Academic literature on the topic 'Cancer tumer'
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Journal articles on the topic "Cancer tumer"
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Blaich, Günter, Hella Raade, and Manfred Metzler. "Modification of 7,8–benzoflavone metabolism in hamster liver and kidney microsomes by hepatic tumer inducing treatments." Carcinogenesis 11, no. 1 (1990): 95–101. http://dx.doi.org/10.1093/carcin/11.1.95.
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Parsons, Heather A., Timothy Blewett, Xiangying Chu, Sainetra Sridhar, Katheryn Santos, Kan Xiong, Vandana Abramson, et al. "Abstract PD11-06: PD11-06 Circulating tumor DNA association with residual cancer burden after neoadjuvant therapy in triple negative breast cancer in TBCRC 030." Cancer Research 83, no. 5_Supplement (March 1, 2023): PD11–06—PD11–06. http://dx.doi.org/10.1158/1538-7445.sabcs22-pd11-06.
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Abstract Background. Patients (pts) with early triple negative breast cancer (eTNBC) are at increased risk of breast cancer recurrence and death. Recent studies have focused on escalation of therapy, with current treatment standard of at least five drugs – and associated toxicities - for eTNBC. Though presence of residual disease after neoadjuvant therapy (NAT) as measured by residual cancer burden (RCB) helps guide addition of adjuvant treatment, more effective tools to tailor therapy are limited. Persistence of circulating tumor DNA (ctDNA) in the setting of residual disease is associated with high risk of distant recurrence. However, more sensitive minimal residual disease (MRD) assays are needed to potentially guide optimization of systemic therapy. Methods. TBCRC 030 is a phase II randomized study of 12 weeks of NAT single agent cisplatin or paclitaxel for stage II-III TNBC, followed by surgery. The primary objective of the parent study was to correlate baseline biomarker for homologous recombination deficiency and RCB by study arm. From this group, responders (RCB 0/1) and non-responders (RCB 2/3) from both study arms who did not receive additional NAT prior to surgery were selected for analysis from the study cohort, matched on baseline nodal status and tumor size. As a post hoc study amendment, available pts were followed for event free survival (EFS). Plasma samples were collected prior to treatment initiation (W0), at three weeks (W3), and at twelve weeks, prior to surgery (W12). Whole genome sequencing (WGS) was performed on primary tumor tissue to identify somatic mutations and design for each pt a tumor-informed, ctDNA assay tracking up to 1000 mutations to detect MRD. Detection limit was computed for each tested sample as previously described. For each sample assayed, we report tumor fraction (TFx) when MRD was detected and the detection limit at 90% power when MRD was not detected. Results. Of 139 study pts, 68 had complete tissue and plasma samples and no receipt of additional NAT. Of these, 22 were responders. These responders, and 22 matched non-responders were identified for analysis. Data from 22 pts – 11 responders, 11 non-responders - are described here; full analysis on all 44 pts will be presented at the meeting. Personalized ctDNA assays were designed targeting 434 to 1000 variants (median 1000) and applied to 66 plasma samples. At W0, 100% (22/22) were positive for ctDNA; 73% (16/22) and 55% (12/22) were positive at W3, and W12, respectively. In pts with T1-T2 tumors median TFx was 4.1e-3(7.8e-6, 3.4e-2) and 4.7e-1(4.3e-2, 9.0e-1) in pts with T3-T4 tumors. TFx decreased from W0 to W3 and from W0 to W12 in responders (Table 1). By W12, ctDNA had cleared in 7/8 pts with RCB 0, 1/3 with RCB 1, 2/8 with RCB 2, and 0/3 with RCB 3. Overall, ctDNA levels were broad with median TFx of 1.5e-3 (range 2.9e-6 to 0.90). Detection limit at 90% power for all tested samples was a median of 8.8e-6 (range 9.9e-7 to 6.8e-3). To investigate whether ctDNA persistence after NAT was associated with BC recurrence, we analyzed a separate group of all 8 pts with known recurrence and with complete data and samples. All pts had persistent ctDNA at W12 (median TFx 6.8e-3, [2.9e-6 to 6.6e-2]). Conclusions. After 3 weeks of NAT for eTNBC, ctDNA TFx decreased, with a 3900-fold change in responders and 18-fold change in non-responders. By W3, TFx for most pts with RCB 0/1 were below the 1 in 10,000 limit of detection for many currently available assays, emphasizing the need for sensitive tests to potentially guide therapy. Additional studies will determine if ctDNA-guided approaches in eTNBC can improve pt outcomes. Table 1: Tumer Fraction and Tumer Fraction Fold Change by Response to Neoadjuvant Therapy Citation Format: Heather A. Parsons, Timothy Blewett, Xiangying Chu, Sainetra Sridhar, Katheryn Santos, Kan Xiong, Vandana Abramson, Ashka Patel, Ju Cheng, Adam M. Brufsky, Justin Rhoades, Jeremy Force, Ruolin Liu, Tiffany A. Traina, Lisa Carey, Mothaffar Rimawi, Ahmed Elkhanany, Vered Stearns, Jennifer M. Specht, Harold Burstein, Antonio C. Wolff, Eric Winer, Nabihah Tayob, Ian Krop, Todd Golub, Erica L. Mayer, Viktor Adalsteinsson. PD11-06 Circulating tumor DNA association with residual cancer burden after neoadjuvant therapy in triple negative breast cancer in TBCRC 030 [abstract]. In: Proceedings of the 2022 San Antonio Breast Cancer Symposium; 2022 Dec 6-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2023;83(5 Suppl):Abstract nr PD11-06.
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Cho, Bong Jun, Hans H. Kim, David J. Lee, Eun Jung Choi, Yeo Hyun Hwang, Sun Ha Chun, and In Ah Kim. "MicroRNA-21 inhibitor potentiates anti-tumor effect of radiation therapy in vitro and in vivo." Tumor Microenvironment and Therapy 2, no. 1 (January 10, 2014): 1–13. http://dx.doi.org/10.2478/tumor-2014-0001.
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AbstractMicroRNA-21 (miR-21) plays important roles in carcinogenesis and is highly expressed in diverse human cancers. We evaluated the potential of targeting miRNA-21 to overcome the radioresistance of human cancer cells having an activated EGFR2-associated signaling and also aimed to elucidate the mechanisms of radiosensitization, and the effect on epithelial- mesenchymal transition (EMT). Ectopic overexpression of miR-21 up-regulated EGFR/HER2-associated signaling and increased radioresistance of a panel of human cancer cells (U251, U87, and A549 cells). In contrast, a specific inhibitor of miR-21 attenuated this signaling and radiosensitized a panel of human cancer cells. Inhibition of miR-21 was associated with persistent γH2AX foci formation. Inhibition of miR-21 decreased the typical features of EMT, such as invasion and migration and vascular tube formation. Treatment with anti-miR-21 decreased tumor burden in nude mice bearing intracranial U251 xenografts compared to controls. Combined treatment of anti-miR-21 and radiation further decreased tumor burden compared to each treatment alone. In summary, miR-21 is an important onco-miR, which confers radioresistance and diverse features of EMT. Inhibition of miR-21 could be a potential strategy for improving the efficacy of radiation therapy via unique modulation of pro-survival signaling implicated in radiation response and EMT.
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Lavekar, G. S. "Arbud-Tumor-Cancer- a concise integrative review." Journal of Clinical Oncology Reports 1, no. 1 (January 20, 2023): 01–05. http://dx.doi.org/10.58489/2836-5062/001.
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The Cancerous diseases will cause 10 million deaths in 2020 and may increase in coming years (1). Since ancient times Cancer-Arbud has been considered a mega disease and critical for treatment. A review is presenting the conception, description and treatment modalities as described in ayurveda, a short review is presented in this article.
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GARCÍA CEBRIÁN, MARÍA JOSÉ, MONIKA BAUDEN, ROLAND ANDERSSON, STEFAN HOLDENRIEDER, and DANIEL ANSARI. "Paradoxical Role of HMGB1 in Pancreatic Cancer: Tumor Suppressor or Tumor Promoter?" Anticancer Research 36, no. 9 (September 9, 2016): 4381–90. http://dx.doi.org/10.21873/anticanres.10981.
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SK, Deshmukh. "Immune Cells in the Tumor Microenvironment and Cancer Stem Cells: Interplay for Tumor Progression." Journal of Embryology & Stem Cell Research 2, no. 2 (2018): 1–2. http://dx.doi.org/10.23880/jes-16000109.
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Fejzić, Hanifa. "Tumor marker CA 15-3 in breast cancer patients." Acta Medica Academica 44, no. 1 (June 2, 2015): 39–46. http://dx.doi.org/10.5644/ama2006-124.125.
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Singh, Dr Ravi Pratap. "HLA A24 Associated Tumor Immunity in HER2/neu Positive Breast Cancer." Recent Advances in Pathology & Laboratory Medicine 3, no. 2 (August 21, 2017): 13–16. http://dx.doi.org/10.24321/2454.8642.201702.
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Li, Lin, Mengyuan Li, Zehang Jiang, and Xiaosheng Wang. "ARID1A Mutations Are Associated with Increased Immune Activity in Gastrointestinal Cancer." Cells 8, no. 7 (July 4, 2019): 678. http://dx.doi.org/10.3390/cells8070678.
