Relevant bibliographies by topics / Tumor Infiltrating

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Tumor Infiltrating'

Author: Grafiati
Published: 4 June 2021
Last updated: 27 January 2023

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Journal articles on the topic "Tumor Infiltrating"

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Rodin, William Carl Ivar, Patrik Sundström, Filip Ahlmanner, Elinor Bexe Lindskog, and Marianne Quiding Järbrink. "Potent anti-tumor effector functions in tumor-infiltrating MAIT and γδ T cells isolated from colon cancer patients." Journal of Immunology 202, no. 1_Supplement (May 1, 2019): 138.13. http://dx.doi.org/10.4049/jimmunol.202.supp.138.13.

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Abstract In colon cancer, tumor progression and patient outcome is affected by the cytokine balance in the tumors. IFNγ, TNFα and Granzyme B expression are associated with favorable patient outcome, while high IL-17 expression is associated with accelerated tumor progression. However, knowledge of the regulation and activation of unconventional T cell subsets in colon tumors is limited. The aim of this study was to characterize unconventional T cells in colon tumors and unaffected tissue, determine their capacity to produce cytokines affecting tumor progression as well as the In vitro cytotoxic capabilities of MAIT and γδ T cells. Using flow cytometry, we show that MAIT cells accumulate in colon tumors and that the frequencies of γδ T cells are reduced in the tumor epithelium. Using polyclonal stimulation, we show that IFNγ production by tumour infiltrating MAIT cells is impaired whilst tumour infiltrating γδ T have an increased expression of IFNγ, TNFα and Granzyme B. IL-17 expression was also elevated in tumour infiltrating γδ T cells, but at lower levels than the TH1 - associated cytokines. Tumor infiltrating MAIT cells had an exhausted (PD-1highTim-3+) phenotype compared to MAIT cells from unaffected tissue. Analyzing cytokine expression, we show that while no single molecule is lost the polyfunctional capacity of tumour infiltrating MAIT cells is decreased compared to MAIT cells from unaffected tissue. Altogether, this study shows that γδ T cells and MAIT cells contribute to the cytokine balance in colon tumors with a TH1 – dominated profile and that they have potent cytotoxic capacity, which may reduce tumor progression and improve patient outcome.
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Wirth, Thomas, Farizan Ahmad, Agnieszka Pacholska, Haritha Samaranayake, and Seppo Ylä-Herttuala. "The Syngeneic BT4C Rat Malignant Glioma is a Valuable Model to study Myelomonocytic cells in Tumors." Cancer Growth and Metastasis 5 (January 2012): CGM.S9314. http://dx.doi.org/10.4137/cgm.s9314.

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Background The impact of infiltrating macrophages on tumor progression in malignant gliomas has been studied extensively. However, there is a lack of animal models for studying the role of infiltrating macrophages in malignant gliomas. Material and methods: The BT4C rat malignant glioma model was characterized by immunohistochemical analysis of inflammatory cell types associated with the tumors. Results BT4C malignant gliomas are highly vascularized tumors with an infiltrative behavior. BT4C gliomas demonstrated a high infiltration rate of macrophages. Particularly, a CD68/VEGFR-1 positive subtype of macrophages was detected at the edges of malignant gliomas. Also, CD133 positive cells were located mainly at the infiltrative edges of gliomas, whereas VEGFR-2 was highly expressed throughout the malignant glioma. Conclusion The immunocompetent BT4C rat malignant glioma model shows features similar to its human counterpart, which makes it a valuable model to study the impact of tumor associated macrophages in the pathology of malignant gliomas.
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Whiteside, Theresa L., Lorenz M. Jost, and Ronald B. Herberman. "Tumor-infiltrating lymphocytes." Critical Reviews in Oncology/Hematology 12, no. 1 (January 1992): 25–47. http://dx.doi.org/10.1016/1040-8428(92)90063-v.

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Besser, Michal J., Ronnie Shapira-Frommer, and Jacob Schachter. "Tumor-Infiltrating Lymphocytes." Cancer Journal 21, no. 6 (2015): 465–69. http://dx.doi.org/10.1097/ppo.0000000000000154.

