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Milas, L. "Tumor Bed Effect in Murine Tumors: Relationship to Tumor Take and Tumor Macrophage Content." Radiation Research 123, no. 2 (August 1990): 232. http://dx.doi.org/10.2307/3577551.
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Bai, Ren-Kui, Julia Chang, Kun-Tu Yeh, Mary Ann Lou, Jyh-Feng Lu, Duan-Jun Tan, Hao Liu, and Lee-Jun C. Wong. "Mitochondrial DNA Content Varies with Pathological Characteristics of Breast Cancer." Journal of Oncology 2011 (2011): 1–10. http://dx.doi.org/10.1155/2011/496189.
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Changes in mitochondrial DNA (mtDNA) content in cancers have been reported with controversial results, probably due to small sample size and variable pathological conditions. In this study, mtDNA content in 302 breast tumor/surrounding normal tissue pairs were evaluated and correlated with the clinico-pathological characteristics of tumors. Overall, mtDNA content in tumor tissues is significantly lower than that in the surrounding normal tissues,P<0.00001. MtDNA content in tumor tissues decreased with increasing tumor size. However, when the tumor is very large (>50 cm3), mtDNA content started to increase. Similarly, mtDNA content decreased from grades 0 and I to grade II tumors, but increased from grade II to grade III tumors. Tumors with somatic mtDNA alterations in coding region have significantly higher mtDNA content than tumors without somatic mtDNA alterations (P<0.001). Tumors with somatic mtDNA alterations in the D-Loop region have significantly lower mtDNA content (P<0.001). Patients with both low and high mtDNA content in tumor tissue have significantly higher hazard of death than patients with median levels of mtDNA content. mtDNA content in tumor tissues change with tumor size, grade, and ER/PR status; significant deviation from the median level of mtDNA content is associated with poor survival.
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Watanabe, Satoru, Junko Kamiyama, Hiroo Chigasaki, and Shigetake Yoshioka. "Polyol content of cerebrospinal fluid in brain-tumor patients." Journal of Neurosurgery 70, no. 2 (February 1989): 183–89. http://dx.doi.org/10.3171/jns.1989.70.2.0183.
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✓ In order to investigate whether cerebrospinal fluid (CSF) polyols are consumed by brain tissue, the concentration of seven polyols in the CSF and the serum of 30 patients with intracranial tumor and 17 control individuals was measured by gas chromatography. The mean polyol content in the control samples showed that the fructose, inositol, and glucitol levels were significantly greater in CSF than in serum. A comparison of the lumbar CSF from control subjects and 11 patients with malignant tumors exposed to the CSF snowed the fructose and inositol levels to be significantly lower (54% and 45%, respectively) and the glucose content to be slightly higher (110%) in the tumor cases. These differences were markedly greater in the ventricular than in the lumbar CSF and greater in patients with tumors exposed to the CSF space than in those with tumors buried in the brain tissue. In ventricular CSF obtained from seven patients with malignant brain tumors before and after radio— and/or chemotherapy, significant increases in fructose (34%) and glucitol (48%) levels were found, but the other polyols did not change significantly. In culture, the human glioblastoma cell growth rate was higher in the medium containing fructose and glucose than in that containing glucose alone. A notable amount of fructose and glucose was consumed by cultured glioblastoma cells. The roles of polyols contained in CSF and the effects of fructose on the growth of cultured glioblastoma cells are discussed in light of these findings and of previous reports.
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Sawaya, Raymond, O. Juhani Rämö, Mei Lin Shi, and George Mandybur. "Biological significance of tissue plasminogen activator content in brain tumors." Journal of Neurosurgery 74, no. 3 (March 1991): 480–86. http://dx.doi.org/10.3171/jns.1991.74.3.0480.
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✓ Fresh brain-tumor samples were obtained at operation and analyzed for their content of tissue type plasminogen activator (tPA) using an activity assay (gel chromatography zymogram) and an enzyme-linked immunospecific assay. The specimens were taken from 23 glioblastomas, 35 metastatic tumors, 42 meningiomas, 16 low-grade gliomas, and seven acoustic neurinomas; seven specimens were from normal brain. A strong correlation was found between the results of the two assays (r = 0.77, p < 0.0001). There was a threefold difference in the tPA content of the benign tumors as compared to malignant tumors (p = 0.0006), the latter having less tPA. Histologically benign meningiomas contained higher tPA than malignant meningiomas (p = 0.01); however, the difference between low-grade gliomas and high-grade gliomas was less evident. Overall regression analysis data have shown an inverse relationship between the tissue content in tPA and the presence and degree of tumor necrosis and peritumoral brain edema (p = 0.004 and p = 0.0004, respectively). This finding was most consistent in the glioblastoma group where the correlation coefficient values were r = 0.53 and r = −0.55, respectively. There was no significant correlation between the tissue tPA content and the age and sex, steroid use, or plasma tPA of the patients or the duration of symptoms. In summary, this is the first demonstration of tPA in a large series of human brain tumors and in normal brain. The differences observed have clear biological significance and, although the source of tPA in tumor tissue is still unknown, a relative reduction in tPA in tumor tissue may play an integral role in the development of tissue necrosis and tissue edema. The lack of tPA in tumor necrosis was not due to tissue destruction and cell death since urokinase was readily detectable in that tissue.
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García, I., F. Vizoso, A. Andicoechea, P. Raigoso, P. Vérez, E. Alexandre, J. L. García-Muñiz, and M. T. Allende. "Clinical Significance of Epidermal Growth Factor Receptor Content in Gastric Cancer." International Journal of Biological Markers 16, no. 3 (January 2001): 183–88. http://dx.doi.org/10.1177/172460080101600305.
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The objective of this work was to evaluate the epidermal growth factor receptor (EGFR) content in gastric cancer, its possible relationship with clinicopathological parameters of tumors and its prognostic significance. Membranous EGFR levels were examined by radioligand binding assays in 110 patients with gastric cancer. The mean follow-up period was 30.7 months. EGFR levels of tumors ranged widely, from 0.3 to 510 fmol/mg protein. EGFR levels were significantly higher (p<0.0005) in neoplastic tissue than in paired adjacent mucosa samples (median) (n= 84; 8.7 vs. 3.9 fmol/mg protein). Intratumoral EGFR levels were significantly correlated with tumor stage (p<0.05), and were higher in patients with stage III tumors (median) (7.6, 6.4, 12.3 and 7.5 fmol/mg protein for stages I, II, III and IV, respectively). In addition, the tumor/mucosa ratios of the EGFR content were significantly higher (p<0.05) in patients with stage III tumors (1, 1.8, 3.9, and 0.92, respectively). Although there was no significant relationship between EGFR levels of tumors and overall survival, the results suggest a role for EGFR in tumor progression of gastric cancer.
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O'Brien, T. D., D. W. Hayden, T. P. O'Leary, D. D. Caywood, and K. H. Johnson. "Canine Pancreatic Endocrine Tumors: Immunohistochemical Analysis of Hormone Content and Amyloid." Veterinary Pathology 24, no. 4 (July 1987): 308–14. http://dx.doi.org/10.1177/030098588702400404.
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Thirty-one primary canine pancreatic endocrine tumors and their metastases were studied histologically and immunohistochemically for the presence of insulin, glucagon, somatostatin, pancreatic polypeptide (PP), gastrin, and adrenocorticotrophic hormone (ACTH). Tumors were also evaluated for the presence of amyloid. The cytoarchitectural pattern of 25 of 31 primary tumors was predominantly solid, whereas three tumors were mostly glandular, two were unclassified, and one had a gyriform pattern. Cells with insulin immunoreactivity were found in 30 of 31 tumors and were found in all cases in which there was clinical evidence of inappropriate insulin secretion. Insulin was the only hormone demonstrable in three of the 30 tumors, but cells immunoreactive for other hormones were also present in various combinations in most tumors [i.e., glucagon (13 of 30), somatostatin (17 of 30), PP (25 of 30), and gastrin (2 of 30)]. One tumor contained only cells with glucagon and PP immunoreactivity. Amyloid was found in ten of 31 primary tumors but was not detected in metastases. Cells with insulin immunoreactivity were the only cell type consistently present in tumors containing amyloid. Amyloid deposits did not immunoreact with any of the antisera. Seventeen of 31 dogs had metastasis of the pancreatic endocrine tumor to regional lymph nodes, liver, or both. All metastases available for study (15 of 17) contained cells with insulin immunoreactivity and some contained cells with PP or somatostatin immunoreactivity. No statistically significant ( P > 0.05) differences in tendency to metastasize were found when pancreatic endocrine tumors were compared by region of origin, cytoarchitectural pattern, presence of amyloid, or by number of hormones contained within the tumor.