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Because traditional treatment strategies for advanced gastrointestinal (GI) cancers often have a limited therapeutic effect, immunotherapy could be a viable approach for the therapy of advanced GI cancers, considering the recent success of immunotherapy in treating various refractory malignancies, including the DNA mismatch repair-deficient GI cancers. However, only a subset of cancer patients currently respond to immunotherapy. Thus, it is important to identify useful biomarkers for predicting cancer immunotherapy response. The tumor suppressor gene ARID1A has a high mutation rate in GI cancers and its deficiency is correlated with the microsatellite instability (MSI) genomic feature of cancer. We investigated the correlation between ARID1A mutations and tumor immunity using three GI cancer genomics datasets by the bioinformatic approach, and found that diverse antitumor immune signatures were more highly enriched in ARID1A-mutated GI cancers than in ARID1A-wildtype GI cancers. The elevated immune activity in ARID1A-mutated GI cancers was associated with the higher tumor mutation burden and lower tumor aneuploidy level, as well as a higher proportion of MSI cancers in this GI cancer subtype. Moreover, we found that ARID1A-mutated GI cancers more highly expressed PD-L1 than ARID1A-wildtype GI cancers. The elevated antitumor immune signatures and PD-L1 expression could contribute to the more active immunotherapeutic responsiveness and better survival prognosis in ARID1A-mutated GI cancers than in ARID1A-wildtype GI cancers in the immunotherapy setting, as evidenced in three cancer cohorts receiving immunotherapy. Thus, the ARID1A mutation could be a useful biomarker for identifying GI cancer patients responsive to immunotherapy.
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Nenciu, Adina-Elena, C. G. Nenciu, R. Fodoroiu, Florica Șandru, and M. C. Dumitrașcu. "TUMOR MARKERS IN OVARIAN CANCER." Journal of Surgical Sciences 7, no. 2 (September 1, 2020): 79–84. http://dx.doi.org/10.33695/jss.v7i2.356.
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Even if today’s society is rapidly evolving there is still much that can be done. This applies in theoncological field. One of the main female health problems worldwide is represented by thegynecological cancers. Ovarian cancer is the main cause of mortality among women withgynecological cancers. Although its prevalence is lover compared to breast, uterine or cervicalcancer, the mortality and morbidity rates are significantly higher. The first step in the managementof ovarian cancer is represented by regular screening and rapid diagnosis. One of the most importanttolls is represented by serological markers dosage in order to estimate the type of tumor before thegynecological specific intervention. There is a real need to identify correctly the ovarian cancer asearly as possible in order to obtain the favorable prognosis that comes with the diagnosis in earlystage. Most of the ovarian cancers (above 90%) are represented by carcinomas which are frequentlydiagnosed in advanced stages. The roles of the biomarkers are to indicate the malignancy of anovarian tumor and to predict the relapse risk. The aim of this paper is to update the indicationsregarding the usage of serological markers in ovarian cancers and the importance of using them forour patients.
Dissertations / Theses on the topic "Cancer tumer"
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Lale, Shantanu Vijay. "Development of stimuli responsive polymeric nanosystems for cancer therapeutics." Thesis, IIT Delhi, 2016. http://localhost:8080/xmlui/handle/12345678/6999.
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McGinley, Susan. "Sensitizing Tumor Response to Cancer Therapy." College of Agriculture and Life Sciences, University of Arizona (Tucson, AZ), 2008. http://hdl.handle.net/10150/622086.
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Hoarau, Jessica. "Halfway Between 2D Models and Animal Models : a New Multicellular 3D Spheroid Model Organized to Study Tumor-Endothelium Interactions in Ovarian Cancer." Thesis, Université Paris-Saclay (ComUE), 2019. http://www.theses.fr/2019SACLS111.
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Le cancer de l'ovaire (CO) est la cinquième cause de décès chez les femmes qui se caractérise par son diagnostic tardif (stades FIGO III et IV) et par l’importance de ses métastases abdominales souvent observées au moment du diagnostic. Le traitement repose sur une chirurgie cytoréductive complète associée à une chimiothérapie. Malheureusement, parmi les patientes ayant une rémission clinique complète après la fin du traitement initial, 60% des personnes atteintes d'un cancer épithélial de l'ovaire (CEO) à un stade avancé rechuteront dans les cinq ans.L'importance de la néo-angiogenèse dans le développement des tumeurs a poussé les chercheurs à étudier d'autres stratégies. Les thérapies anti-angiogéniques ciblant le système vasculaire tumoral sont désormais utilisées en association avec la thérapie cytotoxique standard dans le traitement des CEO. Malheureusement, les progrès réalisés grâce à cette approche offrent encore un succès limité, qui peut s'expliquer en partie par l'interaction hétérotypique entre les cellules endothéliales et la tumeur. Plusieurs études suggèrent un dialogue complexe entre les cellules cancéreuses de l'ovaire (OCC) et les cellules endothéliales (EC) pouvant entraîner une sensibilité différente à la chimiothérapie et aux traitements anti-angiogéniques conduisant à la progression tumorale.L’objectif de la présente étude est d’étudier le rôle des interactions entre EC et OCC dans la prolifération et la chimiorésistance des CEO. Pour modéliser l'endothélium de la tumeur, nous avons utilisé notre modèle de cellules endothéliales AKT activées (E4+EC). Nous avons démontré en utilisant un modèle de coculture 2D que l’endothélium activé induit une prolifération et une chimiorésistance accrues dans les CEO par l’activation de la signalisation de Notch. Nous avons montré que l’expression et l’activation des récepteurs Notch étaient augmentées dans les cultures en coculture et dans les OCC résistantes à la chimiothérapie.L’accumulation d’ascite dans l’abdomen des patientes atteintes de CO semble jouer un rôle clé dans le mécanisme de propagation des OCC. Les OCC isolées flottent généralement dans l'ascite et forment des sphéroïdes multicellulaires. Dans ce contexte, nous avons développé un nouveau modèle 3D de sphéroïde pour étudier les interactions tumeur-endothélium dans un modèle plus proche des conditions in vivo. Nous avons démontré que les E4+EC et OCC formaient des angiosphères organisées avec un noyau de cellules endothéliales entourées par des OCC qui prolifèrent rapidement. Nous avons établi que l'activation de l'AKT dans les EC était nécessaire pour la formation d'angiosphères organisées. Fait intéressant, dans les ascites de patientes CEO, nous avons pu trouver des structures très similaires à nos angiosphères. De plus, dans une cohorte rétrospective de 59 patientes, nous avons montré que les EC étaient AKT activé chez des patientes atteintes de CEO, ce qui confirme l'importance de l'activation d’AKT dans la CEO. De plus, nous avons démontré l'importance du FGF2, de la Pentraxine 3 (PTX3), du PD-ECGF et du TIMP-1 dans l'organisation de l'angiosphères. Enfin, nous avons confirmé le rôle de Notch3/Jag1 dans le cross-talk des OCC-EC dans la prolifération et l'invasion des OCC au péritoine.En conclusion, notre étude illustre l’importance des EC AKT activé dans les CEO. Au vu des résultats mitigés des traitements anti-angiogéniques, se concentrer sur la normalisation vasculaire dans l'angiogenèse pathologique pourrait être plus efficace. Bien que l'AKT soit difficilement ciblable, la caractérisation génétique des tumeurs pourrait potentiellement identifier un sous-ensemble de tumeurs avec une signalisation NOTCH aberrante qui constituerait une cible idéale pour des inhibiteurs spécifiques. Alors que nous nous dirigeons vers la médecine personnalisée et de précision, il pourrait y avoir une place pour l'inhibition de NOTCH dans les CO en combinaison avec d'autres stratégies thérapeutiquesOvarian cancer (OC) is the most lethal gynecologic malignancy in developed countries and the fifth cause of death among women. OC is a heterogeneous disease, which is characterized by its late diagnosis (FIGO III and IV stages) and the importance of abdominal metastases often observed at the time of diagnosis. The mainstay of treatment involves complete cytoreductive surgery associated with platinum and taxane-based chemotherapy. Unfortunately, among patients achieving complete clinical remission after completion of initial treatment, 60% with advanced epithelial ovarian cancer (EOC) will relapse within five years.The importance of neo-angiogenesis in tumor formation, growth and dissemination has driven researchers to investigate into alternative strategies. Anti-angiogenic therapies targeting tumor vasculature are now used in combination with standard cytotoxic therapy in the treatment of EOC. Unfortunately, the progress achieved by this approach still offers limited success which can partly be explained by the heterotypic interaction between the tumor and endothelial cells. Evidence suggests a complex cross-talk between ovarian cancer cells (OCCs) and endothelial cells (ECs) that can result in the emergence of a heterogeneous tumoral and endothelial population with different sensitivity to chemotherapy and anti-angiogenic therapies leading to an increase of OCC proliferation and dissemination.The objective of the present study is to investigate the role of ECs and OCCs interactions in the proliferation and chemoresistance of EOC. To model tumor endothelium, we used our model of Akt-activated endothelial cells (E4+ECs). We demonstrated using a 2D co-culture model that activated endothelium induces increased proliferation and chemoresistance in EOC through the activation of Notch signaling. We showed that Notch receptor expression and activation are increased in co-culture and in OCCs resistant to chemotherapy.The accumulation of ascites in the abdomen of an OC patient seems to play a key role in the mechanism of OCC spreading. Detached cancer cells usually float in ascites and form multicellular spheroids. In this context, we developed a new model of organized multicellular 3D spheroid to study tumor-endothelium interactions in a model closer to in vivo conditions. We demonstrated that when cocultured in 3D condition, E4+ECs and OCCs formed organized tumor angiospheres with a core of endothelial cells surrounded by highly proliferating OCCs. We established that AKT activation in ECs was mandatory for the formation of organized angiospheres. Interestingly, in EOC patient ascites, we were able to find structures that were very similar to our angiospheres. In addition, in a retrospective cohort of 59 patients, we showed that ECs were AKT activated in EOC patients which support the importance of AKT activation in EC in EOC. Besides, we demonstrated the importance of FGF2, Pentraxin 3 (PTX3), PD-ECGF and TIMP-1 in angiosphere organization. Finally, we confirmed the role of Notch3/Jagged1 in OCCs-ECs crosstalk for OCC proliferation but also during peritoneum invasion.Altogether, our study illustrates the importance of AKT activated ECs in EOC. In a context of poor results of anti-angiogenic therapies in clinical settings, focusing on vascular normalization in pathological angiogenesis could be more efficient. While AKT is hardly targetable, the genetic characterization of tumors could potentially identify a subset of tumors with aberrant NOTCH signaling that would constitute an ideal target for specific inhibitors. As we move toward personalized and precision medicine, there might be a place for notch inhibition in advanced ovarian cancer in combination with other therapeutic strategies
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Stemmer, Kerstin. "Molecular Characteristics of Kidney Cancer." [S.l. : s.n.], 2008. http://nbn-resolving.de/urn:nbn:de:bsz:352-opus-73925.
