joint function. Guidelines provide physicians with treatment advice aiming to limit mortality and morbidity and assist future research.
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Sieper, Joachim. Ankylosing spondylitis. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0113.
Full textAbstract:
Ankylosing spondylitis (AS) is a chronic inflammatory disease predominantly of the sacroiliac joint (SIJ) and the spine. It starts normally in the second decade of life and has a slight male predominance. The prevalence is between 0.2 and 0.8% and is strongly dependent on the prevalence of HLA B27 in a given population. For the diagnosis of AS, the presence of radiographic sacroiliitis is mandatory. However, radiographs do not detect active inflammation but only structural bony damage. Most recently new classification criteria for axial spondyloarthritis (SpA) have been developed by the Assessement of Spondylo-Arthritis international Society (ASAS) which cover AS but also the earlier form of non-radiographic axial SpA. MRI has become an important new tool for the detection of subchondral bone marrow inflammation in SIJ and spine and has become increasingly important for an early diagnosis. HLA B27 plays a central role in the pathogenesis but its exact interaction with the immune system has not yet been clarified. Besides pain and stiffness in the axial skeleton patients suffer also from periods of peripheral arthritis, enthesitis, and uveitis. New bone formation as a reaction to inflammation and subsequent ankylosis of the spine determine long-term outcome in a subgroup of patients. Currently only non-steroidal anti-inflammatory drugs (NSAIDs) and tumour necrosis factor (TNF) blockers have been proven to be effective in the medical treatment of axial SpA, and international ASAS recommendations for the structured management of axial SpA have been published based on these two types of drugs. Conventional disease-modifying anti-rheumatic drugs (DMARDs) such as methotrexate are not effective.
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Sieper, Joachim. Axial spondyloarthropathies. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199642489.003.0113_update_003.
Full textAbstract:
Axial spondyloarthritis (axSpA) is a chronic inflammatory disease predominantly of the sacroiliac joint (SIJ) and the spine. It starts normally in the second decade of life and has a slight male predominance. The prevalence is between 0.2% and 0.8% and is strongly dependent on the prevalence of HLA-B27 in a given population. AxSpA can be split in patients with radiographic axSpA (also termed ankylosing spondylitis (AS)) and in patients with non-radiographic axSpA (nr-axSpA). For the diagnosis of AS, the presence of radiographic sacroiliitis is mandatory. However, radiographs do not detect active inflammation but only structural bony damage. Most recently new classification criteria for axSpA have been developed by the Assessment of Spondylo-Arthritis International Society (ASAS) which cover AS but also the earlier form of nr-axSpA. MRI has become an important new tool for the detection of subchondral bone marrow inflammation in SIJ and spine and has become increasingly important for an early diagnosis. HLA-B27 plays a central role in the pathogenesis but its exact interaction with the immune system has not yet been clarified. Besides pain and stiffness in the axial skeleton patients suffer also from periods of peripheral arthritis, enthesitis, and uveitis. New bone formation as a reaction to inflammation and subsequent ankylosis of the spine determine long-term outcome in a subgroup of patients. Currently only non-steroidal anti-inflammatory drugs (NSAIDs) and tumour necrosis factor (TNF) blockers have been proven to be effective in the medical treatment of axial SpA, and international ASAS recommendations for the structured management of axial SpA have been published based on these two types of drugs. Conventional disease-modifying anti-rheumatic drugs (DMARDs) such as methotrexate are not effective.
Book chapters on the topic "Subsequent tumours"
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Harrington, Kevin J., Charleen M. L. Chan Wah Hak, Antonio Rullan, and Emmanuel Patin. "DNA Repair Mechanisms as a New Target in Head and Neck Cancer." In Critical Issues in Head and Neck Oncology, 23–35. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-23175-9_3.