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Hao, Qiongyu, Yong Wu, Yanyuan Wu, Piwen Wang, and Jaydutt V. Vadgama. "Tumor-Derived Exosomes in Tumor-Induced Immune Suppression." International Journal of Molecular Sciences 23, no. 3 (January 27, 2022): 1461. http://dx.doi.org/10.3390/ijms23031461.
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Exosomes are a class of small membrane-bound extracellular vesicles released by almost all cell types and present in all body fluids. Based on the studies of exosome content and their interactions with recipient cells, exosomes are now thought to mediate “targeted” information transfer. Tumor-derived exosomes (TEX) carry a cargo of molecules different from that of normal cell-derived exosomes. TEX functions to mediate distinct biological effects such as receptor discharge and intercellular cross-talk. The immune system defenses, which may initially restrict tumor progression, are progressively blunted by the broad array of TEX molecules that activate suppressive pathways in different immune cells. Herein, we provide a review of the latest research progress on TEX in the context of tumor-mediated immune suppression and discuss the potential as well as challenges of TEX as a target of immunotherapy.
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Nesseler, Jean Philippe, Mi-Heon Lee, Christine Nguyen, Anusha Kalbasi, James W. Sayre, Tahmineh Romero, Philippe Nickers, William H. McBride, and Dörthe Schaue. "Tumor Size Matters—Understanding Concomitant Tumor Immunity in the Context of Hypofractionated Radiotherapy with Immunotherapy." Cancers 12, no. 3 (March 18, 2020): 714. http://dx.doi.org/10.3390/cancers12030714.
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The purpose of this study was to determine the dynamic contributions of different immune cell subsets to primary and abscopal tumor regression after hypofractionated radiation therapy (hRT) and the impact of anti-PD-1 therapy. A bilateral syngeneic FSA1 fibrosarcoma model was used in immunocompetent C3H mice, with delayed inoculation to mimic primary and microscopic disease. The effect of tumor burden on intratumoral and splenic immune cell content was delineated as a prelude to hRT on macroscopic T1 tumors with 3 fractions of 8 Gy while microscopic T2 tumors were left untreated. This was performed with and without systemic anti-PD-1. Immune profiles within T1 and T2 tumors and in spleen changed drastically with tumor burden in untreated mice with infiltrating CD4+ content declining, while the proportion of CD4+ Tregs rose. Myeloid cell representation escalated in larger tumors, resulting in major decreases in the lymphoid:myeloid ratios. In general, activation of Tregs and myeloid-derived suppressor cells allow immunogenic tumors to grow, although their relative contributions change with time. The evidence suggests that primary T1 tumors self-regulate their immune content depending on their size and this can influence the lymphoid compartment of T2 tumors, especially with respect to Tregs. Tumor burden is a major confounding factor in immune analysis that has to be taken into consideration in experimental models and in the clinic. hRT caused complete local regression of primary tumors, which was accompanied by heavy infiltration of CD8+ T cells activated to express IFN-γ and PD-1; while certain myeloid populations diminished. In spite of this active infiltrate, primary hRT failed to generate the systemic conditions required to cause abscopal regression of unirradiated microscopic tumors unless PD-1 blockade, which on its own was ineffective, was added to the RT regimen. The combination further increased local and systemically activated CD8+ T cells, but few other changes. This study emphasizes the subtle interplay between the immune system and tumors as they grow and how difficult it is for local RT, which can generate a local immune response that may help with primary tumor regression, to overcome the systemic barriers that are generated so as to effect immune regression of even small abscopal lesions.
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Paradiso, Angelo, Annita Mangia, Anna Barletta, Francesco Marzullo, Vincenzo Ventrella, Angela Racanelli, Francesco Schittulli, and Mario De Lena. "Mammography and Morphobiologic Characteristics of Human Breast Cancer." Tumori Journal 79, no. 6 (December 1993): 422–26. http://dx.doi.org/10.1177/030089169307900611.
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Aims A comparative analysis was performed to verify a possible correlation between mammographic features and morphobiologic characteristics of the tumor in a series of 176 invasive primary breast cancer patients. Methods Breast cancers were grouped according to mammographic features as follows: tumor mass with spiculated borders; tumor mass with well-circumscribed borders; tumor with density alteration of parenchyma with no clear borders; a cluster of micro-calcifications as the only sign of tumor presence; tumor without mammographic abnormality. The tumor tissue biologic characteristics investigated were: hormone receptor content, tumor proliferative activity, DNA content and cytohlstologic tumor-grade differentiation. Results Spiculated tumors showed a significantly higher percentage of estrogen-receptorpositive cases with respect to circumscribed tumors, independently of the patient's menopausal status. Tumors with only microcalcifications were all from premenopausal patients and showed a significantly higher percentage of progesterone-receptor-positive cases (83 %). Tumor proliferative activity did not significantly differ in the 5 mammographic breast cancer groups; aneuploidy was less frequent in tumors with spiculated borders than in mammographic types (39 % vs 57 %; p = 0.05); percentages of G1-G2-G3 tumors did not differ significantly among the mammographic groups considered. Conclusions Certain relationships between mammographic features and biologic characteristics could be of potential clinical interest and stimulate more detailed studies on this issue.
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von Au, A., M. Vasel, S. Kraft, M. G. Cecchini, A. Wetterwald, and I. Nakchbandi⁎. "Circulating fibronectin increases tumor growth and fibronectin content of tumors correlates with survival." Bone 50 (May 2012): S50—S51. http://dx.doi.org/10.1016/j.bone.2012.02.138.
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KOKAL, WILLIAM A., ROBERT L. GARDINE, KHALIL SHEIBANI, PETER L. MORRIS, ELLIOT PRAGER, IRENE W. ZAK, and JOSE J. TERZ. "Tumor DNA Content in Resectable, Primary Colorectal Carcinoma." Annals of Surgery 209, no. 2 (February 1989): 188–93. http://dx.doi.org/10.1097/00000658-198902000-00009.
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Conley, Andrew, Huazhang Li, and Alex V. Kotlar. "Abstract 5066: Accurate detection of tumor sequence at low tumor content for MRD." Cancer Research 82, no. 12_Supplement (June 15, 2022): 5066. http://dx.doi.org/10.1158/1538-7445.am2022-5066.
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Abstract Background Accurate detection of tumor sequence when the overall tumor content (TC) of the sample is low (<0.01%) is critical for tumor-informed minimal residual disease (MRD) monitoring. Current methodology generally relies on detection of multiple low-VAF (variant allele fraction) co-mutations. At low TC and low DNA input (<30ng, 9,000 genome equivalents), many variant sites are not expected to have any tumor-derived fragments or will be only marginally above background noise. A method that does not rely on the positive identification of mutations would be useful for detecting early disease recurrence. Methods We developed a maximum likelihood (ML) method for inferring the TC of MRD samples, rather than VAF at individual sites. This method considers the frequency of non-reference reads at each variant site along with estimated error rates. To evaluate our method at low TC, we carried out spike-in simulations of MRD samples across a range of sample TC from 0 to 0.1%. For each simulation, we randomly selected a single normal from a pool of sequenced normal samples to serve as background. Using this background, we randomly selected sites and mutations to represent somatic variants, sampled the existing noise at each site, and the number of ctDNA fragments and reads given the tumor content. Intrinsic error rates were modeled as either the mean error of the sample, the per-reference base error, or the mutation error. An additional randomly selected normal sample was used for extrinsic, per-site error estimates. We created contrived tumor-informed MRD samples by serial two-fold dilution of tumor DNA in a normal background (0.2%-0.0125% sample TC), followed by amplicon sequencing and characterization by our ML method. Results In our spike-in simulations, using 32 variants sites, we achieved 99% sensitivity in detecting tumor sequence at a TC of 0.01% (average ~1 tumor fragment per site), 73% sensitivity at 0.005% (average ~0.5 tumor fragments per site), and 99.9% specificity when using extrinsic error from a normal sample. At 16 sites we achieved 95% and 68% sensitivity respectively, and 99.6% specificity. Without the extrinsic error, specificity was greatly reduced to 71% (16 sites) and 77% (32 sites) at .005% TC. This highlights the advantage of extrinsic error in estimating low TC. In our contrived samples, we found that TC estimates from our ML approach correlated well with the expected values (r = 0.99). Conclusions With our approach, we were able to accurately quantify TC in both simulated and contrived samples. In simulated samples, we can detect TC well below 0.01% with high specificity and using only 16 sites. Importantly, the TC estimation does not rely on identifying individual positive sites. While modeling the intrinsic sequencing error rates in a sample does increase our ability to characterize TC, extrinsic, per-site error rates are needed to control false positives introduced by constitutively noisy sites. Citation Format: Andrew Conley, Huazhang Li, Alex V. Kotlar. Accurate detection of tumor sequence at low tumor content for MRD [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 5066.