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Dacheux, Estelle. "Implication de la protéine onco-suppressive BRCA1 dans la régulation de la traduction." Thesis, Lyon 1, 2013. http://www.theses.fr/2013LYO10077.
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BRCA1 est l’un des deux gènes majeur de prédisposition au cancer du sein. Les multiples partenaires protéiques de BRCA1 lui confèrent de nombreuses fonctions par lesquelles elle peut assurer la surveillance de l’intégrité cellulaire. L’équipe dans laquelle j’ai mené ma thèse a identifié un nouveau partenaire protéique de BRCA1, la protéine de liaison au poly(A) des ARN messagers PABP1, et a ainsi mis en lumière l’implication de BRCA1 dans la régulation de la traduction [1]. Durant ma thèse, j’ai étudié cette nouvelle fonction de BRCA1 et essayé de comprendre si, et comment, elle pourrait contribuer à son rôle de suppresseur de tumeur. J’ai tout d’abord montré que BRCA1 est associée avec la fraction ribosomique des cellules, et plus particulièrement à la fraction subpolysomique, ce qui pourrait indiquer sa participation à l’initiation de la traduction. De plus, nos résultats indiquent que BRCA1 pourrait participer à un complexe non canonique d’initiation de la traduction. Dans la mesure où BRCA1 n’est pas un facteur canonique d’initiation de la traduction, il est peu probable qu’elle intervienne dans la traduction de tous les ARNm. Notre hypothèse est qu’elle pourrait réguler la traduction d’ARNm spécifiques codant pour des protéines impliquées dans ses différentes fonctions de surveillance de l’intégrité cellulaire. Afin d’identifier les cibles traductionnelles de BRCA1, j’ai réalisé une analyse transcriptomique comparative du contenu des polysomes de cellules épithéliales mammaires MCF7 exprimant de façon transitoire un ARN interférent dirigé contre BRCA1 ou contrôle. Parmi les ARNm cibles de l’activité traductionnelle de BRCA1, beaucoup codent effectivement pour des protéines impliquées dans les fonctions auxquelles elle participe. Ce travail confirme que la participation de BRCA1 à la régulation de la traduction pourrait être une autre voie par laquelle BRCA1 exerce son rôle de suppresseur de tumeur. De plus, l’analyse des cibles traductionnelle de BRCA1 pourrait conduire à l’identification de nouvelles fonctions de cette protéine ainsi qu’à la découverte de marqueurs tumoraux ou de cibles thérapeutiques pour les patients porteurs d’une mutation de BRCA1BRCA1 is one of the two major genes of breast cancer susceptibility. The numerous binding partners of BRCA1 allow it to participate to several cellular pathways which globally contribute to its cell surveillance capacity. The team in which I performed my PhD identified a new bindind partner of BRCA1, the Poly(A)-Binding Protein 1 and, consequently, a new function of this tumor suppressor, namely, the translation regulation [1]. During my PhD, I studied this new function and try to elucidate if, and how, this function could participates to the BRCA1’s tumor suppressive activity. I first showed that BRCA1 is associated with the ribosomal fraction of the cell, and more precisely, with the subpolysomal fraction, which could indicate that BRCA1 participates to the initiation step of translation. Moreover, our results suggest that BRCA1 could participate to a non canonical initiation complex. Given that BRCA1 is not a canonical translation initiation factor, it is unlikely that BRCA1 regulates the translation of all mRNAs. Our hypothesis is that BRCA1 could regulate the translation of specific mRNAs involved in its various cell surveillance functions. In an attempt to identify the BRCA1 translational targets, we performed a microarray analysis of polysomes-bound mRNAs in MCF7 cells transiently expressing siRNA directed against BRCA1 or control siRNA. We found that, among the translational targets of BRCA1, many indeed encode proteins involved in the same main functions as BRCA1’s. Altogether, our results suggest that the involvement of BRCA1 in translation regulation could be another way by which BRCA1 exerts its tumor suppressor role. Moreover, the analysis of the BRCA1’s translational targets could lead to the identification of new functions for BRCA1 as well as to the discovery of new tumoral markers and therapeutic targets for the BRCA1 mutated patients
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Bonneau, Claire. "Étude des mécanismes de récidive métastatique dans les cancers du sein luminaux de stade précoce : impact du microenvironnement tumoral Caractérisation moléculaire des cancers du sein en pratique clinique A subset of activated cancer associated fibroblasts is associated with distant relapse in early luminal breast cancers." Thesis, Sorbonne Paris Cité, 2018. https://wo.app.u-paris.fr/cgi-bin/WebObjects/TheseWeb.woa/wa/show?t=2365&f=17162.
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Les cancers du sein de stade précoce constituent un enjeu de santé publique du fait de leur fréquence élevée (70% des nouveaux cas diagnostiqués). Parmi eux, les cancers luminaux (exprimant les récepteurs hormonaux sans surexpression de l’HER2) de stade T1N0, de moins de 2cm sans envahissement ganglionnaire, ont un pronostic spontanément favorable et font ainsi l’objet de peu d’études dédiées. Néanmoins certaines de ces patientes (5 à 10% à 10 ans) vont récidiver avec des métastases à distance et mourir. L’identification de facteurs pronostiques pour ces tumeurs et une meilleure compréhension des mécanismes de récidive pourraient permettre de discriminer les tumeurs réellement indolentes pour lesquelles le traitement pourrait être diminué et au contraire, les tumeurs les plus à risque de récidive pour lesquelles un traitement devrait être renforcé. L’objectif de ce travail de thèse était d’identifier les mécanismes de la récidive métastatique dans les cancers du sein luminaux de stade T1b-cN0M0 au diagnostic en analysant plus spécifiquement le microenvironnement tumoral. Pour cela, nous avons constitué une cohorte de patientes ayant eu un cancer du sein T1b-cN0, de type luminal (exprimant les récepteurs hormonaux sans surexpression de l’HER2) de type cas (patientes avec récidive métastatique à distance) / témoin (patiente sans récidive à distance), à partir de la cohorte de patientes suivies à l’Institut Curie. Les témoins étaient choisis appariés aux cas sur les principaux facteurs pronostiques connus : âge, grade tumoral et prolifération tumorale estimée par le Ki67. Nous avons ensuite évalué les facteurs de récidive dépendant des cellules tumorales. En analyse univariée, on montre qu’une moins bonne différenciation (baisse de l’expression de la E-cadhérine) est associée à la récidive. Par ailleurs, le score de récidive prédit par la signature transcriptomique ProsignaTM est plus élevé chez les cas que chez les contrôles sans que la discrimination entre les deux ne soit parfaite pour cette population de cancers du sein. L’originalité de notre étude reposait sur l’étude détaillée du microenvironnement tumoral. Sur le plan immunologique, l’analyse systématique quantitative et qualitative, en immunohistochimie, de l’infiltrat immun montre une absence d'association avec les lymphocytes B, macrophages et cellules dendritiques. En revanche, on observe une baisse des lymphocytes T CD4+ tumoraux chez les cas, sans autres association concernant les différents sous-types de lymphocytes T. Dans la continuité des travaux déjà réalisé au laboratoire du Dr Fatima Mechta-Grigoriou, l’analyse des différents sous-types de fibroblastes associés au cancer (CAF) dans notre cohorte révélait que les cas étaient plus spécifiquement enrichis en CAF activés de type CAF-S1 alors que la quantité globale de stroma ne soit pas associée à la récidive. Ici, l’action des CAF-S1 est médiée par la cadhérine-11 qui augmente les capacités de migration et invasion des cellules tumorales in vitro par stratégie siRNA. En analyse multivariée, les caractéristiques du microenvironnement et en particulier l’enrichissement en CAF-S1 restent significativement associées à la récidive.En conclusion, nous avons identifié que la survenue de métastases dans les cancers du sein luminaux de stade précoce repose sur des mécanismes associés au micro-environnement tumoral tels que la présence de CAF-S1 et leur expression de la cadhérine-11, indépendamment des cellules tumorales elles-mêmes. L’enrichissement en CAF-S1 dans le stroma tumoral était également un facteur de mauvais pronosticPurpose: Early luminal breast cancers (BC) represent 70% of newly diagnosed BC. Their prognosis is generally favorable but some patients (around 5 to 10% at 10 years) will relapse with distant metastases and most of them will die. Because this dismal prognosis concerns a small number of patients, T1N0 BC have been rarely studied. The aim of this work was to identify the mechanisms of metastatic recurrence in luminal breast cancers T1b-cN0M0 at diagnosis by deciphering characteristics of both epithelial cancer cells and their surrounding tumor microenvironment (TME). Experimental Design: We constituted a cohort of luminal T1b-cN0 BC patients with metastatic recurrence (defined as "cases”) and corresponding "controls" (i. e. patients without metastatic relapse) matched (1:1) to cases on the main known prognostic factors: age, tumor grade and tumor proliferation (assessed by Ki67). Results: We found that properties in both epithelial compartment and TME are indicative of relapse in early luminal breast cancers. In univariate analysis, the loss of differentiation (assessed by the reduced expression of CDH1/E-cadherin) in cancer cells is associated with recurrence, as also predicted by high ROR score using ProsignaTM test. In TME, quantitative and qualitative immunohistochemical analyzes reveals that “cases” are characterized by a significant decrease in CD4+ T lymphocytes and an accumulation of a particular subset of Cancer Associated Fibroblasts (CAF-S1) compared to “controls”, without any other association of T lymphocyte subtypes, B lymphocytes, macrophages or dendritic cells. In multivariate analysis, TME features, in particular CAF-S1 enrichment, remain significantly associated with recurrence, which demonstrates their biological and clinical relevance. Finally, by performing functional analyses, we demonstrated that CAF-S1 pro-metastatic properties are -at least in part- mediated by CDH11/Osteoblast cadherin, consistent with the fact that the bones are a major site of metastases in these patients. Conclusions: Distant recurrence in early luminal BC is strongly associated with TME features, such as the presence of CAF-S1 and their expression of CDH11. This is independent of tumor cells and represents a new prognostic factor of distant relapse in early luminal BC patients. This could justify targeted therapies against CAF-S1 or CDH11 in these cases
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Pålsson, Birger. "Tumour marker CA-50 in pancreatic cancer." Lund : Dept. of Surgery, Lund University, 1993. http://catalog.hathitrust.org/api/volumes/oclc/38154714.html.