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Oliver, Gary, John Yannelli, and Diane Solomon. "Tumor-Infiltrating Lymphocytes." Acta Cytologica 40, no. 4 (1996): 691–94. http://dx.doi.org/10.1159/000333941.

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Mantovani, Alberto, and Robert Evans. "Tumor-infiltrating leukocytes." Immunology Today 6, no. 5 (May 1985): 144–45. http://dx.doi.org/10.1016/0167-5699(85)90134-3.

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Torcellan, Tommaso, Henry R. Hampton, Jacqueline Bailey, Michio Tomura, Robert Brink, and Tatyana Chtanova. "In vivo photolabeling of tumor-infiltrating cells reveals highly regulated egress of T-cell subsets from tumors." Proceedings of the National Academy of Sciences 114, no. 22 (May 15, 2017): 5677–82. http://dx.doi.org/10.1073/pnas.1618446114.

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Immune therapy is rapidly gaining prominence in the clinic as a major weapon against cancer. Whereas much attention has been focused on the infiltration of tumors by immune cells, the subsequent fate of these infiltrates remains largely unexplored. We therefore established a photoconversion-based model that allowed us to label tumor-infiltrating immune cells and follow their migration. Using this system, we identified a population of tumor-experienced cells that emigrate from primary tumors to draining lymph nodes via afferent lymphatic vessels. Although the majority of tumor-infiltrating cells were myeloid, T cells made up the largest population of tumor-egressing leukocytes. Strikingly, the subset composition of tumor-egressing T cells was greatly skewed compared with those that had infiltrated the tumor and those resident in the draining lymph node. Some T-cell subsets such as CD8+ T cells emigrated more readily; others including CD4−CD8− T cells were preferentially retained, suggesting that specific mechanisms guide immune cell egress from tumors. Furthermore, tumor-egressing T cells were more activated and displayed enhanced effector function in comparison with their lymph node counterparts. Finally, we demonstrated that tumor-infiltrating T cells migrate to distant secondary tumors and draining lymph nodes, highlighting a mechanism whereby tumor-experienced effector T cells may mediate antitumor immunity at metastatic sites. Thus, our results provide insights into migration and function of tumor-infiltrating immune cells and the role of these cells in tumor immunity outside of primary tumor deposits.
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Ho-Tin-Noe, Benoit H., Carla Carbo, Melanie Demers, Stephen M. Cifuni, Tobias Goerge, and Denisa D. Wagner. "Platelets Protect Tumors from Hemorrhage Induced by Stroma-Infiltrating Leukocytes." Blood 112, no. 11 (November 16, 2008): 3916. http://dx.doi.org/10.1182/blood.v112.11.3916.3916.

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Abstract In a recent study, we showed that platelets are crucial regulators of tumor vascular homeostasis in that they continuously prevent tumor hemorrhage through secretion of their granules. However, it remains unclear what platelets target to prevent tumor bleeding. Tumors are associated with inflammation, a cause of hemorrhage in thrombocytopenia. We hypothesized that platelets protect tumors from vascular damages induced by infiltrating inflammatory cells. Here, we report that thrombocytopenia-induced tumor hemorrhage preferentially occurs at the periphery of tumors, where massive accumulation of monocytes/macrophages and neutrophils was revealed by tumor histology. To further investigate the role of tumor-infiltrating leukocytes in the induction of tumor hemorrhage in thrombocytopenic mice, we used genetically-engineered mice with a deficiency in either beta2 or beta3 integrins, or in integrin activation. We show that these mice have decreased leukocyte infiltration in the tumor stroma and are protected from thrombocytopenia-induced tumor hemorrhage. Using a model of TNFa-induced skin inflammation, we demonstrate that releasates from collagen- and thrombin-stimulated platelets inhibit neutrophil-induced vascular damage. Our results show that platelets protect tumors from vascular leakage induced by infiltrating leukocytes and that releasate from activated platelets has potent in vivo healing properties needed after leukocyte transmigration.
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Hendry, Shona, Roberto Salgado, Thomas Gevaert, Prudence A. Russell, Tom John, Bibhusal Thapa, Michael Christie, et al. "Assessing Tumor-Infiltrating Lymphocytes in Solid Tumors." Advances In Anatomic Pathology 24, no. 6 (November 2017): 311–35. http://dx.doi.org/10.1097/pap.0000000000000161.