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Okada, Yoshikazu, Otmar Kloiber, and Konstantin A. Hossmann. "Regional metabolism in experimental brain tumors in cats: relationship with acid/base, water, and electrolyte homeostasis." Journal of Neurosurgery 77, no. 6 (December 1992): 917–26. http://dx.doi.org/10.3171/jns.1992.77.6.0917.
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✓ Experimental brain tumors were produced in cats by xenotransplantation of the rat glioma clone F98 into the white matter of the left hemisphere. One to 4 weeks after implantation, local adenosine triphosphate (ATP), glucose, lactate, and tissue pH were measured via imaging techniques in cryostat sections passing through the center of the tumor and correlated with changes in water and electrolyte content. The tumors exhibited a heterogeneous metabolic pattern, with a tendency for ATP to decrease and lactate to increase during tumor development. Tissue pH was above 7.5 in tumors with high ATP content but it sharply declined at low ATP levels. In peritumoral edema, ATP also decreased and lactate increased but, in contrast to tumor tissue, pH became more alkaline. Metabolic changes were associated with edema formation, as evidenced by the rise in water and sodium content. There was a distinct difference between tumor tissue and peritumoral edema: in tumor tissue, pH declined with increasing water content, whereas in peritumoral edema it increased. These observations are interpreted as follows: 1) in tumor tissue, “lactacidosis” and ATP depletion are attributed to disturbances in blood flow, resulting in metabolic failure and the intracellular “cytotoxic” accumulation of water; 2) in peritumoral edema, “lactalkalosis” is the result of an efflux of (alkaline) lactate salts from the tumor into the expanded extracellular compartment, and the decrease in ATP is the volumetric effect of extracellular “vasogenic” edema fluid and not the result of cellular energy failure. These findings are of importance for the interpretation of volume-selective magnetic resonance spectroscopy and may contribute to the establishment of spectroscopic criteria for the evaluation of therapeutical interventions.
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de Guzman, Rafael Barona, M. A. Martorell, J. Basterra, M. Armengot, A. Montoro, and J. Montoro. "Analysis of DNA Content in Supraglottic Epidermoid Carcinoma." Otolaryngology–Head and Neck Surgery 108, no. 6 (June 1993): 706–10. http://dx.doi.org/10.1177/019459989310800613.
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DNA analysis by flow cytometry is considered to be of prognostic value in epidermoid carcinoma of the head and neck. However, few and contradictory studies have been made on laryngeal carcinomas. We studied 48 epidermoid carcinomas in patients subjected to horizontal supraglottic laryngectomy with a 5-year- followup. The technique described by Hedley for fixated and paraffin-embedded tumors was used. Thirteen tumors were excluded on the grounds of presenting variation coefficients in excess of 10. Of the 35 cases analyzed, 28 (80%) were diploid and seven (20%) aneuploid. No correlation was observed between tumor ploldy and patient survival, recurrence, or any of the histopathological variables studied.
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Guigni, Blas A., Jos van der Velden, C. Matthew Kinsey, James A. Carson, and Michael J. Toth. "Effects of conditioned media from murine lung cancer cells and human tumor cells on cultured myotubes." American Journal of Physiology-Endocrinology and Metabolism 318, no. 1 (January 1, 2020): E22—E32. http://dx.doi.org/10.1152/ajpendo.00310.2019.
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Factors secreted from tumors/tumor cells are hypothesized to cause skeletal muscle wasting in cancer patients. We examined whether cancer cells secrete factors to promote atrophy by evaluating the effects of conditioned media (CM) from murine lung cancer cells and primary cultures of human lung tumor cells on cultured myotubes. We evaluated murine Lewis lung carcinoma (LLC) and KRASG12D cells, and primary cell lines derived from tumor biopsies from patients with lung cancer (hTCM; n = 6). In all experiments, serum content was matched across treatment groups. We hypothesized that CM from murine and human tumor cells would reduce myotube myosin content, decrease mitochondrial content, and increase mitochondrial reactive oxygen species (ROS) production. Treatment of myotubes differentiated for 7 days with CM from LLC and KRASG12D cells did not alter any of these variables. Effects of murine tumor cell CM were observed when myotubes differentiated for 4 days were treated with tumor cell CM and compared with undiluted differentiation media. However, these effects were not apparent if tumor cell CM treatments were compared with control cell CM or dilution controls. Finally, CM from human lung tumor primary cell lines did not modify myosin content or mitochondrial content or ROS production compared with either undiluted differentiated media, control cell CM, or dilution controls. Our results do not support the hypothesis that factors released from cultured lung cancer/tumor cells promote myotube wasting or mitochondrial abnormalities, but we cannot dismiss the possibility that these cells could secrete such factors in vivo within the native tumor microenvironment.
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Reith, Thomas P., Melissa A. Prah, Eun-Jung Choi, Jongho Lee, Robert Wujek, Mona Al-Gizawiy, Christopher R. Chitambar, Jennifer M. Connelly, and Kathleen M. Schmainda. "Basal Ganglia Iron Content Increases with Glioma Severity Using Quantitative Susceptibility Mapping: A Potential Biomarker of Tumor Severity." Tomography 8, no. 2 (March 15, 2022): 789–97. http://dx.doi.org/10.3390/tomography8020065.
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Background and Purpose: Gliomas have been found to alter iron metabolism and transport in ways that result in an expansion of their intracellular iron compartments to support aggressive tumor growth. This study used deep neural network trained quantitative susceptibility mapping to assess basal ganglia iron concentrations in glioma patients. Materials and Methods: Ninety-two patients with brain lesions were initially enrolled in this study and fifty-nine met the inclusion criteria. Susceptibility-weighted images were collected at 3.0 T and used to construct quantitative susceptibility maps via a deep neural network-based method. The regions of interest were manually drawn within basal ganglia structures and the mean voxel intensities were extracted and averaged across multiple slices. One-way ANCOVA tests were conducted to compare the susceptibility values of groups of patients based on tumor grade while controlling for age, sex, and tumor type. Results: The mean basal ganglia susceptibility for patients with grade IV tumors was higher than that for patients with grade II tumors (p = 0.00153) and was also higher for patients with grade III tumors compared to patients with grade II tumors (p = 0.020), after controlling for age, sex, and tumor type. Patient age influenced susceptibility values (p = 0.00356), while sex (p = 0.69) and tumor type (p = 0.11) did not. Conclusions: The basal ganglia iron content increased with glioma severity. Basal ganglia iron levels may thus be a useful biomarker in glioma prognosis and treatment, especially with regard to iron-based cancer therapies.
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Pol, Jay. "Brain Tumor Image Classification using CNN." International Journal for Research in Applied Science and Engineering Technology 10, no. 6 (June 30, 2022): 1934–41. http://dx.doi.org/10.22214/ijraset.2022.44191.
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Abstract: We present a method for segmenting and categorizing brain tumors in the challenge of content of brain tumor with segmentation is enrolled and skull is exposed for bar graph equivalent high-level contradiction refer amount. Preprocessing, segmentation, feature extraction, optimization, and classification are used to detect tumors. The tissue is then classified using preprocessed images. We utilized leave-one-out cross-validation to generate a Dice overlap of 88 for the whole tumor area, 75 for the core tumor region, and 95 for the enhancing tumor region, which is higher than the Dice overlap reported
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Meyer, Hanno S., Friederike Liesche-Starnecker, Mona Mustafa, Igor Yakushev, Benedikt Wiestler, Bernhard Meyer, and Jens Gempt. "[18F]FET PET Uptake Indicates High Tumor and Low Necrosis Content in Brain Metastasis." Cancers 13, no. 2 (January 19, 2021): 355. http://dx.doi.org/10.3390/cancers13020355.