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Muller, Laure. "Modélisation et traitement du signal de rétrodiffusion lumineuse dans les tissus vivants appliques à la détection de bas niveaux de saturation en oxygène : contribution à l'optimisation de la dosimétrie en thérapie photodynamique anticancéreuse." Vandoeuvre-les-Nancy, INPL, 1994. http://www.theses.fr/1994INPL120N.
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La thérapie photodynamique, basée sur l'affinité pour les tissus tumoraux d'un agent photosensibilisant est un traitement anticancéreux prometteur mais encore en phase de recherche. Parmi les paramètres inconnus, l'action de l'oxygène est un élément essentiel a la définition d'une dosimétrie efficace de la lumière. En effet, sa détermination permet une optimisation de l'action phototoxique ainsi que la détermination d'un seuil de réussite thérapeutique. A ces fins, le développement d'un système adapte aux mesures par voie endoscopique, seul accès au site tumoral, permettant l'évaluation de l'état d'oxygénation des tissus au cours du traitement en temps réel et in situ est nécessaire. Reposant sur le principe de différenciation optique, éprouve par les oxymétries dits de pouls, la saisie des données s'effectue par un capteur original issu de la technologie fibres optique. La métrologie associée comporte une phase de modélisation de la réponse de la masse tumorale a une excitation lumineuse. Cette démarche s'apparente parfaitement au traitement de signal physiologique, puisque les tissus tumoraux, soumis a un échelon de lumière, sont identifies par un modèle de type arx. Celui-ci a été valide tant par des simulations numériques que par des expérimentations sur fantômes optiques. Il ouvre d'ailleurs de nouveaux horizons a l'oxymétrie pulsée en général. La gestion des données est assurée par le biais d'un logiciel débouchant sur une surveillance en temps réel du site opératoire. L'optimisation du système comporte une gestion dynamique de l'espace mémoire par un échantillonnage sélectif des données expérimentales. L'élaboration de fantômes a base de colorants, destines a la validation du principe est décrite. Enfin un protocole de mesures in vivo confirme les bons résultats obtenus in vitro
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Payne, Kyle K. "Immunotherapy of Cancer: Reprogramming Tumor/Immune Cellular Crosstalk to Improve Anti-Tumor Efficacy." VCU Scholars Compass, 2015. http://scholarscompass.vcu.edu/etd/3939.
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Immunotherapy of cancer has been shown to be promising in prolonging patient survival. However, complete elimination of cancer and life-long relapse-free survival remain to be major challenge for anti-cancer therapeutics. We have previously reported that ex vivo reprogramming of tumor-sensitized immune cells by bryostatin 1/ionomycin (B/I) and the gamma-chain (γ-c) cytokines IL-2, IL-7, and IL-15 resulted in the generation of memory T cells as well as CD25+ NKT cells and CD25+ NK cells. Adoptive cellular therapy (ACT) utilizing these reprogrammed immune cells protected FVBN202 mice from tumor challenge, and overcame the suppressive functions of myeloid-derived suppressor cells (MDSCs). We then demonstrated that the presence of CD25+ NKT cells was required for anti-tumor efficacy of T cells as well as their resistance to MDSCs. Similar results were obtained by reprogramming of peripheral blood mononuclear cells (PBMC) from patients with early stage breast cancer, demonstrating that an increased frequency of CD25+ NKT cells in reprogrammed immune cells was associated with modulation of MDSCs to CD11b-HLA-DR+ immune stimulatory cells. Here, we tested the efficacy of immunotherapy in a therapeutic setting against established primary breast cancer (Chapter One), experimental metastatic breast cancer (Chapter Three) as well as against minimal residual disease (MRD) in patients with multiple myeloma (Chapter Two). We evaluated the ability of reprogrammed immune cells, including CD25+ NKT cells, to convert MDSCs to myeloid immune stimulatory cells, in vivo; this resulted in the identification and characterization of a novel antigen presenting cell (APC). These novel immune stimulatory cells differed from conventional APCs, including dendritic cells (DCs) and macrophages. We have also demonstrated that enhancing immunogenicity of mammary tumors by treatment with Decitabine (Dec) along with overcoming MDSCs by utilizing reprogrammed T cells and NKT cells in ACT prolongs survival of animals, but fails to eliminate the tumor. However, targeting cancer during a setting of MDR, when tumor cells are dormant, results in objective responses as evidenced in our multiple myeloma studies. This suggests that targeting breast cancer with immunotherapy following conventional therapies, in a setting of residual disease when tumor cells are dormant, may be effective in eliminating such residual cells or maintaining dormancy and extending time-to-relapse for breast cancer patients.
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Fumagalli, Debora. "Evaluation of tumor heterogeneity in breast cancer." Doctoral thesis, Universite Libre de Bruxelles, 2016. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/229735.
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Le cancer du sein est le cancer le plus fréquent chez la femme et représente la principale cause de mortalité liée au cancer. Le décés est habituellement causé par le développement de résistance aux traitements et la propagation métastatique de la maladie. Malgré la pertinence clinique, la complexité moléculaire de la maladie et sa dynamique restent à ce jour peu connues.Depuis longtemps, l’hétérogénéité du cancer du sein a été observée au niveau histologique et du profil évolutif clinique, et ces différences ont servi de base pour la classification de la maladie. Avec le développement des technologies à haut débit, telles que les puces à damier (microarrays) et le séquençage à haut débit, cette classification a été affinée et une complexité génétique jusqu'alors inconnue a été révélée.Des études utilisant ces techniques ont montré que des différences moléculaires existent non seulement entre les différentes patientes atteintes d’un cancer du sein (hétérogénéité inter-tumorale), mais aussi chez la même patiente (hétérogénéité intra-tumorale). En outre, l'hétérogénéité intra-tumorale peut exister non seulement entre les différentes parties d'une tumeur (hétérogénéité intra-tumorale spatiale) mais elle peut aussi résulter de l’évolution moléculaire d'une tumeur au cours du temps (hétérogénéité intra-tumorale temporelle). Cette complexité pourrait avoir un impact important sur la façon dont les patientes atteintes d’un cancer du sein sont prises en charge et traitées.La recherche que j’ai menée dans le Breast Cancer Translational Research Laboratory sous la direction du Professeur Christos Sotiriou avait deux objectifs principaux. Le premier était de déterminer l'ampleur et les implications cliniques de l'hétérogénéité intra-tumorale dans deux scénarios cliniques courants, à savoir: les cancers du sein multifocaux (MFBCs) et les cancers du sein métastatiques ER positif / HER2 négatif. Le deuxième était d'étudier l'impact de l'édition de l'ARN dans la détermination de l'hétérogénéité inter-tumorale, phénomène encore peu caractérisé. Notre recherche a notamment montré que:1) Les lésions de tous les MFBCs que l’on a étudiés partagent une origine commune. Malgré cela, et malgré des caractéristiques pathologiques similaires, chez un tiers des patientes, les lésions multifocales d’une même patiente ne partageaient aucune substitution et aucune insertion/déletion. De plus, l’hétérogénéité inter-lésion a été observée pour des mutations oncogéniques dans des gènes tels que PIK3CA, TP53, GATA3 et PTEN;2) En se concentrant sur un nombre défini de gènes associés au cancer, une concordance substantielle des mutations et du nombre de copies des gènes a été observée entre les lésions primaires et métastatiques appariées de cancers du sein ER positif / HER2 négatif. Des différences entre les lésions appariées ont cependant été trouvées pour les niveaux d’expression de certains gènes. Dans les lésions primaires, seuls les niveaux d’expression de quelques gènes et un niveau élevé d'amplification de FGFR1 ont été associés à la survie;3) L'édition de l’ARN est une source généralisée de variation du transcriptome dans le cancer du sein. Dans ce cancer, et potentiellement dans tous les cancers, l'édition de l’ARN est principalement contrôlée par deux facteurs, à savoir l'amplification de 1q et l'inflammation, qui sont toutes deux très répandues parmi les cancers humains. La magnitude de l'édition de l’ARN, en combinaison avec la conservation des sites d'édition détectés dans les tissus et les patientes, suggère qu'il pourrait y avoir des implications cliniques et thérapeutiques pour un large éventail de patientes atteintes d’un cancer.Nos résultats suggèrent qu'une caractérisation moléculaire approfondie des cancers du sein multifocaux et métastatiques est importante pour apprécier leur complexité, et que dans la recherche sur le cancer du sein, plus d’importance devrait être accordée à l'édition de l'ARN, un phénomène encore peu étudié qui pourrait influencer notre connaissance sur le développement et l'évolution de la maladie.Breast cancer still represents the most frequently diagnosed cancer and the leading cause of cancer-related mortality in women. Death is usually caused by the development of resistance to treatments and the resulting metastatic spread of the disease. Despite the clinical relevance, little is known about the molecular complexity of the disease and its dynamics.Breast tumor heterogeneity has been observed at the level of the histology and the natural history of the disease for a long time, and these differences have served as the basis for disease classification. With the advent of high-throughput technologies, such as gene expression microarrays and massively parallel sequencing, this classification has been refined and a previously unknown genetic complexity has been revealed. Studies implementing these technologies have shown that molecular dif¬ferences exist not only between different breast cancer patients (inter-tumor heterogeneity), but also within the same patient (intra-tumor heterogeneity). Furthermore, intra-tumor heterogeneity could occur either between different regions of a tumor (spatial intra-tumor heterogeneity), or as the result of the molecular evolu¬tion of a tumor over time (temporal intra-tumor heterogeneity). This complexity might have a profound impact on the way breast cancer patients are managed and treated. The research work that I carried out in the Breast Cancer Translational Research Laboratory under the direction of Prof Christos Sotiriou had two main aims. The first was to determine the extent and the clinical implications of intra-tumor heterogeneity in two common clinical scenarios, namely: multifocal breast cancers (MFBCs) and metastatic ER positive/HER2 negative breast cancers. The second was to investigate the potential impact of yet poorly characterized phenomenon, such as RNA editing, in determining inter-tumor heterogeneity. For this purpose, I have conducted three main projects, which resulted in three manuscripts.We showed that:1) The lesions of all the investigated MFBCs shared a common origin. Despite this, and despite having similar pathological features, in up to a third of the patients the lesions of the same MFBC didn’t share any substitution/indels, and inter-lesion heterogeneity was observed for oncogenic mutation(s) in genes such as PIK3CA, TP53, GATA3, and PTEN; 2) When focusing on a defined number of cancer-associated genes, a substantial concordance for mutations and copy number aberrations could be found between primary and matched metastatic lesions of ER positive/HER2 negative breast cancers. Differences between matched pairs could however be found for the level of expressions of few genes. In primary lesions, only the expression levels of few genes and high FGFR1 amplification levels were associated with OS;3) A-to-I RNA editing is a pervasive source of transcriptome variation in breast cancer. In breast and potentially all cancers, A-to-I editing is mainly controlled by two factors, namely 1q amplification and inflammation, both of which are highly prevalent among human cancers. The wide-spread editing observed, in combination with the conservation of editing sites detected across tissues and patients, suggests that there might be clinical and therapeutic implications for a wide range of cancer patients.Our results suggest both that a thorough molecular characterization of multifocal and metastatic breast cancers is important to appreciate their genomic complexity, and that in breast cancer research more relevance should be given to RNA editing, a yet poorly investigated phenomenon that has the potential to impact the development and the evolution of the disease.