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AbstractUntil recently, radiotherapy was viewed solely from a tumour cell-autonomous perspective, whereby successful therapy resulted from inflicting breaks in nuclear DNA above an unspecified threshold that exceeded the tumour cell’s capacity for repair. Greater understanding of the importance of non-tumour cell-autonomous, immunological aspects of radiation-induced cell death in the context of the tumour micro-environment (TME) has altered this rather narrow perception. We now know that clinical responses to radiotherapy are inextricably linked to the immune system: loco-regional radiotherapy can trigger abscopal, immune-mediated responses at distant unirradiated sites (albeit rarely), while patients who are pathologically or iatrogenically immunosuppressed may derive less benefit from radiotherapy. The intrinsic biology of individual tumours, their associated microenvironments, and the physical characteristics of the delivered radiation, can all influence the immunogenicity of radiotherapy. By understanding and modulating cross-talk between molecular responses to radiation-induced DNA damage, associated mechanisms of cell death and subsequent innate and adaptive immune responses, we may be able to improve clinical outcomes of radiotherapy.In this chapter, the focus will be on mechanisms of DNA damage repair and how tumours exploit alterations in these to enhance their survival. However, tumour cell-intrinsic aberrations in DNA repair can render tumour cells vulnerable to the effects of radiotherapy and this may be enhanced further by rational use of targeted DNA damage-response inhibitors. In particular, we will focus on how disordered DNA repair and its pharmacological modulation through ataxia telangiectasia and Rad3-related kinase inhibition can lead to radiation-induced immunostimulation and how this can be exploited further in the clinic through the use of specific immunotherapies, such as immune checkpoint blockers. As part of the discussion, specific mechanisms of radiation-induced cell death will be discussed, with emphasis on mechanisms of triggering immunologically visible, pro-inflammatory modes of cell death.
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Thomsen, A. R., M. R. Saalmann, N. H. Nicolay, A. L. Grosu, and Peter Vaupel. "Temperature Profiles and Oxygenation Status in Human Skin and Subcutis Upon Thermography-Controlled wIRA-Hyperthermia." In Water-filtered Infrared A (wIRA) Irradiation, 69–80. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-92880-3_5.
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AbstractEfficacy of wIRA immediately followed by hypofractionated radiation in the treatment of locally recurrent breast cancer and other superficial tumors is documented. A prerequisite for the additive and synergistic radiosensitizing properties of hyperthermia is the assessment of resulting temperatures of tumors and normal tissues. To assess the role of hyperthermia in reversing tumor hypoxia through its effects on local blood flow, oxygen profiles in skin, subcutis, and superficial tumors have been additionally assessed during mild hyperthermia (39–43 °C).Upon wIRA-exposure, skin surface temperatures increased from 35 to 41.6 °C within 5–12 min. Maximum temperatures of 42 °C were found in subepidermal regions, with a steady decline in deeper layers reaching 40.1 °C at a depth of 20 mm. Heating was accompanied by increases in tissue oxygen tensions. Effective hyperthermia levels (≥ 39 °C) were established in depths up to 25 mm. Following wIRA exposure, tissue temperatures returned to pretreatment levels within a few minutes, with the decay time depending on tissue depths, while pO2 values remained on therapeutical levels for 30–60 min postheat, outlasting the period needed for subsequent radiotherapy. Monitoring in the upper dermis layer of skin and recurrent breast cancers confirmed the improved O2 status during wIRA exposure and outlasted the time needed for subsequent radiotherapy.
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Mertens, Ann C., and Thorsten Langer. "Rare Subsequent Primary Cancers in Pediatric Cancer Survivors." In Rare Tumors In Children and Adolescents, 529–36. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-04197-6_46.
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Smits, Daan, and Antoine A. Khalil. "Multimodal Techniques to Study Tumor Growth, Basement Membrane Breaching, and Invasion in 3D Matrices." In Cell Migration in Three Dimensions, 281–303. New York, NY: Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-2887-4_17.
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AbstractCancer-derived organoids and three-dimensional (3D) extracellular matrix (ECM) are taking center stage as in vitro models to study neoplastic cell behavior, since they recapitulate the heterogeneous cellular composition of tumors and their extracellular environment. In combination with imaging and molecular/biochemical techniques, 3D organoid models have contributed substantially to our knowledge about the cellular and molecular mechanisms that regulate the growth of tumors and invasion into the surrounding tissue. We here outline a set of protocols that describe culturing of cancer-derived organoids in 3D matrices and various strategies that allow modeling of tumor growth, tumor cell penetration into basement membranes, and invasion into Collagen I-rich ECM. Furthermore, we specify protocols for subsequent handling of organoids cultured in 3D ECM for confocal microscopy and analysis of gene expression at the protein and mRNA level. Although we here use breast cancer-derived organoids, these protocols can be directly applied or adapted for organoids derived from other cancer types or healthy tissues. Thus, in addition to investigating cell behavior of multiple cancer types, the combination of protocols described here may be used to study processes such as cell differentiation and migration during homeostasis and normal development.