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Amino acid positron emission tomography (PET) has been employed in the management of brain metastases. Yet, histopathological correlates of PET findings remain poorly understood. We investigated the relationship of O-(2-[18F]Fluoroethyl)-L-tyrosine ([18F]FET) PET, magnetic resonance imaging (MRI), and histology in brain metastases. Fifteen patients undergoing brain metastasis resection were included prospectively. Using intraoperative navigation, 39 targeted biopsies were obtained from parts of the metastases that were either PET-positive or negative and MRI-positive or negative. Tumor and necrosis content, proliferation index, lymphocyte infiltration, and vascularization were determined histopathologically. [18F]FET PET had higher specificity than MRI (66% vs. 56%) and increased sensitivity for tumor from 73% to 93% when combined with MRI. Tumor content per sample increased with PET uptake (rs = 0.3, p = 0.045), whereas necrosis content decreased (rs = −0.4, p = 0.014). PET-positive samples had more tumor (median: 75%; interquartile range: 10–97%; p = 0.016) than PET-negative samples. The other investigated histological properties were not correlated with [18F]FET PET intensity. Tumors were heterogeneous at the levels of imaging and histology. [18F]FET PET can be a valuable tool in the management of brain metastases. In biopsies, one should aim for PET hotspots to increase the chance for retrieval of samples with high tumor cell concentrations. Multiple biopsies should be performed to account for intra-tumor heterogeneity. PET could be useful for differentiating treatment-related changes (e.g., radiation necrosis) from tumor recurrence.
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Oliveira, Marcelo Magaldi, Audrey Beatriz Araujo, Arthur Nicolato, Andre Prosdocimi, Joao Victor Godinho, Ana Luiza Martins Valle, Marcilea Santos, et al. "Face, Content, and Construct Validity of Brain Tumor Microsurgery Simulation Using a Human Placenta Model." Operative Neurosurgery 12, no. 1 (September 22, 2015): 61–67. http://dx.doi.org/10.1227/neu.0000000000001030.
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Abstract BACKGROUND Brain tumors are complex 3-dimensional lesions. Their resection involves training and the use of the multiple microsurgical techniques available for removal. Simulation models, with haptic and visual realism, may be useful for improving the bimanual technical skills of neurosurgical residents and neurosurgeons, potentially decreasing surgical errors and thus improving patient outcomes. OBJECTIVE To describe and assess an ex vivo placental model for brain tumor microsurgery using a simulation tool in neurosurgical psychomotor teaching and assessment. METHODS Sixteen human placentas were used in this research project. Intravascular blood remnants were removed by continuous saline solution irrigation of the 2 placental arteries and placental vein. Brain tumors were simulated using silicone injections in the placental stroma. Eight neurosurgeons and 8 neurosurgical residents carried out the resection of simulated tumors using the same surgical instruments and bimanual microsurgical techniques used to perform human brain tumor operations. Face and content validity was assessed using a subjective evaluation based on a 5-point Likert scale. Construct validity was assessed by analyzing the surgical performance of the neurosurgeon and resident groups. RESULTS The placenta model simulated brain tumor surgical procedures with high fidelity. Results showed face and content validity. Construct validity was demonstrated by statistically different surgical performances among the evaluated groups. CONCLUSION Human placentas are useful haptic models to simulate brain tumor microsurgical removal. Results using this model demonstrate face, content, and construct validity.
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Lisyaniy, N. I., D. N. Stanetskaya, A. N. Lisyaniy, and L. N. Belskaya. "CONTENT OF STEM TUMOR CD133+ CELLS IN BRAIN NEOPLASMS OF DIFFERENT HISTOLOGICAL TYPE." Experimental Oncology 39, no. 3 (September 22, 2017): 219–23. http://dx.doi.org/10.31768/2312-8852.2017.39(3):219-223.
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Today, there are conflicting data on the content of cancer stem cells responsible for recurrence and resistance to chemotherapy in tumors of human brain. The aim of the study was to analyze the content of CD133+ cells in different brain tumors by immunofluorescence assay and immunohistochemical method. Materials and Methods: The samples of different brain tumors removed during neurosurgical operations were studied for CD133 expression. Results: Immunofluorescence assay of tumor imprints revealed CD133+ cells in 40–85% of tumors regardless of histological type. In malignant tumors, the count of CD133+ cells was higher than in benign tumors. Immunohistochemical method used for detection of CD133+ cells was less sensitive than immunofluorescence technique. The number of CD133+ cells may vary even in tumors of the same histological type. In 20–30% of malignant tumors (glioblastomas, medulloblastomas), the content of CD133+ cells was very low or not detected at all. Conclusions: In tumors of the brain of different genesis and degree of anaplasia CD133+ cells are found out. In malignant tumors (glioblastomas and medulloblastomas), CD133+ cells are much more frequently detected than in benign brain tumors. The content of CD133+ cells in brain tumors is highly variable being small and some malignant tumors, indicating low predictive and diagnostic value of cancer stem cell content in clinical practice.
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Welkoborsky, Hans-J., Wolf J. Mann, Gabriele Haibt, and Ronald G. Amedee. "Comparison of Cytophotometric Characteristics to Histology and Proliferation Markers in Acoustic Neuromas." Annals of Otology, Rhinology & Laryngology 103, no. 1 (January 1994): 49–53. http://dx.doi.org/10.1177/000348949410300109.
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Specimens of histologically confirmed acoustic neuromas obtained during operation in 25 patients were examined. Quantitative DNA measurements were performed with an image analysis system. From the single cell measurements, the mean DNA content of all tumor cells, 2c deviation index (2c DI), DNA entropy, DNA grade of neoplasia, and percentage of tumor cells with a DNA content of more than 5c (5c exceeding rate) were derived, as well as the mean nuclear area of the tumor cells. Proliferating cell nuclear antigen (PCNA) was identified immunohistochemically. A PCNA score was developed in determining PCNA-positive cells in a total amount of 1,000 cells. Results of quantitative DNA measurements and PCNA scores were compared to clinical symptoms, histology, and time between first onset of symptoms and diagnosis of the tumor. Quantitative DNA measurements revealed the existence of hyperdiploid tumor cells in all neuromas. According to the frequency with which they occurred, tumors could be divided into two categories: 1) tumors with a high percentage of hyperdiploid cells (“hyperdiploid tumors”) and 2) those with a low percentage (“diploid tumors”). Hyperdiploid tumors showed increased values for the 2c DI, mean DNA content, DNA grade of neoplasia, and DNA entropy as signs of increased proliferation. In addition, the PCNA scores were higher in these tumors, indicative of increased DNA synthesis. The mean nuclear area was higher in these tumors. No correlation was found between the results of the DNA analysis and the PCNA score, or the clinical data and the predominant histologic subtype. The results of this study could explain the known differences in growth rate of acoustic neuromas and might also have clinical relevance in identifying patients at high risk for developing tumor recurrences.
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Mijatov, Ivana, Bojan Pejakovic, Benjamin Nalic, Sasa Mijatov, and Aleksandar Kiralj. "Infratemporal fossa schwannoma." Medical review 66, no. 5-6 (2013): 250–53. http://dx.doi.org/10.2298/mpns1306250m.
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Introduction. Due to its contents and relations with neighboring regions, the infratemporal fossa has a great clinical significance. Primary tumors of this region, both benign and malignant, are rare, but they do require surgical treatment, which is determined by the size and localization of the tumor. Case Report. The paper presents the case of a 72-year-old female patient who was referred to hospital for paresthesia in the left half of the face after having been found to have a tumor of left infratmeporal fossa by imaging methods. The tumor was completely removed by transfacial-transzygomatic approach and, according to histopathological findings, it was a schwannoma. The postoperative course was without complications and the patient did not have any discomforts at the check-up a month later. Conclusion. In addition to the accurate diagnosis, the success rate of the surgical treatment of tumors depends on the appropriate surgical approach to ensure the complete removal of the tumor while preserving the content of the infratemporal region.
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Ravensbergen, Cor J., Meaghan Polack, Jessica Roelands, Stijn Crobach, Hein Putter, Hans Gelderblom, Rob A. E. M. Tollenaar, and Wilma E. Mesker. "Combined Assessment of the Tumor–Stroma Ratio and Tumor Immune Cell Infiltrate for Immune Checkpoint Inhibitor Therapy Response Prediction in Colon Cancer." Cells 10, no. 11 (October 28, 2021): 2935. http://dx.doi.org/10.3390/cells10112935.