Doctorat en Sciences médicales (Médecine)
info:eu-repo/semantics/nonPublished
Books on the topic "Cancer tumer"
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Janes-Hodder, Honna. Childhood cancer: A parent's guide to solid tumor cancers. 2nd ed. Beijing: O'Reilly, 2002.
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1935-, Sell Stewart, ed. Serological cancer markers. Totowa, N.J: Humana Press, 1992.
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1954-, Srivastava Sudhir, ed. Early detection of cancer: Molecular markers. Armonk, N.Y: Futura Pub. Co., 1994.
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H, Goldfarb Ronald, ed. Brain tumor invasiveness. Dordrecht: Kluwer Academic, 1994.
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F, Oettgen Herbert, ed. Gangliosides and cancer. Weinheim, Federal Republic of Germany: VCH Verlagsgesellschaft, 1989.
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T, Garrett Carleton, and Sell Stewart 1935-, eds. Cellular cancer markers. Totowa, N.J: Humana Press, 1995.
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Marry M. van den Heuvel-Eibrink, ed. Wilms Tumor. Brisbane, Australia: Codon Publications, 2016.
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Tumor models in cancer research. 2nd ed. New York: Humana Press, 2011.
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Teicher, Beverly A. Tumor Models in Cancer Research. New Jersey: Humana Press, 2001. http://dx.doi.org/10.1385/1592591000.
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Pag�, Michel. Tumor Targeting in Cancer Therapy. New Jersey: Humana Press, 2002. http://dx.doi.org/10.1385/1592591671.
Full textBook chapters on the topic "Cancer tumer"
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Camelo, Felipe, and Anne Le. "The Intricate Metabolism of Pancreatic Cancers." In The Heterogeneity of Cancer Metabolism, 77–88. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-65768-0_5.
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AbstractCurrently, approximately 95% of pancreatic cancers are pancreatic ductal adenocarcinomas (PDAC), which are the most aggressive form and the fourth leading cause of cancer death with extremely poor prognosis [1]. Poor prognosis is primarily attributed to the late diagnosis of the disease when patients are no longer candidates for surgical resection [2]. Cancer cells are dependent on the oncogenes that allow them to proliferate limitlessly. Thus, targeting the expression of known oncogenes in pancreatic cancer has been shown to lead to more effective treatment [3]. This chapter discusses the complexity of metabolic features in pancreatic cancers. In order to comprehend the heterogeneous nature of cancer metabolism fully, we need to take into account the close relationship between cancer metabolism and genetics. Gene expression varies tremendously, not only among different types of cancers but also within the same type of cancer among different patients. Cancer metabolism heterogeneity is often prompted and perpetuated not only by mutations in oncogenes and tumor-suppressor genes but also by the innate diversity of the tumor microenvironment. Much effort has been focused on elucidating the genetic alterations that correlate with disease progression and treatment response [4, 5]. However, the precise mechanisms by which tumor metabolism contributes to cancer growth, survival, mobility, and aggressiveness represent a functional readout of tumor progression (Fig. 1).
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van Herpen, Carla M. L. "Patients with Rare Head Neck Cancers: Do They Need a Different Approach?" In Critical Issues in Head and Neck Oncology, 309–15. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-63234-2_20.
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AbstractA cancer is considered rare when the annual cancer incidence is less than 6 per 100,000 inhabitants. In absolute numbers more than 500,000 patients per year are diagnosed with a rare cancer, and 4,300,000 rare cancer patients are prevalent in Europe. The definition is widely adopted among the different scientific international societies like ESMO and ESTRO. This means that 22% of all diagnosed cancers are rare and out of the 260 cancer types identified (www.rarecare), 223 (86%) are rare. The European Network for Rare Solid Cancers (EURACAN) uses this definition to create reference networks in order to improve rare cancer care.In Europe rare cancer patients have poorer survival as compared to common cancer patients. Moreover, the survival of rare cancer patients in the Netherlands has barely increased over time (from 50% in 1995–2000 to 56% in 2012–2016), in contrast to the common cancers (from 59% in 1995–2012 to 72% in 2012–2016). Clinical decision-making is more problematic in the case of a rare cancer because clinical studies on that tumor will be more difficult to do; so, the quality of available evidence tends to be limited. Furthermore, the decreased survival is partly caused by a delay in the diagnostic trajectory and found to be related to more advanced staging resulting in less effective treatment options.Examples of rare cancers in the head and neck region are salivary gland cancers, which can be divided in 22 histological subtypes, and epithelial tumors of the nasal cavity and sinuses, e.g. intestinal type adenocarcinoma. Furthermore, soft tissue sarcoma and bone sarcoma and Merkel cell carcinoma, which are rare and frequently located in the head and neck area (Table 20.1).New developments in the treatment of (recurrent/metastatic) salivary gland cancer, especially salivary duct cancer, will be discussed. By unraveling tumor characteristics, such as genetic alterations and protein expression profiles, therapeutic strategies tailored to the patient’s tumor can be rationalized. This genomic profiling and mapping of immunohistochemical expression profiles is essential in the search for a suitable treatment or study approach. Thereby, it alleviates the paucity in systemic treatment options and can significantly alter the prognosis of patients with rare cancers.
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Zarisfi, Mohammadreza, Tu Nguyen, Jessie R. Nedrow, and Anne Le. "The Heterogeneity Metabolism of Renal Cell Carcinomas." In The Heterogeneity of Cancer Metabolism, 117–26. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-65768-0_8.
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AbstractAccording to data from the American Cancer Society, cancer is one of the deadliest health problems globally. Annually, renal cell carcinoma (RCC) causes more than 100,000 deaths worldwide [1–4], posing an urgent need to develop effective treatments to increase patient survival outcomes. New therapies are expected to address a major factor contributing to cancer’s resistance to standard therapies: oncogenic heterogeneity. Gene expression can vary tremendously among different types of cancers, different patients of the same tumor type, and even within individual tumors; various metabolic phenotypes can emerge, making singletherapy approaches insufficient. Novel strategies targeting the diverse metabolism of cancers aim to overcome this obstacle. Though some have yielded positive results, it remains a challenge to uncover all of the distinct metabolic profiles of RCC. In the quest to overcome this obstacle, the metabolic oriented research focusing on these cancers has offered freshly new perspectives, which are expected to contribute heavily to the development of new treatments.
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Ferrari, Marco, Nausica Montalto, and Piero Nicolai. "Novel Approaches in Surgical Management: How to Assess Surgical Margins." In Critical Issues in Head and Neck Oncology, 95–110. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-63234-2_7.
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AbstractThe concept of surgical margins was born a long time ago but still lacks a univocal and sound understanding. The current biological rationale behind the recommendations on margins management relies on two pillars: (1) the observation that groups of cancer cells can leave the macroscopic tumor and disseminate throughout adjacent tissues with different degrees of aggressiveness; (2) the belief that removal of all (or most of) cancer cells can cure the patient. However, this background is undermined by some pieces of evidence. For instance, it has been proven that tissues surrounding cancer often bear precancerous traits, which means that cutting through non-cancerous tissues does not equate to cut through healthy tissues. The head and neck exquisitely poses a number of challenges in the achievement of negative margins, with special reference to anatomical complexity, high density in relevant structures, and unique histological heterogeneity of cancers. Currently, intraoperative margins evaluation relies on surgeons’ sight, palpation, ability to map tumor extension on imaging, and knowledge of anatomy, with some optical imaging technologies aiding the delineation of the mucosal margins of excision. Frozen sections are currently used to intraoperatively evaluate margins, yet with debate on whether and how this practice should be performed. Future perspectives on improvement of margins control are threefold: research is oriented towards refinements of understanding of cancers local progression, implementation of technologies to intraoperatively render tumor extension, and employment of optical imaging modalities capable of detecting foci of residual tumor in the surgical bed.