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Turmak, Mehmet. "Embolization Procedures in Oncological Patients." In The Radiology of Cancer, 569–89. Istanbul: Nobel Tip Kitabevleri, 2024. http://dx.doi.org/10.69860/nobel.9786053359364.37.
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Embolization is a vascular interventional procedure that employs various materials to obstruct the blood flow of a vessel or tumor. Embolization in oncologic patients serves a multitude of purposes, including the cessation of tumor or tissue blood flow by means of catheterization with various materials, the reduction of tumor size by creating ischemia through the coverage of the most distal region, and the mitigation of bleeding risk during surgery by the administration of preoperatively in hypervascular tumors. It is of great importance that the embolization targets the distal bed, as proximal embolization may cause neovascularization at a later stage, which may ultimately lead to failure of the technically correct procedure. Therefore, the choice of embolizing particles is a crucial step. The use of too large particles may result in proximal occlusion, whereas the use of too small particles may lead to mucosal necrosis, chronic pain, or unwanted tissue and/or organ embolization via microcollaterals. In this chapter, our objective is to provide a concise overview of embolizing agents and subsequently discuss embolization procedures in head and neck, renal, pelvic-gynecological, and bone tumors, respectively.
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Wirtz, Ralph M. "Molecular In Vitro and In Vivo Diagnostics as the Impartible Basis of Multimodal Therapy Approaches in Precision Oncology." In Beyond Becquerel and Biology to Precision Radiomolecular Oncology: Festschrift in Honor of Richard P. Baum, 361–65. Cham: Springer International Publishing, 2024. http://dx.doi.org/10.1007/978-3-031-33533-4_36.
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AbstractIn 2000, more than two decades ago, genome-wide gene expression profiling became available and thereafter led to the dissection of cancer biology across almost all entities [1–3]. First, the molecular portraits based on RNA expression profiling (termed “heat maps”) were used in breast cancer to identify luminal, ERBB2-positive, and basal tumors. Interestingly, these subtypes not only elucidated the underlying biology but also directly suggested targeted treatment intervention with luminal tumors being hormone-dependent, ERBB2-positive tumors exposing the transmembrane receptor Her-2/neu and basal tumors lacking homogenous expression of typical targeted treatment options, with the latter being termed “triple negative” later on. Interestingly, genome-wide mutation analysis later on revealed that the luminal subtype, while bearing most mutations (such as PIK3CA) exhibited lowest immunogenicity and frequently absence of tumor-infiltrating lymphocytes. In contrast, the basal subtype turned out to have lowest rate of classical oncogens, but was dominated by loss-of-function mutation of p53 [4], while almost half of basal tumors being infiltrated by large amounts of immune cells. This led to the assumption that hormone regulation affects immune cell recognition and three biological axes (hormone, immune, and proliferation axis) were built up for breast cancer as being the coordinates of the biological universe of breast cancer [5, 6]. The therapeutic implication of these fundamental insights were further explored and validated the distinct sensitivity towards antihormonal treatment, ERBB2 targeting, and chemotherapy. Interestingly, the hormone-insensitive, highly proliferating basal and ERBB2-positive tumors with higher amounts of immune cell infiltrates did respond best to neoadjuvant treatment with superior outcome [7]. As one consequence, the concept arose to develop RNA-based vaccination concepts in the post-neoadjuvant situation of triple negative breast cancer not responding to neoadjuvant chemotherapy by targeting individual neo-epitope patterns [8], which has been investigated in the subsequent “Merit” trial with positive proof of concept [9]. In line with this, the first approval of checkpoint therapy treatment in breast cancer happened in the triple negative breast cancer subtype [10].