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The best current biomarker strategies for predicting response to immune checkpoint inhibitor (ICI) therapy fail to account for interpatient variability in response rates. The histologic tumor–stroma ratio (TSR) quantifies intratumoral stromal content and was recently found to be predictive of response to neoadjuvant therapy in multiple cancer types. In the current work, we predicted the likelihood of ICI therapy responsivity of 335 therapy-naive colon adenocarcinoma tumors from The Cancer Genome Atlas, using bioinformatics approaches. The TSR was scored on diagnostic tissue slides, and tumor-infiltrating immune cells (TIICs) were inferred from transcriptomic data. Tumors with high stromal content demonstrated increased T regulatory cell infiltration (p = 0.014) but failed to predict ICI therapy response. Consequently, we devised a hybrid tumor microenvironment classification of four stromal categories, based on histological stromal content and transcriptomic-deconvoluted immune cell infiltration, which was associated with previously established transcriptomic and genomic biomarkers for ICI therapy response. By integrating these biomarkers, stroma-low/immune-high tumors were predicted to be most responsive to ICI therapy. The framework described here provides evidence for expansion of current histological TIIC quantification to include the TSR as a novel, easy-to-use biomarker for the prediction of ICI therapy response.
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Kraxner, Anton, Franziska Braun, Wei-Yi Cheng, Marta Canamero, Emilia Andersson, Suzana Vega Harring, Sebastian Dziadek, et al. "930 Fibroblast activation protein alpha expression in tumor stroma and its association with immuno-regulatory circuits across epithelial tumors." Journal for ImmunoTherapy of Cancer 9, Suppl 2 (November 2021): A976. http://dx.doi.org/10.1136/jitc-2021-sitc2021.930.
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BackgroundCarcinoma associated fibroblasts (CAFs) play important roles in modulating tumor development and prognosis through biochemical and biomechanical signals, but also through their immuno-modulatory characteristics. Fibroblast activation protein alpha (FAP), a serine protease with selectively high expression on CAFs, may be an ideal target for therapeutic intervention, including cancer immunotherapy. Therefore, a thorough understanding of FAP expression, but also immune cell composition and especially their interaction is key to optimally inform drug development and patient enrichment strategies.MethodsFormalin-fixed paraffin embedded tissue specimens comprising 253 primary tumors and 277 metastatic lesions were included in this study. Tumor sections were analyzed by digital immunohistochemistry (IHC) to assess tumor-stroma composition, FAP content and immune cell infiltration, complemented by transcriptomic analyses.ResultsAcross different types of epithelial tumors, FAP was detected by digital IHC in the tumor-associated stroma at a low to moderate proportion and with heterogeneous distribution patterns. Primary tumors in breast and lung cancer demonstrated a higher median FAP content (6.5% and 6.6% area coverage, respectively) compared to renal cell carcinoma (0.2% area coverage), which was confirmed on mRNA expression level. Median FAP levels were similar between primary and metastatic lesions in most tumor types except for renal cancer, for which FAP levels were significantly increased in metastasis lesions (3.3% area coverage). FAP content positively correlated with the density of FoxP3 positive regulatory T cells, but indication and tissue type specific differences were observed. Transcriptomic analysis revealed that both stroma-richness as well as higher FAP content were positively correlated with macrophage and dendritic cell gene signatures. However, while a higher stromal content was associated with signatures related to endothelial cells and preadipocytes, higher FAP content showed a stronger correlation with regulatory T cells. These findings are suggestive of a distinct biological role of FAP positive stroma in human tumors.ConclusionsFAP-targeted therapy is a promising strategy to optimize accumulation and action of anti-cancer drugs in the tumor microenvironment, potentially leading to more specific and effective therapies. Our study further elucidates the role of FAP by providing a comprehensive and granular landscape of FAP content in primary and metastatic tumor lesions derived from the same patient population and its association with immune cell composition. Future studies aim to elucidate the complex and dynamic interplay between malignant, stromal and immune cell populations in both temporal and spatial contexts and how that contributes to outcome in cancer immunotherapy.
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Markopoulos, Georgios S., Georgios K. Glantzounis, Anna C. Goussia, Georgios D. Lianos, Anastasia Karampa, George A. Alexiou, and George Vartholomatos. "Touch Imprint Intraoperative Flow Cytometry as a Complementary Tool for Detailed Assessment of Resection Margins and Tumor Biology in Liver Surgery for Primary and Metastatic Liver Neoplasms." Methods and Protocols 4, no. 3 (September 15, 2021): 66. http://dx.doi.org/10.3390/mps4030066.
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Liver resection is the main treatment for primary and metastatic liver tumors in order to achieve long-term survival with good quality of life. The ultimate goal of surgical oncology is to achieve complete tumor removal with adequate clear surgical margins. Flow cytometry is a powerful analytical technique with applications such as phenotypic analysis and quantification of DNA content. Intraoperative flow cytometry (iFC) is the application of flow cytometry for DNA content/ploidy and cell cycle distribution analysis during surgery for tumor cell analysis and margin evaluation. It has been used for cell analysis of intracranial tumors and recently of head and neck carcinomas and breast carcinomas, as well as for tumor margin evaluation. Herein, we present a novel touch imprint iFC protocol for the detailed assessment of tumor margins during excision of malignant hepatic lesions. The protocol aims to offer information on surgical margins after removal of malignant liver tumors based on DNA content of cancer cells and to corroborate the results of iFC with that of histopathological analysis. Based on the established role of iFC in other types of malignancies, our specialized protocol has the potential, through characterization of cells in liver transection surface post hepatectomy, to offer significant information on the type of resection and tumor biology. This information can be used to effectively guide intra- and postoperative patient management.
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Salloum, Rabih M., Helena J. Mauceri, Nader N. Hanna, David H. Gorski, Mitchell C. Posner, and Ralph R. Weichselbaum. "Dual Induction of the Epo-Egr-TNF-α Plasmid in Hypoxic Human Colon Adenocarcinoma Produces Tumor Growth Delay." American Surgeon 69, no. 1 (January 2003): 24–27. http://dx.doi.org/10.1177/000313480306900105.
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Gene therapy is a modality for the treatment of solid tumors that involves the introduction of a suicide gene into the tumor cells. Genetic radiotherapy involves the placement of a radiation-sensitive promoter upstream from a suicide gene. Because of their irregular vasculature some solid tumors are chronically hypoxic and hence are resistant to conventional treatment with chemotherapy and ionizing radiation (IR). The purpose of this study was to demonstrate that regional tumor hypoxia could be exploited to improve local tumor control. The cDNA coding the erythropoietin hypoxia-responsive element (EPO) was placed upstream from the Egr-TNF-α construct. WIDR human colon adenocarcinoma cells were injected into the right hind limb of nude mice and treated with Epo-Egr-TNF-α plasmid with or without IR. Tumor volumes were measured by calipers and tumor necrosis factor (TNF)-α content of the tumor was determined by enzyme-linked immunosorbent assay. Treatment with the combined regimen of Epo-Egr-TNF-α plasmid + IR resulted in significant tumor growth delay. Tumor TNF-α content was increased by 30 per cent in the combined treatment group compared with each treatment alone. Regional tumor hypoxia can be exploited successfully to induce tumor growth delay, enhance local control, and enhance the therapeutic ratio.
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Cheng, Noah C., Nune Markosyan, and Robert H. Vonderheide. "Abstract C013: Response to combination immunotherapy in a mouse model of PDAC is a function of baseline T cell content." Cancer Research 82, no. 22_Supplement (November 15, 2022): C013. http://dx.doi.org/10.1158/1538-7445.panca22-c013.