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Hendry, Shona, Roberto Salgado, Thomas Gevaert, Prudence A. Russell, Tom John, Bibhusal Thapa, Michael Christie, et al. "Assessing Tumor-infiltrating Lymphocytes in Solid Tumors." Advances In Anatomic Pathology 24, no. 5 (September 2017): 235–51. http://dx.doi.org/10.1097/pap.0000000000000162.

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Dissertations / Theses on the topic "Tumor Infiltrating"

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Monteiro, Vasconcelos Ines [Verfasser]. "Epigenetic quantification of tumor-infiltrating T-lymphocytes in epithelial ovarian tumors / Ines Monteiro Vasconcelos." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2014. http://d-nb.info/1052529828/34.

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Schlecker, Eva [Verfasser], and Viktor [Akademischer Betreuer] Umansky. "The role of tumor-infiltrating MDSC subsets in tumor progression / Eva Schlecker ; Betreuer: Viktor Umansky." Heidelberg : Universitätsbibliothek Heidelberg, 2011. http://d-nb.info/1179229649/34.

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Kurt, Robert Anthony 1968. "Characterization of T lymphocytes infiltrating sites of tumor progression and regression during concomitant tumor immunity." Diss., The University of Arizona, 1996. http://hdl.handle.net/10150/282126.

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The cellular infiltration of solid tumors is indicative of an immune response to cancerous growths. Unfortunately, most tumors grow progressively despite this infiltration. Therefore, the infiltrate from a regressing tumor is necessary in order to examine the requirements for tumor rejection. Due to the rarity of tumor rejection, elucidating the requirements is difficult without an animal model. The sponge model of concomitant tumor immunity allowed the examination of the components associated with tumor rejection. In the model of concomitant tumor immunity an animal is given a primary tumor followed by a secondary tumor challenge. Despite the progression of the primary tumor, the secondary tumor challenge is rejected. In this model the secondary tumor challenge is delivered into a preimplanted gelatin sponge matrix which can be retrieved in order to capture the components associated with tumor rejection. Retrieval of both the primary progressing tumor and the gelatin sponge allowed a direct comparison of the factors associated with tumor progression and rejection. Using this model, we have examined the progressing and rejected tumor sites for differences in T cell cytotoxicity, V beta T cell receptor usage, and the expression of cytokine genes and signal transducing proteins. The results from this study demonstrated that the T cells isolated from progressing tumor sites were not cytolytic, whereas the T cells from the rejection sites showed significant cytolysis towards the autologous tumor cells in vitro. Surprisingly, the T cell infiltration into the progressing and rejected tumor sites were similar with V beta 1 and V beta 8 T cell receptor bearing T cells predominating at both locations. The T cell response also showed clonal restriction upon examination of the complementarity determining region 3 (CDR3) of the T cell receptor. Significantly, the rejection site showed higher gene expression levels of IFN-γ, TNF-α, IL-2, IL-4, IL-10, and IL-12 and reduced TGF-β gene expression compared to the progressing tumor site. Finally, although the T cells from the progressing tumor site showed an altered pattern of tyrosine phosphorylation, the signaling molecules p59ᶠʸⁿ and CD3 ζ were expressed at comparable levels in the T cells from both sites. These data strongly suggest that the tumor microenvironment may play a major role in orchestrating an anti-tumor immune response.
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Morgan, Clifford Grant. "Characterization of Tumor Infiltrating Lymphocytes in Pediatric Cancers and the Development of Novel Immunotherapies." Thesis, The George Washington University, 2015. http://pqdtopen.proquest.com/#viewpdf?dispub=3705722.