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Armstrong, Gregory T., Raja B. Khan, and Wassim Chemaitilly. "Long-Term Outcomes Among Survivors of Childhood Central Nervous System Malignancies: Late Mortality, Subsequent Neoplasms, Endocrine and Neurologic Morbidity." In Brain Tumors in Children, 347–78. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-43205-2_15.
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Gosa, Laura, Lisa Ta, and David A. Nathanson. "Processing of Primary Patient Tumors and Subsequent Generation of Primary Cell Lines." In Methods in Molecular Biology, 425–31. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8935-5_34.
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Iwamoto, Shungo, Naoki Itano, and Hiroshi Nakada. "Tumor Progression through Interaction of Mucins with Lectins and Subsequent Signal Transduction." In Glycosignals in Cancer, 171–211. Singapore: Springer Nature Singapore, 2023. http://dx.doi.org/10.1007/978-981-19-7732-9_9.
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Colli, Benedicto Oscar, Carlos Gilberto Carlotti Junior, Ricardo Santos de Oliveira, and Guilherme Gozzoli Podolski Gondim. "Venous Compromise/Deep Venous Thrombosis During Parasagittal Meningiomas Resection." In Acta Neurochirurgica Supplement, 27–32. Cham: Springer Nature Switzerland, 2024. http://dx.doi.org/10.1007/978-3-031-61601-3_5.
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AbstractWe are reporting the case of JB, a 28-year-old male who presented to our hospital in 2009. The patient reported a progressive increase in a known mass that had been deforming their head since 2005. He had suffered from a first-time seizure four years later (in 2009). Neurological examination revealed a large tumor protruding in the parietal region, which was confirmed by CT. A subsequent MRI demonstrated a hyperostotic contrast-enhancing parasagittal tumor occluding the middle third of the superior sagittal sinus, with cortical veins joining the sinus adjacent to the tumor.The patient was taken to the OR for a craniotomy and a resection of the tumor with cranioplasty in the same setting. The tumor was exposed by using a straight incision on the scalp. A craniotomy was performed around the tumor by using multiple burr holes; now the bone could be separated from the dura and removed. The intradural tumor was exposed, and a cortical vein draining into the tumor could not be preserved. Some residual tumor was left close to the anterior part of the superior sagittal sinus. The dura was reconstructed with pericranium, and the bony defect was closed with titanium mesh. The patient woke up initially paraplegic, but 7 days later, he started with proximal movements in both legs. Unfortunately, he died suddenly in the second postoperative week, due to pulmonary embolism. The case is reviewed in this manuscript to analyze the contributing factors of the complications that were observed and to suggest management strategies to avoid them.
Conference papers on the topic "Subsequent tumours"
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Mukhopadhyay, Asima, Nicola Curtin, and Richard Edmondson. "Clinico-pathological correlation of homologous recombination status in epithelial ovarian cancer: Surgeon’s perspective." In 16th Annual International Conference RGCON. Thieme Medical and Scientific Publishers Private Ltd., 2016. http://dx.doi.org/10.1055/s-0039-1685292.
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Background: TCGA data using expensive multi-modality diagnostic platforms have shown that 50% epithelial ovarian cancers (EOCs) are estimated to be homologous recombination (HR) deficient (HRD). We developed a functional assay for HR using gamma H2AX-Rad51 immunofluoresence.[1] Methods: Primary cultures were developed in 50 consecutive EOCs from ascetic fluid and HR assay was performed. Results: 50% patients were HRD based on the functional assay and show improved ex-vivo chemosensitivity to PARP inhibitor (PARPi) (PPV = 92%, NPV = 100%). HRD patients showed improved platinum sensitivity (53.8% vs 16.7%), survival (12 month OS - 41.7% vs. 11.5%) and optimal cytoreduction (80% vs. 62%) rates compared to HR competent (HRC) tumours which are less responsive and represent an unmet clinical need. Conclusions: Personalised surgical and chemotherapeutic strategies may be developed for HR stratified EOCs. Primary surgery may be the preferred approach in HRC due to poor chemoresponse; surgical expertise/environment should be optimised to ensure optimal surgical outcome. Intra-operative hyperthermic treatment and selective HR inhibitors may improve subsequent chemoresponse in HRC and are currently being investigated.