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Watson, Geoffrey Alan, Kirsty Taylor, and Lillian L. Siu. "Innovation and Advances in Precision Medicine in Head and Neck Cancer." In Critical Issues in Head and Neck Oncology, 355–73. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-63234-2_24.
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AbstractThe clinical utility of precision medicine through molecular characterization of tumors has been demonstrated in some malignancies, especially in cases where oncogenic driver alterations are identified. Next generation sequencing data from thousands of patients with head and neck cancers have provided vast amounts of information about the genomic landscape of this disease. Thus far, only a limited number of genomic alterations have been druggable, such as NTRK gene rearrangements in salivary gland cancers (mainly mammary analogue secretory carcinoma), NOTCH mutations in adenoid cystic cancers, HRAS mutations in head and neck squamous cell cancers, and even a smaller number of these have reached regulatory approval status. In order to expand the scope of precision medicine in head and neck cancer, additional evaluation beyond genomics is necessary. For instance, there is increasing interest to perform transcriptomic profiling for target identification. Another advance is in the area of functional testing such as small interfering RNA and drug libraries on patient derived cell cultures. Liquid biopsies to detect specific tumor clones or subclones, or viral sequences such as HPV, are of great interest to enable non-invasive tracking of response or resistance to treatment. In addition, precision immuno-oncology is a tangible goal, with a growing body of knowledge on the interactions between the host immunity, the tumor and its microenvironment. Immuno-oncology combinations that are tailored to immunophenotypes of the host-tumor-microenvironment triad, personalized cancer vaccines, and adoptive cell therapies, among others, are in active development. Many therapeutic possibilities and opportunities lie ahead that ultimately will increase the reality of precision medicine in head and neck cancer.
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Parker, Nicole N., and Dietmar W. Siemann. "The Microenvironment in Cancer." In Tumor Microenvironment, 1–6. Chichester, UK: John Wiley & Sons, Ltd, 2010. http://dx.doi.org/10.1002/9780470669891.ch1.
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Imai, Kohzoh, and Toshiro Sugiyama. "Tumor Markers." In Gastric Cancer, 218–30. Tokyo: Springer Japan, 1993. http://dx.doi.org/10.1007/978-4-431-68328-5_16.
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Parmiani, G. "Tumor Immunology." In Cancer Metastasis, 226–29. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74236-1_32.
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Walser, Tonya C., Jane Yanagawa, Edward Garon, Jay M. Lee, and Steven M. Dubinett. "Tumor Microenvironment." In Lung Cancer, 27–69. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-524-8_2.
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Ryu, Ji Kon. "Tumor Markers." In Pancreatic Cancer, 89–92. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-47181-4_6.
Full textConference papers on the topic "Cancer tumer"
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Sztejnberg, Manuel L., and Tatjana Jevremovic. "Advanced Application of BNCT in Advanced Cancers." In 17th International Conference on Nuclear Engineering. ASMEDC, 2009. http://dx.doi.org/10.1115/icone17-75906.
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We present a new concept of one form of radiation binary targeted therapy that may offer hope for the often fatal relapsed and/or metastasized HER2+ cancers. The idea is to deliver boronated (boron-10 isotope) anti-HER2 monoclonal antibodies (mAbs) to the patient to be deposited preferentially into the tumor followed by one session of a low energy neutron irradiation. Based on actual computed tomography data, we present the comprehensive theoretical (numerical) modeling of the new approach in designing the treatment conditions for the boron neutron capture therapy (BNCT) using the MITRII-FCB neutron beam facility. The results show the effectiveness of the proposed treatment option for the advanced breast cancers and the metastasized breast cancers in the lungs of a patient. Our theoretical analysis concludes that with a boron concentration of ∼316 μg/g in tumor and a tumor-to-healthy tissue boron concentration ratio of 35:1, this new BNCT breast cancer treatment can be performed with very low doses to normal tissue and 50 Gy, or higher, doses delivered to the tumor regions. In particular, when applied to the breast cancer treatment, the resulting doses to skin and lung remain under the tolerance dose values. We also went beyond the traditional application of the BNCT and analyzed its applicability in targeting the metastasized breast cancer; using the same theoretical approach we determined the doses delivered into the patient lung with scattered cancer loci.
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Stokol, Tracy, Mandy B. Esch, Nozomi Nishimura, Chris Schaffer, Janelle L. Daddona, David J. Post, and Dhruv P. Desai. "Little Channels, Big Disease: Using Microfluidics to Investigate Cancer Metastasis." In ASME 2011 9th International Conference on Nanochannels, Microchannels, and Minichannels. ASMEDC, 2011. http://dx.doi.org/10.1115/icnmm2011-58298.
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The leading cause of death in human patients with malignant cancer is the dissemination of the primary tumor to secondary sites throughout the body. It is well known that cancers metastasize to certain tissues (e.g. breast cancer typically spreads to the lungs. brain and bone), in a pattern that cannot be explained by blood flow from the primary tumor or simple mechanical arrest. Circulating tumor cells usually arrest in the microvasculature of target tissues. At these sites, they must adhere to the endothelium, survive, proliferate and extravasate in order to form a secondary tumor. In vitro tools that appropriately mimic the microvasculature in which cancer metastasis occurs have been largely unavailable. With the advent of microfluidic and nanotechnology, we can now more accurately model the complexity of the microvascular environment, in terms of representative endothelial cells, geometry, shear stress and exposure to organ-specific environmental cues. This talk will focus on the use of microfluidic devices to explore mechanisms involved in tumor-endothelial cell interactions that govern cancer metastasis to organ specific sites.
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Soucy, P., W. Ehringer, C. Klinge, H. Frieboes, and A. Gobin. "An Innovative Approach for Curcumin Delivery for Breast Cancer Using Albumin Nanoparticles." In ASME 2013 2nd Global Congress on NanoEngineering for Medicine and Biology. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/nemb2013-93295.
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Triple-negative breast cancer (TNBC) accounts for ∼25% of breast cancer among premenopausal African-American and Latino women1. Curcumin (diferuloylmethane; CCM), a natural polyphenol extracted from turmeric, has chemopreventive and chemotherapeutic activity in various cancers 2,3 and inhibits growth and invasion of TNBC/basal-like MDA-MB-231 human breast cancer cells 4. CCM has been reported to affect all stages of tumor progression and metastases due to its interactions with multiple targets. We employ a novel approach utilizing both computational and experimental modeling to characterize and analyze TNBC and the 3D tumor microenvironment responses to albumin bound CCM particles (ACP) versus CCM alone.
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Lima, Beatriz Alves, Andressa da Silva Pereira, Bruna Alves Lima, Diana Gonçalves Lima, Leonardo Ferreira Pucci, Renato Moraes Ferreira, Tiago Castro Ferreira, and Henrique Ferreira Pucci. "PREDICTORS OF BREAST CANCER PROGNOSIS BASED ON TUMOR BIOMARKERS." In Abstracts from the Brazilian Breast Cancer Symposium - BBCS 2021. Mastology, 2021. http://dx.doi.org/10.29289/259453942021v31s2022.
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Objective: To analyze the tumor biological markers of breast cancer associated with the prognostic of the disease. Methodology: A systematic review was carried out on the Scielo, PubMed, and the National Cancer Institute databases on the topic. Descriptors used were: tumor biomarkers, breast cancer, and prognosis. Thus, 15 articles published between 2001 and 2020 were selected. Results: Breast cancer, characterized by the disordered multiplication of breast cells, is the most incident in women in the world, representing 24.2% of the total cases in 2018, and the most frequent cause of death in this gender. Accordingly, tumor markers are complementary tests for early diagnosis, since they are macromolecules derived from the tumor and biological fluids. The evaluation of tumor markers is of paramount importance due to the great diversity in clinical progression of breast cancer, for example, those hormone receptors (estrogen and progesterone), MIB-1, Ki-67, PCNA, p53, and c-erbB-2. Hence, about two-thirds of breast cancers are positive for hormone receptors and are related to a more favorable prognosis. PCNA (36 kDa protein perceptible in the cell nucleus from the late G1 to the S phase of the cell cycle) and MIB-1 (direct antibody against parts of the Ki-67 antigen) have a high proportion of tumor cells associated with a high-degree tumor differentiation, indicating a worse prognosis. Furthermore, mutations in the p53 and c-erbB-2 genes report low levels of estrogen and progesterone receptors, leading to a worse prognosis. Conclusion: In brief, the recognition of the main markers helps in the identification of patients with potentially aggressive tumors and in the mortality reduction of breast cancer, through treatments that can alter the course of the disease. On account of this, it is known that the tumor markers must be used in combination with the other methods such as diagnostic, prognostic, and therapeutic modifications.
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Queiroz, Andrei Alves de, Debora Garcia y. Narvaiza, Ana Maria Kemp, and Gisele Tolaini Gomes Pereira. "LOBULAR BREAST CARCINOMA: THE RISK FOR CONTRALATERAL BREAST IS NOT PERMANENT." In Scientifc papers of XXIII Brazilian Breast Congress - 2021. Mastology, 2021. http://dx.doi.org/10.29289/259453942021v31s1028.