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Cytotoxic T lymphocytes (CTLs) are the primary component of the adaptive immune system responsible for clearance of virally infected and tumorigenic cells. In cancer however, this tumor-specific immune response is often impaired. The impairment is multifactorial; some cancers utilize mechanisms to evade the immune system through downregulation of Major Histocompatability Complex I or lack of tumor-specific antigens, while others use methods to actively inhibit local function of tumor-induced immune responses via production of immunosuppressive cytokines, Fas-mediated apoptosis, or recruitment of T regulatory cells (Tregs). These Tregs function to further immune regulate and inhibit CTLs, using methods such as suppressive cytokines, and cytotoxic killing. All of these components lead to an “on/off” phenotype, where CTL effector function is shut down within the Tumor Immunosuppressive Microenvironment (TIM), but can be recovered quickly upon removal of CTLs from the TIM. The transient impairment of Tumor Infiltrating Lymphocytes (TIL) has been described in mouse models, but is poorly characterized in humans.

In this dissertation, we examined infiltration of CTLs across several types of human pediatric cancers, taken from patients who had not undergone prior treatment. We found tumors associated with favorable prognoses, including Wilms’ Tumor and Neuroblastoma (NB), had higher levels of CTL infiltration than those with less favorable prognoses, e.g. Ependymoma, which possessed no observable infiltration. Additionally, we demonstrate the TIL “on/off” phenotype in a case of Pilocytic Astrocytoma, demonstrating significant recovery of TIL effector function.

We proposed that the poor infiltration and impaired effector function in these pediatric tumors was a direct result of the TIM, and sought to improve this immune response by developing an attenuated live cell vaccine, utilizing a murine NB model, Neuro2a, to create a NB line with knock down (KD) of Inhibitor of Differentiation 2 (Id2), which impaired their ability to form tumors in vivo. In prophylactic and therapeutic models, introduction of Id2-KD cells in combination with the immune checkpoint blockade inhibitor anti-CTLA-4, induced an increase in CTLs capable of homing to the tumor, that were also able to employ effector function within the TIM, resulting in clearance of wild-type Neuro2a tumors.

A separate emerging immunotherapeutic approach is to express a Chimeric Antigen Receptor (CAR) on CTLs that allows them to be activated to kill cells expressing the CAR-specific protein, bypassing MHC presentation. Using a murine Rhabdomyosarcoma model, we demonstrate that tumor infiltrating Tregs express lytic molecules, encouraging us to develop a method of successfully transducing Tregs with a CAR (DC101), rather than CTLs, thereby exploiting characteristics of the Treg in the TIM, specifically their cytotoxic capability and their unique recruitment and ability to thrive in that environment. We demonstrate in vitro CAR-mediated redirection of lytic effector function using DC101-expressing CTLs against tumor cell lines, though attempting to increase Treg cytotoxicity in vitro via known inducers of CTL cytotoxicity (IFNα or IL-12) or known inducers of Tregs within the TIM (TGF-β1) showed no increase in Treg cytotoxicity.

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Rieger, Jan Hendrik [Verfasser], and Viktor [Akademischer Betreuer] Umansky. "Targets of tumor infiltrating lymphocyte reactivity in pancreatic cancer / Jan Hendrik Rieger ; Betreuer: Viktor Umansky." Heidelberg : Universitätsbibliothek Heidelberg, 2019. http://d-nb.info/1199611484/34.

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Ko, Kuibeom. "Treatment of advanced tumors with agonistic anti-GITR mAb and its effects on tumor-infiltrating Foxp3[+]CD25[+]CD4[+] regulatory T cells." Kyoto University, 2006. http://hdl.handle.net/2433/135631.

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Hansmann, Leo Alexander [Verfasser]. "A single cell approach to tumor-infiltrating lymphocytes in solid and hematopoietic malignancies / Leo Alexander Hansmann." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2019. http://d-nb.info/1200409574/34.

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Ito, Takeshi. "The therapeutic potential of multiclonal tumoricidal T cells derived from tumor infiltrating lymphocyte-derived iPS cells." Doctoral thesis, Kyoto University, 2021. http://hdl.handle.net/2433/265194.