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Wu, Jie, Shixiong Xu, Quan Long, Michael W. Collins, Carola S. Koenig, Gaiping Zhao, Yuping Jiang, and Anwar R. Padhani. "Simulation of Blood Perfusion in Tumour Microvasculature." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176335.
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Solid tumor has become one of the most serious diseases that threaten mankind’s health and life all over the world. It is well recognized that structural and functional abnormalities of tumor vascularity and the subsequent microenvironment and cellular adaptive consequences creates a great barrier for drug delivery in solid tumors, contributing to treatment resistance. Hence, the investigation of microcirculatory dynamics in solid tumors has important significance for improving the effectiveness of many anticancer therapies.
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Mattingly, M., R. B. Roemer, and S. Devasia. "Optimal Actuator Placement in Hyperthermia: A Reduced-Order Modeling Approach." In ASME 1997 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1997. http://dx.doi.org/10.1115/imece1997-0211.
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Abstract Studies have shown a positive correlation between the effective temperature maintained inside a cancerous tumor during hyperthermia treatments and the response rate of that tumor to subsequent radiation therapy (see, for example, [1]). In addition, effective temperature control is crucial to avoid the premature abortion of hyperthermia treatments from patient discomfort due to overheating of the normal tissue surrounding these tumors. Hence, there is a need to optimally heat tumors and surrounding tissue — this is significantly affected by the choice of actuator placement and input powers. In this work, we show how the extended balanced realization model reduction approach [2] can be employed to efficiently determine the optimal scan path for a given hyperthermia treatment.
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Elliott, G. D., D. Fron, J. J. McGrath, C. Seip, and E. Crockett-Torabi. "Development of a Novel In Vivo Assay for Assessment of Tissue Viability: A Cryosurgery Application." In ASME 2000 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2000. http://dx.doi.org/10.1115/imece2000-2238.
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Abstract Our recent success with applying a novel Green Fluorescent Protein (GFP) viability assay to isolated cells after freezing has suggested possible utility for assessing viability of cells within tissues, both in situ, and intravitally. The current work seeks to establish that following freezing, changes in the fluorescent intensity of tumors grown from GFP-transfected cells will correlate with tissue damage as assessed by histological methods, thereby evaluating the use of a transfection-based assay for in vivo purposes. GFP-fluorescing R3230AC tumors were grown inside implanted dorsal skin flap chambers, and treated cryosurgically after 6-9 days of growth. Fluorescent images of the tumors were acquired at the center of the viewing area before, during, and for 6 hours following freezing. Following the observation period the animal was immediately euthanized and the tissue within the chamber was fixed in formalin and stained for histological analysis. The results of intravital microscopy in a centrally located test area revealed a large reduction in fluorescent intensity within the tumor tissue immediately following the final freeze-thaw cycle, with little subsequent change during the subsequent 6 hour observation period. In H&E section significant damage was observed in the central test areas. Taken together, this evidence suggests that the GFP assay is not limited to isolated cells, but can serve as the basis for intravital assessment of viability.
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Evrensel, Cahit A., Lisbeth A. Welniak, Alan Fuchs, Jigar Patel, William J. Murphy, and Faramarz Gordaninejad. "Utilization of Biocompatible Ferrous Particles for a New Cancer Therapy." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206803.
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Magneto-rheologiacal Fluid (MRF), suspensions of polarizable micron size particles, is synthesized from suspensions of iron particles (micron and nano size) in phosphate buffered saline (PBS). The iron particles have been surface coated using atom transfer radical polymerization (ATRP) with various polymers, such as poly(N-isopropylacrylamide) (poly(NIPAAm)), and poly(acrylamide) (poly(AAm)). The surface grafted polymer has been characterized using differential scanning calorimetry (DSC), and properties of resulting fluid have been measured using a rheometer. A mathematical model is developed to explore the force induced by the particles on the neighboring tissue under externally applied magnetic field. This force results in the damage of the tumor cell lines and trigger the immune system response. The effect of MRF on primary and metastasized tumor growth were evaluated by using an orthotopic murine breast cancer model (4T1). Tumors were evaluated by growth measurements and histological changes following injection of MRF or carrier fluid alone into the tumor and the effects of subsequent application of a magnetic field to the site. Results indicate slowed tumor growth and increased dendritic cell activation with this therapy and they are encouraging.