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Introduction: The invasive lobular carcinoma of the breast occurs in approximately 10% of breast cancers. The increased risk for multicentric and bilateral breast tumor is well-documented in the literature, but few data is available regarding the interval for occurrence of contralateral tumors. Objectives: This study aims to analyze the characteristics of the bilaterality of the lobular tumor and time to the occurrence of the bilateral tumor in comparison with non-lobular tumors. Methods: Retrospective, analytical study from the American Surveillance, Epidemiology and End Results Program (SEER) database. Patients with unilateral and bilateral breast cancer (synchronous and metachronous) were filtered from this database in women aged 20 to 75 years from 2000 to 2017. Patients with cancers diagnosed in other organs were excluded. Definitions: Lobular carcinoma at the first diagnosis (LC): patients with lobular breast cancer at the diagnosis of the first neoplasm. Non-lobular carcinoma (NLC): patients with non-lobular carcinoma (ductal or special type) at diagnosis of the first neoplasm. Results: We identified 560,608 patients with breast cancer, 19,792 of which were patients with bilateral tumors (3.5%) and 45,156 (8.0%) lobular tumors at the first diagnosis. Patients with LC had significantly more tumors in both breasts throughout the research period (6.3% vs. 3.3%; OR: 1.97; 95%CI 1.89–2.06, p <0.001). The time for occurrence of contralateral tumor varied widely between patients with lobular and non-lobular tumors. The LC patients presented the diagnosis of contralateral breast tumor much earlier, with 50% of the contralateral tumors diagnosed within one month, and 75% in the first three months, while the NLC patients presented 50% of the contralateral tumors in the first three months and 75% after 54 months of follow-up. Cox’s multivariate analysis shows a higher risk of contralateral breast involvement in LC patients when corrected by age and estrogen receptor expression (RR 2.0; 95%CI 1.93–2.09; p <0.001). This increased risk is not sustained when patients with a tumor in an interval greater than 12 months (RR 1.04; 95%CI 0.96–1.14; p=0.3). Conclusions: Invasive lobular carcinoma is associated with a higher incidence of contralateral disease, but the higher risk occurs in the first year of follow-up. After the one-year period, the incidence of contralateral breast cancer is similar in lobular and non-lobular cancers.
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Zielinski, Rachel, Cosmin Mihai, and Samir Ghadiali. "Multi-Scale Modeling of Cancer Cell Migration and Adhesion During Epithelial-to-Mesenchymal Transition." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53511.
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Cancer is a leading cause of death in the US, and tumor cell metastasis and secondary tumor formation are key factors in the malignancy and prognosis of the disease. The regulation of cell motility plays an important role in the migration and invasion of cancer cells into surrounding tissues. The primary modes of increased motility in cancerous tissues may include collective migration of a group of epithelial cells during tumor growth and single cell migration of mesenchymal cells after detachment from the primary tumor site [1]. In epithelial cancers, metastasizing cells lose their cell-cell adhesions, detach from the tumor mass, begin expressing mesenchymal markers, and become highly motile and invasive, a process known as epithelial-to-mesenchymal transition (EMT) (Fig. 1) [2]. Although the cellular and biochemical signaling mechanisms underlying EMT have been studied extensively, there is limited information about the biomechanical mechanisms of EMT. In particular, it is not known how changes in cell mechanics (cell stiffness, cell-cell adhesion strength, traction forces) influence the detachment, migration and invasion processes that occur during metastasis.
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Patel, Sagar S., Ramesh Natarajan, and Rebecca L. Heise. "Mechanotransduction of Primary Cilia in Lung Adenocarcinoma." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80435.
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Lung cancer causes more than 1 million deaths worldwide annually [1]. In a recent study by the American Cancer Society in 2011, more than 221,000 new cases of lung cancers were reported [2]. Out of these, the mortality rate was found in roughly 70% of the cases [2]. Lung cancer is divided into two major categories: small cell and non-small cell. In the United States, non-small cell lung cancer accounts for 85% of all lung cancers and is considered the most common type of lung cancer [2]. It is usually resistant to chemotherapy, therefore making it extremely difficult to treat [3]. Furthermore adenocarcinomas, a type of non-small cell lung cancer, occur towards the periphery of the lungs and are the most common type accounting for 40–45% of all lung cancer cases [3]. Epithelial cells in the healthy lungs undergo stresses during inhalation and expiration of normal breathing. In addition to the forces of normal breathing, lung cancer cells may also experience abnormal mechanical forces due to pre-existing lung diseases such as asthma, bronchitis and chronic obstructive pulmonary disease or other tumor associated structural changes. These conditions can significantly alter the structure of the lungs and cell phenotype [4]. The change in the structure of the lungs affects the mechanical environment of the cells. Changes in extracellular (ECM) stiffness, cell stretch, and shear stress influence tumorigenesis and metastasis [5]. One mechanism through which the cells sense and respond to the cellular mechanical environment is through the primary cilia [6–7]. Primary cilia are non-motile, solitary structures formed from the cellular microtubules and protrude out of each cell. They have also been shown to play an important role in facilitating common cancer signaling pathways such as Sonic Hedgehog and Wnt/β-catenin signaling [8–9]. The objective of this study was to test the hypothesis that lung cancer cells respond to mechanical stimuli with the formation of primary cilia that are necessary for 3 hallmarks of tumor progression: proliferation, epithelial mesenchymal-transition, and migration.
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McClain, Jacob, Sara L. Tuell, and Susan N. Thomas. "Tumors Change the Elastic and Viscoelastic Properties of Draining Lymph Node Tissues." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14419.
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Changes in tissue mechanical properties are often the first indication of malignant disease, with the detection of a stiff lump by a patient. These changes include growth-induced solid stresses, increased matrix stiffness, high fluid pressure, and increased interstitial flow, which in turn enhance fluid flux away from the tumor to downstream lymph nodes (LNs). But in addition to changing the way a tumor feels to a patient, altered tumor tissue mechanics promote cancer cell invasion into lymphatic vessels, allowing their metastatic dissemination to draining LNs. LN swelling and stiffening is another common indicator of tumor growth, and the presence of metastatic cells in the sentinel LN, or tumor draining lymph node (TDLN), is used clinically to stage disease. Recent studies indicate the LN microenvironment determines whether metastatic cancers can spread to the sentinel LNs. Yet despite the known correlation of LN swelling and stiffening with tumorigenesis and the role of the LN microenvironment in metastasis, our understanding of how changes in LN mechanical properties relate to tumor progression, anti-tumor immune response and metastatic colonization of the LN is limited. This lack of a quantitative understanding limits functional analyses of the role of LN mechanics in determining cancer cell colonization of the TDLN, their influence on immune suppression taking place within the TDLN, as well as the development of strategies to mitigate these effects.
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Rabin, Yoed, Thomas B. Julian, Peter Olson, Michael J. Taylor, and Norman Wolmark. "Cryosurgery for Breast Malignancies: Apparatus and Techniques." In ASME 1999 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1999. http://dx.doi.org/10.1115/imece1999-0585.
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Abstract The treatment of breast cancer has evolved from the time of mutilation and ignorance in the middle ages, to one of breast conserving management and an intense study and understanding of the biological mechanisms driving tumor cells. As the treatment is directed to the cellular and sub-cellular level, breast conserving surgical procedures take on a more important role. Recent published results from neoadjuvant trials indicate a decrease in tumor size in 80% of patients and a modest increase in conversion from mastectomy to lumpectomy. By 2010 AD, it is estimated that 50% of all new breast cancers discovered will be less than 10 mm in diameter (Cady et al., 1996), which represents 90,000 patients. Standard surgical treatment would require an open segment resection, an operating room, anesthesia, cosmetic concerns and substantial cost. Add to this the number of patients who require segmental resection following complete clinical or pathological response following neoadjuvant chemotherapy, and the cost increases. An alternative method of tumor removal or destruction for small malignancies is needed to complete the biological assault on breast cancer. Cryosurgery may be one of these alternative means. Cryosurgery has been used successfully for more than three decades to treat benign and malignant neoplasms. To date, there is one reported case of primary breast cancer treatment with cryotherapy (Staren et al., 1997), which was followed up with ultrasound-guided biopsy, and which was found negative for malignancy 12 weeks post-cryosurgery. Cryotherapy carries many benefits in addition to the attractive concept of minimally invasive surgery. Low temperatures generate anaesthetic effect. Hemorrhage is reduced due to thrombosis of small blood vessels. Cryotherapy may cause stimulation of the body’s immune system, which additionally augments local tumor destruction and may also induce a response in metastatic tumor sites (Suzuki, 1995). With multiple treatments such as neoadjuvant therapy, hormone therapy, and radiation, which have the ability to downsize primary cancers and treat small cancers, lumpectomy may be increasingly used. Current diagnostic imaging trends are increasingly detecting small cancers (< 1 cm). The minimization of surgical intervention to compliment these trends is a natural progression of technology and understanding of the biological processes involved. Our ongoing research program to evaluate cryosurgery in the breast is comprised of several phases: (i) development of a miniaturized cryoprobe and a cryodevice for minimally invasive breast cryosurgery; (ii) validation testing of the cryoprobe and device in vivo; (iii) development of a technique to evaluate the injury associated with cryotreatment of the breast; (iv) comparison of the ultrasound imaged “‘ice-ball” in vivo with the resulting cryoinjury immediately post-cryosurgery; and, (v) long-term follow-up post-cryosurgery in a recently-pregnant sheep breast model. The work to date is part of this report.
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Melo, Maria Eduarda Bernardino Martins, Gabriela Prado Lopes, Darley Lima Ferreira Filho, Irnanda Layanna Gomes Oliveira, and Maria Eduarda Vasconcelos Florêncio Cavalcanti. "MALE BILATERAL BREAST CANCER: CASE REPORT." In Scientifc papers of XXIII Brazilian Breast Congress - 2021. Mastology, 2021. http://dx.doi.org/10.29289/259453942021v31s1077.