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Zhang, Hua. "A human monoclonal anti-melanoma single chain Fv (scFv) antibody derived from tumor-infiltrating B lymphocytes." Diss., The University of Arizona, 1995. http://hdl.handle.net/10150/187293.

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The development of recombinant DNA technology has made it feasible to clone, construct and express fully human immunoglobulin molecules. Here we report a novel methodology to make human antitumor scFv antibodies from tumor-infiltrating B lymphocytes (TIL-B). We isolated and expanded TIL-B from melanomas in the presence of EBV. The transformed B cells secreting tumor-specific antibodies were identified and cloned by limiting dilution. From one B cell clone with specific melanoma reactivity, we captured the immunoglobulin variable region genes, V(H) and V(k), by polymerase chain reaction (peR), sequenced the genes and linked them together by peR assembly using a (Gly₄Ser)₃ linker to form the scFv gene that was subsequently cloned into the pET21d vector and expressed. The scFv protein, obtained, with a molecular weight of 29 KD was purified and biotinylated for further characterization. The scFv demonstrated specific tumor reactivity to 21 of 24 different melanoma cell lines and not to 14 non-melanoma tumor cell lines, including breast, ovarian and colon cancer cell lines, normal human melanocytes as well as normal human leukocytes. These results were obtained using 1) a tumor cell ELISA, 2) fixed cell immunofluorescence and 3) live cell flow cytometry. The immunoprecipitation results indicated that a protein antigen of 45 KD was recognized by the scFv. Since we previously reported that about 70% of human tumors of different histologic types contain tumor-infiltrating B lymphocytes producing specific anti-tumor antibodies, this approach offers a rapid. effective method by combining in vitro B cell expansion and peR-gene cloning to elucidate the repertoire of the human anti-tumor immune responses and to make human monoclonal anti-tumor antibody molecules.
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Schnappinger, Julia [Verfasser], and Elfriede [Akademischer Betreuer] Nößner. "Profiling human tumor infiltrating leukocytes comparing renal cell and hepatocellular carcinoma / Julia Schnappinger ; Betreuer: Elfriede Nößner." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2019. http://d-nb.info/1225682452/34.

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Books on the topic "Tumor Infiltrating"

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Tumor-infiltrating lymphocytes in human malignancies. Austin: R.G. Landes Co., 1993.

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Higgins, Catherine Ann. Tumour associated macrophages: Tumour infiltrating lymphocytes : apoptotic and mitotic cells in human colorectal cancer. [S.l: The Author], 1998.

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Hatton, William James. Stereological envmeration of tumour associated macrophages infiltrating human colorectal tumours. [S.l: The Author], 1996.

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J, Silverstein Melvin, ed. Ductal carcinoma in situ of the breast. Baltimore: Williams & Wilkins, 1997.

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Fabre, Aurélie. Immunostaining and DNA analysis of Wilms' tumour (WT1) suppressor gene in ductal carcinoma in situ (DCIS) of the breast: Thesis. 1998.

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Kotlan, Beatrix. Tumor Infiltrating B Lymphocytes: A Novel Approach for Cancer Diagnostics and Therapeutics. Springer, 2020.

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Moerdler, Scott, and Xingxing Zang. PD-1/PDL-1 Inhibitors as Immunotherapy for Ovarian Cancer. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190248208.003.0010.

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Programmed death 1 (PD-1), a member of the B7-CD28 immunoglobulin superfamily, and its ligands PD-L1/PD-L2 inhibit T-cell activation. They also play a key role in the tumor microenvironment, allowing for cancer immune escape. PD-1 is induced on a variety of immune cells, including tumor-infiltrating lymphocytes (TILs), while PD-L1 is found on many types of solid tumors including ovarian cancer and some TILs. The use of immunocheckpoint inhibitors like anti-PD-1 and anti-PD-L1 therapies has been shown to reactivate the immune system to attack tumor cells. Ovarian cancers have been shown to be responsive to anti-PD-1 and anti-PD-L1 therapies, though immunocheckpoint inhibitors are not enough. Current research is evaluating combination therapies to improve response rates.
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Farghaly, Samir A. Adoptive Cell Immunotherapy for Epithelial Ovarian Cancer. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190248208.003.0005.