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Hwang, Larn, Kevin Ng, Wen Wang, and Vuong Trieu. "Abstract 3742: Treatment with trabedersen, an anti-TGF-beta 2 antisense, primed tumors to subsequent chemotherapies." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-3742.
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Mosquéra, Júlia Milhomem, Amanda Ribeiro Alves, Gianna Carolina Pereira Cavalli, Larissa Feitosa de Albuquerque Lima Ramos, and Flávio Lúcio Vasconcelos. "GLOBAL SURVIVAL BASED ON CLINICAL, HISTOLOGICAL, AND BIOLOGICAL TUMOR CRITERIA IN A SECONDARY PUBLIC BRAZILIAN HOSPITAL." In Abstracts from the Brazilian Breast Cancer Symposium - BBCS 2021. Mastology, 2021. http://dx.doi.org/10.29289/259453942021v31s2045.
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Objective: To analyze the overall survival of women with breast cancer based on clinical, histological, and biological tumor data in a secondary hospital in Federal District/Brazil. Method: Retrospective cohort study of women diagnosed with breast cancer from 2012 to 2019, followed up until December 2020, having its data analyzed in 2021. The population studied was from the area covered of the Regional Hospital of Santa Maria (Brasília/Distrito Federal/Brazil), a secondary service, linked to the Brazilian Unified Health System. The information analyzed in this study were state at the last visit (life or dead), the presence of clinically compromised axillary lymph nodes, staging by the TNM system, location of distant metastasis (bone or visceral), histological type and grade, and tumor biological profile. Subsequently, survivals were analyzed in relation to variables previously described. The data were analyzed with the aid of the statistical package SPSS (version 26.0), with p<0.05 is considered significant. Results: This study included a total of 203 patients, of which 158 (77.8%) survived and 45 (22.2%) died. Regarding deaths, 67.5% had a clinically compromised armpit (p<0.001) and 50% were in stage IV (p<0.001). In relation to overall survival, worse survival was observed for patients with clinically suspect lymph nodes (p<0.001), for tumors measuring between 2 and 5 cm and tumors larger than 5 cm in relation to tumors smaller than 2 cm (p<0.001), and for stages III and IV compared to stages I and II (p<0.001). There was no worsening of survival in relation to the histological type (p=0.39), histological grade (p=0.65), location of metastases (bone and visceral) (p=0.76), or biological profile (p=0.40). Conclusion: There were more deaths in relation to the clinically compromised axillary state and in stages III and IV. Larger tumors, more advanced staging, and a clinically compromised armpit worsened overall survival.
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Liu, Jing, Yi-Xin Zhou, Tian-Hua Yu, Lin Gui, Zhong-Shan Deng, and Yong-Gang Lv. "New Cryoprobe System With Powerful Heating Features and Its Performance Tests on Biomaterials." In ASME 2003 International Mechanical Engineering Congress and Exposition. ASMEDC, 2003. http://dx.doi.org/10.1115/imece2003-41357.
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Cryosurgery is a clinical therapy aiming at destroying the target of diseased tissues through a controlled deep freezing and subsequent rewarming [1,2]. Applications of this treatment are quite wide in skin cancers, glaucoma, lung tumor etc. [3]-[10]. In contrast to the freezing therapy, heating of tumors has also long been proved to be an effective way of selectively killing the cells of cancerous tissues [11]-[13]. Clinical tests showed that heating the tumor to above a critical minimum temperature such as 42–43 °C for an extended period could effectively destroy the target. It was recently realized that freezing immediately followed by a rapid and strong heating of the target tissues would significantly improve the treatment effect [14]-[16]. Therefore, an apparatus thus developed will be of great importance in cancer clinics. But until now, most of the currently available cryoprobe systems are only capable of performing a single freezing function, in which the treated tissue is often let to naturally re-warm by simply switching off the apparatus. The first one and only commercially available cryoprobe system aiming at both freezing and heating therapy is perhaps Endocare Corporation’s Ar-He Cryoprobe system [14]. However, the highest tissue temperature for this system to achieve is about 0–20 °C [17], which is not high enough to thermally destroy the target tissues. Presently, there is a strong lack of freezing applicators with powerful heating functions for hyperthermia purposes. Without strong enough heating, tumors may still have a chance to regenerate. This is perhaps one of the critical reasons to impede the widespread of cryosurgery in destroying pathological tissues.