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Abstract Findings from the recently reported phase 2 PRINCE trial for patients with metastatic pancreatic cancer suggest potential clinical benefit with certain combinations of chemotherapy and immunotherapy. Overall survival following gemcitabine/nab-paclitaxel and either PD-1 blocking antibody or CD40 agonistic antibody (aCD40) correlated with the prevalence of distinct T cell subsets in circulation at baseline and with the extent of certain tumor infiltrating T cells (Padron et al., Nature Medicine, 2022). Here, we modeled the therapeutic effect of aCD40/PD-1/CTLA-4 therapy in the absence of chemotherapy in mice bearing tumors derived from the autochthonous pancreatic ductal adenocarcinoma (PDAC) KPC model and studied the dependency of tumor regression on the degree of tumor infiltrating T cells. We used a panel of KPC tumor cell clones that exhibit reproducible and transplantable levels of T cell infiltration ranging between high, intermediate, and low amounts. Mice were subcutaneously injected with clonal PDAC lines and treated 14-21 days later with either aCD40 alone or aCD40/PD-1/CTLA-4 (all i.p., n=5-8 mice per cohort of T cell high, intermediate and low clones). Systemic immune dynamics were surveyed by bleeding mice on day 0, 7, and 14 of treatment and analyzing for immune cell activation and exhaustion markers. In mice bearing T cell high and intermediate tumors, aCD40/PD-1/CTLA-4 induced higher rates of complete tumor regressions (71% for T cell high; 25% for T cell intermediate) and prolonged survival (P < 0.001 for T cell high; P = 0.013 for T cell intermediate) compared to untreated controls. Treatment with aCD40 alone was effective in mice with T cell intermediate tumors, leading to regressions in 29% of mice. In mice bearing T cell low tumors, however, tumor regressions after aCD40/PD-1/CTLA-4 were less frequent (12.5%), although survival was improved significantly following the treatment (P <0.001). aCD40 alone improved overall survival of T cell low bearing mice (P = 0.026) without inducing tumor regressions. Regardless of T cell high, intermediate, or low tumors, aCD40/PD-1/CTLA-4 increased the proportions of circulating activated and exhausted CD4+ and CD8+ T cells. aCD40/PD-1/CTLA-4 also increased T cell infiltration into T cell low tumors, but this enhanced infiltration did not correlate with complete regressions. Thus, using tumor clones derived from the same autochthonous genetic model, we show that response to combination immunotherapy is a function of baseline T cell content, with ‘hot’ tumors responding the best and ‘cold’ tumors responding the worst. Additional tumor cell-intrinsic factors such as those revealed in other mouse experiments and in the human samples from the PRINCE study likely restrict a robust anti-tumor immune response even when T cells have been recruited. Citation Format: Noah C. Cheng, Nune Markosyan, Robert H. Vonderheide. Response to combination immunotherapy in a mouse model of PDAC is a function of baseline T cell content [abstract]. In: Proceedings of the AACR Special Conference on Pancreatic Cancer; 2022 Sep 13-16; Boston, MA. Philadelphia (PA): AACR; Cancer Res 2022;82(22 Suppl):Abstract nr C013.
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Stadler, P., H. J. Feldmann, C. Creighton, H. F. Zeilhoffer, V. Zimmermann, M. Schmitt, and M. Molls. "Clinical Evidence for Correlation of Insufficient Tissue Oxygen Supply (Hypoxia) and Tumor-Associated Proteolysis in Squamous Cell Carcinoma of the Head and Neck." International Journal of Biological Markers 15, no. 3 (July 2000): 235–36. http://dx.doi.org/10.1177/172460080001500306.
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Hypoxic tumors of patients with squamous cell carcinoma of the head and neck show a consistent trend towards poor treatment outcome. We now report that tumor hypoxia in these patients is correlated with elevated antigen content of the tumor-associated serine protease uPA (urokinase-type plasminogen activator), a marker of tumor cell invasion and metastasis.
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Fitzgerald, Allison A., Shangzi Wang, Veena Agarwal, Emily F. Marcisak, Annie Zuo, Sandra A. Jablonski, Melanie Loth, et al. "DPP inhibition alters the CXCR3 axis and enhances NK and CD8+ T cell infiltration to improve anti-PD1 efficacy in murine models of pancreatic ductal adenocarcinoma." Journal for ImmunoTherapy of Cancer 9, no. 11 (November 2021): e002837. http://dx.doi.org/10.1136/jitc-2021-002837.
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BackgroundPancreatic ductal adenocarcinoma (PDAC) is projected to be the second leading cause of cancer death in the USA by 2030. Immune checkpoint inhibitors fail to control most PDAC tumors because of PDAC’s extensive immunosuppressive microenvironment and poor immune infiltration, a phenotype also seen in other non-inflamed (ie, ‘cold’) tumors. Identifying novel ways to enhance immunotherapy efficacy in PDAC is critical. Dipeptidyl peptidase (DPP) inhibition can enhance immunotherapy efficacy in other cancer types; however, the impact of DPP inhibition on PDAC tumors remains unexplored.MethodsWe examined the effects of an oral small molecule DPP inhibitor (BXCL701) on PDAC tumor growth using mT3-2D and Pan02 subcutaneous syngeneic murine models in C57BL/6 mice. We explored the effects of DPP inhibition on the tumor immune landscape using RNAseq, immunohistochemistry, cytokine evaluation and flow cytometry. We then tested if BXCL701 enhanced anti-programmed cell death protein 1 (anti-PD1) efficacy and performed immune cell depletion and rechallenged studies to explore the relevance of cytotoxic immune cells to combination treatment efficacy.ResultsIn both murine models of PDAC, DPP inhibition enhanced NK and T cell immune infiltration and reduced tumor growth. DPP inhibition also enhanced the efficacy of anti-PD1. The efficacy of dual anti-PD1 and BXCL701 therapy was dependent on both CD8+ T cells and NK cells. Mice treated with this combination therapy developed antitumor immune memory that cleared some tumors after re-exposure. Lastly, we used The Cancer Genome Atlas (TCGA) to demonstrate that increased NK cell content, but not T cell content, in human PDAC tumors is correlated with longer overall survival. We propose that broad DPP inhibition enhances antitumor immune response via two mechanisms: (1) DPP4 inhibition increases tumor content of CXCL9/10, which recruits CXCR3+ NK and T cells, and (2) DPP8/9 inhibition activates the inflammasome, resulting in proinflammatory cytokine release and Th1 response, further enhancing the CXCL9/10-CXCR3 axis.ConclusionsThese findings show that DPP inhibition with BXCL701 represents a pharmacologic strategy to increase the tumor microenvironment immune cell content to improve anti-PD1 efficacy in PDAC, suggesting BXCL701 can enhance immunotherapy efficacy in ‘cold’ tumor types. These findings also highlight the potential importance of NK cells along with T cells in regulating PDAC tumor growth.
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Dmytryk, V., O. Savchuk, and I. Andriychenko. "The content of matrix metalloproteinases in bladder cancer tumors." Bulletin of Taras Shevchenko National University of Kyiv. Series: Problems of Physiological Functions Regulation 26, no. 1 (2019): 46–50. http://dx.doi.org/10.17721/1728_2624.2019.26.46-50.
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Bladder cancer (BC) is the 9th in frequency oncologic disease, with the highest number of patients in developed countries. The disease is more commonly diagnosed in men – about 75%. The ability to invade surrounding tissues and metastasis to individual organs is one of the fundamental properties of malignant tumors. According to modern ideas about mechanisms of metastasis, basement membranes and extracellular matrix are the main barriers, and tissue structures are needed to overcome the invasive growth of tumor cells. Almost all of the extracellular matrix components can be destroyed by the use of metal-matrix proteinases (MMP), moreover, the precursors of growth factors and adhesion molecules on the cell surface may be the MMP substrates. MMPs also participate in epithelial-mesenchymal transformation, which provides metastasis. Previous studies by other authors point to an increase in the biosynthesis of various MMPs in the outbreak of tumors and in metastases, such changes associated with the degree of differentiation of the tumor, the depth of the invasion, as well as their association with poor further prognosis and low survival rates in patients with various cancers. The purpose of our work was to investigate the content of MMP-1, 2, 3, 8 and TIMP-1 in the tumors and walls of the healthy bladder in patients with BC, depending on the stage of TNM classification. We investigated the increase in the content of MMP-1, 2, 3, 8 and TIMP-1 in samples of healthy bladder walls for stage 3 and 4 of the BC, indicating the participation of the investigated parameters in the growth and invasion of bladder tumors. The results of our study are consistent with the results of previous studies conducted in the study of other neoplasms, which indicate the relationship between the studied parameters with the development of cancer.
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Bodsch, Wolfram, Thomas Rommel, Bernd Grosse Ophoff, and Jürgen Menzel. "Factors responsible for the retention of fluid in human tumor edema and the effect of dexamethasone." Journal of Neurosurgery 67, no. 2 (August 1987): 250–57. http://dx.doi.org/10.3171/jns.1987.67.2.0250.