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The standard management for epithelial ovarian cancer (EOC) is a combination of aggressive debulking surgery with residual tumor of less than 1 cm and platinum-based chemotherapy. However, a high percentage of patients experience disease recurrence. Extensive efforts to find new therapeutic options have been made, albeit cancer cells develop drug resistance and malignant progression occurs. Novel therapeutic strategies are needed to enhance progression-free survival and overall survival of patients with advanced EOC. Several preclinical and clinical studies investigated feasibility and efficacy of adoptive cell therapy (ACT) in EOC. The aim of this chapter is to present an overview of ACT in EOC, focusing on Human Leukocyte Antigen (HLA)-restricted tumor infiltrating lymphocytes and MHC-independent immune effectors such as natural killer and cytokine-induced killer. The available data suggest that ACT may provide the best outcome in patients with low tumor burden, minimal residual disease, or maintenance therapy. Further preclinical studies and clinical trials are needed.
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Mammoser, Aaron. Infiltrative Astrocytomas. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0126.

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Diffuse astrocytomas are WHO grade II astrocytomas that are distinguished from other WHO grade I and II astrocytomas because they are infiltrative, incurable, and have an intrinsic tendency to undergo malignant transformation to an anaplastic astrocytoma or a secondary glioblastoma. They are most often diagnosed in young adults in their 30s and 40s, and have a genetic profile that is different than primary glioblastoma. Anaplastic astrocytomas frequently arise from diffuse astroctyomas and share many of the same molecular abnormalities but tend to acquire more as they inevitably progress to glioblastoma. Recent studies identified mutations associated with WHO grade II and III tumors that predict a progression to a secondary glioblastoma with a better overall prognosis than primary glioblastoma. WHO grade II and III tumors that do not exhibit this typical mutation pattern often behave more aggressively than their counterparts, with a worse prognosis than higher grade tumors with a more favorable genotype.
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Cellular Therapy Of Cancer. World Scientific Publishing Company, 2010.

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Book chapters on the topic "Tumor Infiltrating"

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Masterpol, Kasia Szyfelbein, Andrea Primiani, and Lyn McDivitt Duncan. "Reporting Tumor Infiltrating Lymphocytes." In Atlas of Essential Dermatopathology, 110–11. London: Springer London, 2012. http://dx.doi.org/10.1007/978-1-4471-4471-7_47.

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Pisapia, David, and Ehud Lavi. "Tumor-Infiltrating T Cells." In Encyclopedia of Medical Immunology, 1230–33. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-0-387-84828-0_10.

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Chaoul, Nada, and Marcello Albanesi. "Tumor Infiltrating T Cell Assay." In Methods in Molecular Biology, 41–54. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1507-2_3.

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Yu, Ping, and Yang-Xin Fu. "The Prognostic Significance of Tumor-Infiltrating Lymphocytes." In The Tumor Microenvironment, 385–407. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-6615-5_19.

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Wickström, Stina, and Tanja Lövgren. "Expansion of Tumor-Infiltrating Lymphocytes from Melanoma Tumors." In Methods in Molecular Biology, 105–18. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-8979-9_7.

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Prasad, Alpana. "Very Large Tumors Not Responding to Chemotherapy/Locally Infiltrating Tumors." In Wilms’ Tumor, 233–38. Singapore: Springer Nature Singapore, 2022. http://dx.doi.org/10.1007/978-981-19-3428-5_26.

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Whiteside, Theresa L. "Tumor-Infiltrating Lymphocytes and Their Role in Solid Tumor Progression." In Interaction of Immune and Cancer Cells, 111–21. Vienna: Springer Vienna, 2013. http://dx.doi.org/10.1007/978-3-7091-1300-4_6.