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Inaba, H., H. Machida, I. Mizumoto, S. Mashiko, S. Kimura, and Y. Taguchi. "Near IR spectral detection of singlet molecular oxygen generated by laser excited chlorin-e6Na taken up in mouse tumor cells and tissues." In OSA Annual Meeting. Washington, D.C.: Optica Publishing Group, 1989. http://dx.doi.org/10.1364/oam.1989.tuu34.
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Photochemical or photodynamic therapy (PDT) involving the combination processes of dye injection, like hematoporphyrin derivative (HpD), and subsequent exposure to visible laser light has proved effective in the diagnosis and treatment of malignant tumors at the clinical level.1 In the mechanism of such photosensitized biochemical reactions, excited singlet molecular oxygen (1O2) is considered to play an essential role, at least, in starting the reaction. Until now, almost all studies on the generation of 1O2 molecules in the photosensitized dye were performed by various chemical methods utilizing scavengers or sensitizers of 1O2 molecules during their chemical reactions. However, the spectroscopic technique for the detection of 1O2 molecules in the near infrared region based on their transitions around 1.06,1.27, and 1.59 μm is believed to be much more reliable and versatile than the conventional chemical method. Accordingly, we have performed the experimental study on the spectroscopic detection of 1O2 molecules in laser-excited photosensitive dye, chlorin-e6Na, contained in aqueous solution as well as in mouse cultured tumor cells in vitro and in tumor tissues in vivo, employing a highly sensitive near infrared spectrometer system constructed by our project. Chlorin-e6Na has a structure similar to pheophorbide a, one of the decomposition products from chlorophyll a, which has been demonstrated for the first time by our group to be a more efficient and appropriate dye for the PDT than HpD.2 Thus in vitro and in vivo experiments using mouse FM3A cultured tumor cells and C3H mouse tumor tissues in chlorin-e6Na have indicated the significant spectroscopic evidence for the generation of 1O2 molecules with excellent signal-to-noise ratio during laser excitation.
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Hanks, Thomas, Spencer Raub, Jessica Eaton, Evgeniya Tyrtova, Malia McEvoy, Zirun Zhao, Samuel Emerson, Manuel Ferreira, and Jacob Ruzevick. "Single-Center Experience of the Incidence and Subsequent Natural History of Residual Pituitary Neuroendocrine Tumors following Subtotal Resection." In 33rd Annual Meeting North American Skull Base Society. Georg Thieme Verlag KG, 2024. http://dx.doi.org/10.1055/s-0044-1780154.
Full textReports on the topic "Subsequent tumours"
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Moxham-Hall, Vivienne, Anton du Toit, Sallie Newell, Stuart Brentnall, Deshanie Rawlings, and Eileen Goldberg. Proton beam therapy: A rapid review of the evidence since 2020. The Sax Institute, April 2023. http://dx.doi.org/10.57022/tjvf1783.
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The purpose of the report is to conduct a rapid review of the recent evidence (since 2020) on proton beam therapy (PBT) for: paediatric cancers, central nervous system (CNS) tumours, head and neck cancer and prostate cancer. The report aims to provide a rapid summary of the current knowledge about PBT’s effectiveness, safety, and potential advantages over conventional radiation therapy. The report includes evidence that has become available subsequent to the evidence submitted in the South Australian Health and Medical Research Institute (SAHMRI)’s Medical Services Advisory Committee (MSAC) application requesting Medicare Benefits Schedule (MBS) listing of PBT for paediatric and rare cancers (MSAC Application No. 1638). In addition, the report presents data on international benchmarking of PBT facilities per million population, and with consideration to Australia’s population and numbers of people with cancers recommended for public funding for PBT by MSAC.