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Introduction: Breast cancer occurring bilaterally in men is extremely rare. Breast cancer represents 1% of all cancers, while bilateral cancer represents 5% of a total number of patients with breast cancer, which may be synchronic or metachronic. Many cases of breast cancer in men are detected between 60 and 70 years, with an average of 67 years of age. In men there is a tendency for late diagnosis at a more advanced stage than in women. Case report: A male patient, JSS, 68 years old, from Afogados da Ingazeira, state of Pernambuco, was seen with breast tumoration in June 2016. He arrived at the service with an existing diagnosis of breast cancer through core-biopsy examination. The physical exam presented bulging in the left retroareolar region and a hardened tumoration in palpation. Radical mastectomy was performed. The histopathological results confirmed an invasive mucinous carcinoma with histological grade I, nuclear grade II and mitotic grade I. Free margins. The most frequent histological type in men is ductal (85%–90%), followed by papillary in 4.5% and mucinous in 2.8% of the cases. Nineteen free axillary lymph nodes were dissected, with Estrogen and Progesterone + receptors, Her-2, negative and with Ki-67 of 5%. Breast cancers in men present with more positivity for hormone receptors and low expression for Her-2. The pathological staging was classified as II a. The patient was being followed by the clinical oncology department, where he was chosen not to do chemotherapy and only hormone therapy, with Tamoxifen 20 mg. However, over a period of six months he noticed the presence of a tumoration in the right breast. An image examination was performed with MG/USG, which confirmed the presence of a tumor in the right retro-areolar region (Birads IV). A core-biopsy of the lesion was requested, which confirmed an invasive breast cancer. The patient underwent right radical mastectomy, whose result confirmed an invasive ductal carcinoma with pathological staging II a. Conclusion: This pathology is extremely rare in men and the evaluation of the contralateral breast is of fundamental importance. Early diagnosis and compliance with treatment will reduce tumor recurrence and provide a better prognosis for these patients.
Reports on the topic "Cancer tumer"
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Wang, Ying yuan, Zechang Chen, Luxin Zhang, Shuangyi Chen, Zhuomiao Ye, Tingting Xu, and Yingying Zhang c. A systematic review and network meta-analysis: Role of SNPs in predicting breast carcinoma risk. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, February 2022. http://dx.doi.org/10.37766/inplasy2022.2.0092.
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Review question / Objective: P: Breast cancer patient; I: Single nucleotide polymorphisms associated with breast cancer risk; C: Healthy person; O: By comparing the proportion of SNP mutations in the tumor group and the control group, the effect of BREAST cancer risk-related SNP was investigated; S: Case-control study. Condition being studied: Breast cancer (BC) is one of the most common cancers among women, and its morbidity and mortality have continued to increase worldwide in recent years, reflecting the strong invasiveness and metastasis characteristics of this cancer. BC is a complex disease that involves a sequence of genetic, epigenetic, and phenotypic changes. Polymorphisms of genes involved in multiple biological pathways have been identified as potential risks of BC. These genetic polymorphisms further lead to differences in disease susceptibility and severity among individuals. The development of accurate molecular diagnoses and biological indicators of prognosis are crucial for individualized and precise treatment of BC patients.
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Deng, Chun, Zhenyu Zhang, Zhi Guo, Hengduo Qi, Yang Liu, Haimin Xiao, and Xiaojun Li. Assessment of intraoperative use of indocyanine green fluorescence imaging on the number of lymph node dissection during minimally invasive gastrectomy: a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, November 2021. http://dx.doi.org/10.37766/inplasy2021.11.0062.
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Review question / Objective: Whether is indocyanine green fluorescence imaging-guided lymphadenectomy feasible to improve the number of lymph node dissections during radical gastrectomy in patients with gastric cancer undergoing curative resection? Condition being studied: Gastric cancer was the sixth most common malignant tumor and the fourth leading cause of cancer-related death in the world. Radical lymphadenectomy was a standard procedure in radical gastrectomy for gastric cancer. The retrieval of more lymph nodes was beneficial for improving the accuracy of tumor staging and the long-term survival of patients with gastric cancer. Indocyanine green(ICG) near-infrared fluorescent imaging has been found to provide surgeons with effective visualization of the lymphatic anatomy. As a new surgical navigation technique, ICG near-infrared fluorescent imaging was a hot spot and had already demonstrated promising results in the localization of lymph nodes during surgery in patients with breast cancer, non–small cell lung cancer, and gastric cancer. In addition, ICG had increasingly been reported in the localization of tumor, lymph node dissection, and the evaluation of anastomotic blood supply during radical gastrectomy for gastric cancer. However, it remained unclear whether ICG fluorescence imaging would assist surgeons in performing safe and sufficient lymphadenectomy.
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Kengsakul, Malika, Gatske Nieuwenhuyzen – de Boer, and Heleen van Beekhuizen. Radiological factors associated with residual disease after cytoreductive surgery for advanced ovarian cancer. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, January 2023. http://dx.doi.org/10.37766/inplasy2023.1.0059.
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Review question / Objective: Which radiological factors associated with incomplete cytoreduction (gross residual disease) after cytoreductive surgery (CRS) for advanced ovarian cancer? Condition being studied: Findings of CT scan and discussion in the multidisciplinary tumor board meeting (MDO) are crucial to determine the therapeutic strategy for individual ovarian cancer patients. Preferably, patients undergo primary cytoreductive surgery (CRS) followed by adjuvant chemotherapy. However, when complete cytoreduction is not considered feasible, neoadjuvant chemotherapy followed by interval cytoreductive surgery and adjuvant chemotherapy is indicated. In patients with advanced stage epithelial ovarian cancer (EOC), maximal cytoreduction to no gross residual tumor (complete cytoreduction) is known to associated with the best overall survival.
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Li, Zhenqi, Guangfu Zhang, Jia Liu, and Xiaolin Li. Risk factors for gallbladder Cancer:A meta-analysis based on nearly a decade of research. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, April 2022. http://dx.doi.org/10.37766/inplasy2022.4.0065.
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Review question / Objective: Gallbladder cancer is a rare tumor that is mostly advanced once detected. The efficacy of surgical treatment is still controversial. Therefore, primary prevention of gallbladder cancer is important. There are many studies on risk factors for gallbladder cancer, but at present it is difficult to identify independent risk factors for gallbladder cancer, except for a history of symptomatic chronic cholecystitis and malignant transformation of a single polyp. Laparoscopic cholecystectomy is popular worldwide and can be a preventive procedure for gallbladder cancer in addition to resolving benign lesions. This study makes a meta-analysis of the latest research results exploring the risk factors of gallbladder cancer in the last decade , expecting to provide evidence-based medical support for the prevention of gallbladder cancer at the clinical level, and to provide some ideas to guide the surgical indications for LC and future research related to gallbladder cancer. Subject of study: Gallbladder cancer. Study content: Risk factors. Type of study: case-control or cohort study. Extract the value: OR, HR, RR.
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Shyam, E., and P. Reddy. Tumor Suppressors and Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 2001. http://dx.doi.org/10.21236/ada403397.
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Shyam, E., and P. Reddy. Tumor Suppressors and Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 2002. http://dx.doi.org/10.21236/ada412779.
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Lin, Yawei, Yi Chen, Rongrong Liu, and Baohua Cao. Effect of exercise on rehabilitation of breast cancer surgery patients: A systematic review and meta-analysis of randomized controlled trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, October 2022. http://dx.doi.org/10.37766/inplasy2022.10.0065.
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Review question / Objective: Exercise after breast cancer surgery has proved beneficial to rehabilitation. We evaluate the best exercise for different post-surgery complications. Information sources: China National Knowledge Infrastructure, Wanfang Data Knowledge Service Platform, VIP China Science and Technology Journal Database, China Biology Medicine, EMBASE and PubMed databases were searched. Combinations of breast cancer (“breast tumor”,“breast carcinoma”,“mammary carcinoma”,“breast neoplasm”) and rehabilitation exercise (“exercise”,“physical therapy”) were employed when screening abstracts/keywords of articles. Two researchers independently searched, read the title and abstract of the literature, read the full text of the preliminary included literature, and extracted the data. In case of divergence, a third researcher was consulted.
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Tenniswood, Martin P. Apoptosis and Tumor Progressionin Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, February 2005. http://dx.doi.org/10.21236/ada443063.
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Uribe Ruíz, Natalia Andrea, and Roberto Benavides Arenas. Enfoque del paciente con cáncer primario de origen desconocido. Facultad de Medicina Universidad de Antioquia, August 2023. http://dx.doi.org/10.59473/medudea.pc.2023.17.
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El cáncer de primario de origen desconocido (en inglés, cancer of unknown primary, CUP) se define como la confirmación histológica de una metástasis para la cual el sitio anatómico del tumor que le dio origen no puede ser identificado luego de una evaluación inicial exhaustiva y racional que incluye: una historia clínica y examen físico completos, paraclínicos básicos e imágenes, entre ellas, tomografía computarizada de tórax, abdomen y pelvis.
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ZHAO, JIE, LIANHUA YE, WEI WANG, YANTAO YANG, ZHENGHAI SHEN, and SUNYIN RAO. Surgical Prognostic Factors of Second Primary Lung Cancer: A Systematic Review and Meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, November 2022. http://dx.doi.org/10.37766/inplasy2022.11.0047.
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Review question / Objective: The objective of this study was to explore the effects of different surgical strategies and potential prognostic factors on the prognosis of patients with SPLC through a systematic review and meta-analysis.Prognostic factors included surgical approach, type of SPLC(Synchronous and metachronous),histology,disease-free interval (DFI),tumor size,CT morphology, lymph node metastasis status, smoking status, gender. Condition being studied: With the development of imaging technology and better survival after primary lung cancer, the detection rate of second primary lung cancer (SPLC) has been increasing. At present, the staging and treatment of the second primary lung cancer are still controversial. Although surgery is widely accepted as the main treatment method, there is no unified diagnostic criteria and diagnosis and treatment strategy. The objective of this study was to explore the effects of different surgical strategies and potential prognostic factors on the prognosis of patients with SPLC through a systematic review and meta-analysis.