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✓ The components of vasogenic edema associated with brain tumors were investigated in human biopsy material sampled from tumor and peritumoral tissue during neurosurgical operations. Tissue from 60 patients with glioblastomas, gliomas, meningiomas, and metastases who had been treated with dexamethasone prior to surgery was used for measurement of water, electrolyte, hemoglobin, serum protein, and dexamethasone concentrations. In all samples except metastases, positive correlations were obtained between water content and both serum protein levels and sodium content in tumors and peritumoral edema, suggesting that these components simultaneously determine forces for extravasation of plasma-derived edema fluid. However, the mean serum protein content varied considerably, being high in glioblastomas (16 mg/ml) and low in peritumoral edema surrounding metastases (4 mg/ml). The mean cerebral blood volume in all samples, as calculated from the tissue hemoglobin content, was 2.5 ml/100 gm wet weight in tumor tissue and 1.6 to 2.0 ml/100 gm wet weight in peritumoral tissue. Sodium concentrations were not significantly different among the tumor types. Both water and serum protein content decreased with increasing dexamethasone concentrations in glioblastomas, while this effect was virtually absent in gliomas and meningiomas. A therapeutic threshold of dexamethasone at 500 mg/gm wet weight was obtained for tumoral and peritumoral tissue of glioblastomas and was effective in a dose-dependent manner as long as the water content and the serum protein concentration remained below 6 ml/gm dry weight and 30 mg/gm dry weight, respectively. These results suggest a previously unknown selectivity among tumor types for the reduction of both water content and serum proteins in corticosteroid-treated edematous tissue.
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Osagbemiro Babatope Bamidele and Soroye Modupeoluwa Omotunde. "http://wjarr.com/content/adjuvant-chemotherapy-malignant-phyllodes-tumor-breast." World Journal of Advanced Research and Reviews 5, no. 3 (March 30, 2020): 055–61. http://dx.doi.org/10.30574/wjarr.2020.5.3.0056.
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Mambo, Elizabeth, Aditi Chatterjee, Mingzhao Xing, Giovanni Tallini, Bryan R. Haugen, Sai-Ching J. Yeung, Saraswati Sukumar, and David Sidransky. "Tumor-specific changes in mtDNA content in human cancer." International Journal of Cancer 116, no. 6 (2005): 920–24. http://dx.doi.org/10.1002/ijc.21110.
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Kokal, William. "Tumor DNA Content in the Prognosis of Colorectal Carcinoma." JAMA: The Journal of the American Medical Association 255, no. 22 (June 13, 1986): 3123. http://dx.doi.org/10.1001/jama.1986.03370220085032.
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Ceriani, R. L., and C. Chan. "Breast epithelial antigen levels and breast tumor antigen content." Breast Cancer Research and Treatment 17, no. 1 (November 1990): 55–58. http://dx.doi.org/10.1007/bf01812685.
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Johnson, Lewis A., Philip T. Lavin, Yogeshwar Y. Dayal, Stephen A. Geller, Wilhelm G. Doos, Harry S. Cooper, John E. Gerber, et al. "Gallbladder adenocarcinoma: Prognostic significance of tumor acid mucopolysaccharide content." Journal of Surgical Oncology 33, no. 4 (December 1986): 243–45. http://dx.doi.org/10.1002/jso.2930330408.
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Kokal, W. "Tumor DNA content in the prognosis of colorectal carcinoma." JAMA: The Journal of the American Medical Association 255, no. 22 (June 13, 1986): 3123–27. http://dx.doi.org/10.1001/jama.255.22.3123.
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Kokal, William A. "Tumor DNA Content in Primary and Metastatic Colorectal Carcinoma." Archives of Surgery 121, no. 12 (December 1, 1986): 1434. http://dx.doi.org/10.1001/archsurg.1986.01400120084014.
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Young, Stephen, Christen Griego-Fullbright, Aaron Wagner, Amanda Chargin, and Bruce Kendrick Patterson. "Simultaneous, single cell, flow cytometric quantification of PD-L1/TILs/cell cycle in non-small cell lung cancer tissue biopsies: Concordance of PD-L1 expression detection between flow cytometry and immunohistochemistry." Journal of Clinical Oncology 36, no. 5_suppl (February 10, 2018): 159. http://dx.doi.org/10.1200/jco.2018.36.5_suppl.159.
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159 Background: Tumor cell expression of PD-L1 leads to the inhibition of immune responses specifically inactivation of cytotoxic T-cells. PD-L1 expression on tumor cells by immunohistochemistry does not provide the complete picture of therapeutic (PD-L1) and prognostic (TILs, aneuploidy) markers. Here, we report a clinical assay that quantifies tumor infiltrating lymphocytes (TILs), cell cycle/DNA content as well as PD-L1 expression on tumor and aneuploid tumor cell populations. Methods: Punch biopsies were taken from 19 fresh tissues specimens and were processed into single cell suspensions using the IVD/CE-IVD IncellPREP Single Cell Preparation Kit. Cells were fixed and permeabilized in 1 mL IncellMax. Cells were tested with the OncoTect iO Lung Assay which contains antibodies directed against PD-L1 (clone 28-8), CD45, CD3, and CD8, and a cell cycle dye. Concordance to IHC was tested by the Dako PD-L1 IHC 28-8 PharmDx Kit. Immune cell populations were quantified and aneuploidy was determined using a DNA index > 1.05. Results: The number of CD8+ CTL were significantly increased (P = 0.02) in tumor compared to normal lung tissue (37.4% to 28.2%). The number of CTL in aneuploid tumors was twice the number of CTL in diploid tumors. The percentage of antigen presenting cells (CD45+, high SSC) was decreased in the tumor cell samples relative to the normal lung tissue (P = 0.01). PD-L1 expression varies in cells depending on the cell cycle. Conclusions: In this study, the concordance between Oncotect iO and IHC was 95% (NPA-97%, PPA-89%). PD-L1 expression varies with DNA content, PD-L1 expression decreases with increasing DNA content. Though CTL are increased in aneuploid tumors, PD-L1 expression decreasing with DNA content may contribute to the association of aneuploidy with distant metastases. PD-L1 expression is a powerful determinant of treatment and aneuploidy is a powerful prognostic factor that combined yield important clinical information.
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Kovaleva, Olga V., Polina Podlesnaya, Maxim Sorokin, Valeria Mochalnikova, Vladimir Kataev, Yuriy A. Khlopko, Andrey O. Plotnikov, Ivan S. Stilidi, Nikolay E. Kushlinskii, and Alexei Gratchev. "Macrophage Phenotype in Combination with Tumor Microbiome Composition Predicts RCC Patients’ Survival: A Pilot Study." Biomedicines 10, no. 7 (June 27, 2022): 1516. http://dx.doi.org/10.3390/biomedicines10071516.
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The identification of new prognostic markers of renal cell carcinoma (RCC) is an urgent problem in oncourology. To investigate the potential prognostic significance of tumor microbiome and stromal inflammatory markers, we studied a cohort of 66 patients with RCC (23 clear cell RCC, 19 papillary RCC and 24 chromophobe RCC). The microbiome was analyzed in tumor and normal tissue by 16S rRNA amplicon sequencing. Characterization of the tumor stroma was performed using immunohistochemistry. A significant difference in alpha diversity was demonstrated between normal kidney tissue and all types of RCC. Further, we demonstrated that the bacterial burden was higher in adjacent normal tissue than in a tumor. For the first time, we demonstrated a significant correlation between bacterial burden and the content of PU.1+ macrophages and CD66b+ neutrophils in kidney tumors. Tumors with high content of PU.1+ cells and CD66b+ cells in the stroma were characterized by a lower bacterial burden. In the tumors with high bacterial burden, the number of PU.1+ cells and CD66b+ was associated with a poor prognosis. The identified associations indicate the great prognostic potential of a combined tumor microbiome and stromal cell analysis.
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Bourhis, J., C. Dominici, H. McDowell, G. Raschella, G. Wilson, M. A. Castello, E. Plouvier, J. Lemerle, G. Riou, and J. Bénard. "N-myc genomic content and DNA ploidy in stage IVS neuroblastoma." Journal of Clinical Oncology 9, no. 8 (August 1991): 1371–75. http://dx.doi.org/10.1200/jco.1991.9.8.1371.