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Whiteside, Theresa L. "Tumor-Infiltrating Lymphocytes and Their Role in Solid Tumor Progression." In Experientia Supplementum, 89–106. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-91311-3_3.

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Ferradini, L., S. Miescher, C. Barras, P. Busson, M. Lipinski, V. von Fliedner, and T. Tursz. "Cytotoxic Tumor Infiltrating Lymphocytes in Nasopharyngeal Carcinoma." In Epstein-Barr Virus and Human Disease • 1988, 213–18. Totowa, NJ: Humana Press, 1989. http://dx.doi.org/10.1007/978-1-4612-4508-7_31.

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Gutkin, Dmitry W. "Tumor-Infiltrating Dendritic Cells: The Pathologist’s Perspective." In Dendritic Cells in Cancer, 33–55. New York, NY: Springer US, 2009. http://dx.doi.org/10.1007/978-0-387-88611-4_3.

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Conference papers on the topic "Tumor Infiltrating"

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Nemejcova, Kristyna, Ivana Ticha, Ondrej Kodet, Miroslav Dura, Michaela Bartu, and Pavel Dundr. "Abstract 4069: Evaluation of inflammatory infiltration (tumor infiltrating lymphocytes - TIL) in malignant melanoma." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-4069.

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Nagle, Luz, Amy Mackay Weber, MacLean Hall, Matthew Beatty, J. Trad Wadsworth, Caitlin McMullen, Krupal Patel, Kathryn Vorwald, Christine Chung, and Shari Pilon-Thomas. "Abstract 2178: Expansion of tumor-specific tumor-infiltrating lymphocytes (TIL) from head and neck tumors." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-2178.

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Korbelik, Mladen, and Gorazd Krosl. "Distribution of photosensitizers between tumor cells and tumor infiltrating host cells." In Europto Biomedical Optics '93, edited by Giulio Jori, Johan Moan, and Willem M. Star. SPIE, 1994. http://dx.doi.org/10.1117/12.168679.

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Evans, Elizabeth E., Holm Bussler, Sebold Torno, Crystal Mallow, Laurie A. Winters, Christine Reilly, Katya Klimatcheva, et al. "Abstract 278: Antibody blockade of semaphorin 4D promotes infiltration of activated tumor infiltrating leukocytes and reverses tumor growth." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-278.

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Gupta, Bindiya, Shalini Rajaram, Sandhya Jain, Neerja Goel, and Naveen Tanwar. "Collision tumor of endometrial stromal sarcoma and squamous cell cancer: A rare entity." In 16th Annual International Conference RGCON. Thieme Medical and Scientific Publishers Private Ltd., 2016. http://dx.doi.org/10.1055/s-0039-1685363.

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A collision tumor is defined by the presence of two separate tumors in one organ on gross, microscopic, and immunohistochemical studies and they should be distinguished from malignant mullerian mixed tumors. A 60 year old lady P8L8 presented with blood stained vaginal discharge and post menopausal bleeding. Examination revealed a 1 x 2 cm cervical growth which was reported as squamous cell carcinoma cervix. Imaging revealed myohyperplasia with normal uterine cavity. The patient underwent Type III radical hysterectomy, bilateral salphingo-oophorectomy and bilateral pelvic lymphadenectomy. The uterine corpus revealed 5 cm growth in uterine cavity which was reported as high grade endometrial stromal sarcoma and the cervical growth was non keratinising squamous cell carcinoma infiltrating the former. The lymph nodes, parametria and vaginal cuff were free of tumor. The patient was referred for adjuvant chemotherapy and radiation therapy.
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Ye, Jian, Xinming Su, Eddy C. Hsueh, Yanping Zhang, Joyce M. Koenig, Daniel F. Hoft, and Guangyong Peng. "Abstract 781: Plasticity of human tumor-infiltrating Th17 cells." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-781.

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Loi, Sherene. "Abstract ES6-3: Tumor infiltrating lymphocytes in breast cancer." In Thirty-Seventh Annual CTRC-AACR San Antonio Breast Cancer Symposium; December 9-13, 2014; San Antonio, TX. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.sabcs14-es6-3.

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Romero Castro, Eduardo, Germán Corredor, Paula Toro, Viviana Arias, Anant Madabhushi, Xiangxue Wang, and Vamsidhar Velcheti. "Quantifying expert diagnosis variability when grading tumor-infiltrating lymphocytes." In 13th International Symposium on Medical Information Processing and Analysis, edited by Jorge Brieva, Juan David García, Natasha Lepore, and Eduardo Romero. SPIE, 2017. http://dx.doi.org/10.1117/12.2286717.

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Kato, Takuya, Kazuhiro Noma, Hajime Kashima, Yuki Katsura, Hiroaki Sato, Takayuki Ninomiya, Toshiaki Ohara, Yasuhiro Shirakawa, and Toshiyoshi Fujiwara. "Abstract 5934: Cancer-associated fibroblasts contribute to tumor immunosuppression by regulating tumor-infiltrating lymphocytes." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-5934.

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Juncker-Jensen, Anna, Nicholas Stavrou, Mate Nagy, Erinn Parnell, Judy Kuo, Eric Leones, Kathy Pham, and Flora Sahafi. "Abstract 408: Reduction of tumor-infiltrating B cells linked to recurrence of NSCLC tumors." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-408.

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Reports on the topic "Tumor Infiltrating"

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Beuneu, Helene, Sandra Demaria, and Michael Dustin. Visualizing Breast Cancer Cell Interaction with Tumor-Infiltrating Lymphocytes During Immunotherapy. Fort Belvoir, VA: Defense Technical Information Center, April 2013. http://dx.doi.org/10.21236/ada577265.

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Leonard, Talayna, Robert Lemme, Cati Kral, Briana Santiago, Chris Elberts, Stephanie Dewald, Patrick McGonagill, et al. High-Percentage of Early Resectable Pancreatic Ductal Adenocarcinoma is Unidentified on Abdominal CT Obtained for Unrelated Diagnosis. Science Repository, December 2021. http://dx.doi.org/10.31487/j.aco.2021.02.03.

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Abstract:
Objective: Pancreatic ductal adenocarcinoma (PDAC) has the best survival when detected early with 5-year survival near 40% for small, resectable PDAC. We evaluate the undiagnosed PDAC imaging features on routine CT and their impact on resectability. Methods: 76 of the screened 134 CTs from 1/1/2012 to 12/31/2018 using our tumor registry were obtained prior to PDAC diagnosis for other indications at least one month before presentation. Each cross-sectional study was reviewed for features of early PDAC: pancreatic mass, pancreatic ductal dilatation, perivascular/peripancreatic soft-tissue infiltration, omental lesions/ascites, and lymphadenopathy. When such features were detectible by the reviewing radiologists, the original CT readings were classified as concordant/discrepant. Descriptive statistics are reported for discrepant reads, tumor resectability, and tumor size. Results: Of the 76 cases from 46 unique subjects (30 male/16 female), 25 CTs (33%) had undetected PDAC imaging features: masses (15/19 unreported), ductal dilatation (16/20 unreported), and peripancreatic/perivascular soft-tissue infiltration (20/36 unreported). 63% of early PDAC features were not identified initially. One year before clinical diagnosis, 75-80% of the PDAC cases were resectable; at < 6 months before clinical diagnosis, only 29% were resectable. Conclusion: Improving early detection of key PDAC features on routine CT examinations can potentially improve patient outcomes.
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Berele, Birhanu Aberha, Guifang Yang, and Yuxiang Cai. Prognostic value of tumour infiltrating lymphocytes in nasopharyngeal carcinoma patients: Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, June 2021. http://dx.doi.org/10.37766/inplasy2021.6.0014.

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Lundgren, D. L., W. C. Griffith, and F. F. Hahn. Inverse relationship of tumors and mononuclear cell leukemia infiltration in the lungs of F344 rats. Office of Scientific and Technical Information (OSTI), December 1995. http://dx.doi.org/10.2172/381384.

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