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DNA ploidy and N-myc genomic content were analyzed in a series of stage IVS neuroblastomas by flow cytometry and Southern blot hybridization, respectively. Of the 12 stage IVS neuroblastomas studied, nine were aneuploid (DNA index [DI] greater than 1), two were diploid (DI = 1), and one was not assessable for DNA content due to insufficient tumor material. N-myc gene amplification was present in two of 12 tumors. None of the aneuploid tumors exhibited N-myc amplification. Among the aneuploid neuroblastomas, the DIs were between 1.27 and 1.60, ie, in the near-triploid range. The follow-up from diagnosis ranged from 1 to 41 months (mean, 20 months). The nine neuroblastomas with near-triploid DNA content were free of disease at the end of the follow-up period. In contrast, a rapid and fatal tumor progression was observed for the three neuroblastomas with N-myc amplification and/or diploidy. Although involving only a limited series, these results strongly suggest that the combined analysis of DNA ploidy and N-myc genomic content could predict clinical outcome in stage IVS neuroblastoma and should help to identify patients for whom a more aggressive therapy is required.
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Bikker, F. J., J. E. van der Wal, A. J. M. Ligtenberg, J. Mollenhauer, J. M. A. de Blieck-Hogervorst, I. van der Waal, A. Poustka, and A. V. Nieuw Amerongen. "Salivary Agglutinin/DMBT1SAG Expression is Up-regulated in the Presence of Salivary Gland Tumors." Journal of Dental Research 83, no. 7 (July 2004): 567–71. http://dx.doi.org/10.1177/154405910408300711.
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Salivary agglutinin (SAG) is encoded by the gene Deleted in Malignant Brain Tumors 1 ( DMBT1) and represents the salivary variant of DMBT1 (DMBT1SAG). While SAG is a bona fide anti-caries factor, DMBT1 was proposed as a candidate tumor-suppressor for brain, digestive tract, and lung cancer. Though DMBT1SAG is expressed in the salivary glands, its expression in salivary gland tumors is unknown. Here we analyzed DMBT1SAG expression in 20 salivary gland tumors and 14 tumor-flanking tissues by immunohistochemistry. DMBT1SAG in salivary gland tumors resembles the changes of expression levels known from DMBT1 in tumors in other cancer types. Particularly, DMBT1SAG was up-regulated in 10/14 tumor-flanking tissues, and a strong staining of the luminal content in the tumor and/or the tumor-flanking tissue was observed in 14/20 cases. This suggests that, in addition to its role in caries defense, SAG may serve as a potential tumor indicator and/or tumor suppressor in salivary gland tissue.
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Satomi, Kaishi, Ryo Nishikawa, Masao Matsutani, Koichi Ichimura, and Hirokazu Takami. "PATH-42. PROGNOSTIC FACTORS OF CNS GERM CELL TUMORS; MOLECULAR AND HISTOPATHOLOGICAL ANALYSES ON 154 CASES FROM THE IGCT CONSORTIUM." Neuro-Oncology 23, Supplement_6 (November 2, 2021): vi124—vi125. http://dx.doi.org/10.1093/neuonc/noab196.494.
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Abstract BACKGROUND Germ cell tumors (GCTs) preferentially occurs in pediatric and young adult age groups. Chemo- and radiation therapies cause long-term sequelae in their later lives. We searched for clinical and histopathological features to predict the prognosis and affect treatment response, with a future goal of treatment stratification. METHODS A total of 154 GCT cases were included in the analysis. Total of 114 germinoma cases underwent measurement of tumor cell content on H-E specimen, and 82 GCT cases underwent 450K methylation analysis. 12p gain was determined on methylation-based copy number computation and FISH. Association with progression-free and overall survival (PFS/OS) was investigated. RESULTS The tumor cell content was widely distributed from < 5% to 90% in the specimens, with a median value of 50%. Patients with a higher tumor cell content (≥50%) showed shorter PFS than those with a lower tumor cell content (< 50 %) (p=0.03). In multivariate analysis with tumor location, tumor cell content was the sole statistically significant prognostic factor (p=0.04). 12p gain was found in 25-out-of-82 cases (30%) and was more frequent in NGGCTs, particularly in cases with malignant components. The presence of 12p gain correlated with shorter PFS and OS, even with histology and tumor markers incorporated in the multivariate analysis. Among NGGCTs, 12p gain still had prognostic significance for PFS and OS. The 12p copy number status was shared among histological components in mixed GCTs. Whole-genome amplification was suggested by FISH. CONCLUSIONS We found that tumor cell content significantly affected the prognosis of germinomas. 12p gain predicts the presence of malignant components of NGGCTs, and poor prognosis of the patients. Furthermore, 12p is likely to be an early event in the tumorigenesis of GCT. These potentially open the possibility of leveraging these pathological and molecular factors in future clinical trials when stratifying the treatment intensity.
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Takami, Hirokazu, Kaishi Satomi, Kohei Fukuoka, Yuko Matsushita, Kai Yamasaki, Taishi Nakamura, Masayuki Kanamori, et al. "BOT-3 Prognostic Factors of CNS Germ Cell Tumors; Molecular and Histopathological Analyses on 154 Cases from the iGCT Consortium." Neuro-Oncology Advances 3, Supplement_6 (December 1, 2021): vi8—vi9. http://dx.doi.org/10.1093/noajnl/vdab159.031.
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Abstract Background: Germ cell tumors (GCTs) preferentially occurs in pediatric and young adult age groups. Chemo- and radiation therapies cause long-term sequelae in their later lives. We searched for clinical and histopathological features to predict the prognosis and affect treatment response, with a future goal of treatment stratification.Methods: A total of 154 GCT cases were included in the analysis. Total of 114 germinoma cases underwent measurement of tumor cell content on H-E specimen, and 82 GCT cases underwent 450K methylation analysis. 12p gain was determined on methylation-based copy number computation and FISH. Association with progression-free and overall survival (PFS/OS) was investigated. Results: The tumor cell content was widely distributed from <5% to 90% in the specimens, with a median value of 50%. Patients with a higher tumor cell content (>=50%) showed shorter PFS than those with a lower tumor cell content (<50 %) (p=0.03). In the multivariate analysis with tumor location, tumor cell content was the sole statistically significant prognostic factor (p=0.04). 12p gain was found in 25-out-of-82 cases (30%) and was more frequent in NGGCTs, particularly in cases with malignant components. The presence of 12p gain correlated with shorter PFS and OS, even with histology and tumor markers incorporated in the multivariate analysis. Among NGGCTs, 12p gain still had prognostic significance for PFS and OS. The 12p copy number status was shared among histological components in mixed GCTs. Whole-genome amplification was suggested by FISH.Conclusions: We found that tumor cell content significantly affected the prognosis of germinomas. 12p gain predicts the presence of malignant components of NGGCTs, and poor prognosis of the patients. Furthermore, 12p is likely to be an early event in the tumorigenesis of CNS GCT. These potentially open the possibility of leveraging these pathological and molecular factors in the future clinical trials when stratifying the treatment intensity.
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Murray, Clare, Anand Kornepati, Alvaro Padron, Myrna Garcia, Haiyan Bai, Yilun Deng, and Tyler Curiel. "755 Pharmacologic tumor PD-L1 depletion reduces Chk2 content and sensitizes tumors to small molecule Chk1 DNA damage repair inhibitors." Journal for ImmunoTherapy of Cancer 9, Suppl 2 (November 2021): A789—A790. http://dx.doi.org/10.1136/jitc-2021-sitc2021.755.
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BackgroundTumor PD-L1 canonically signals to PD-1 on immune cells to evade immune destruction.1 We reported that tumor PD-L1 also mediates diverse pathologic intracellular signals,2 3 including promoting the ATM/Chk2 DNA damage response, and that genetically PD-L1 deficient tumors are sensitized to Chk1 inhibitor therapy.4 DNA damage increases cytosolic DNA, which induces immunogenic STING signals through inflammatory type I interferon and cytokine production.5MethodsWe conducted a high-throughput drug screen that identified the β-lactam cephalosporin antibiotic cefepime as a pharmacologic tumor PD-L1 depleting agent. In vitro tests of β-lactam antibiotics used 80 μM and the Chk1 inhibitors rabusertib and prexasertib were used at indicated concentrations. Cell lines were RT4 human bladder cancer, ID8agg murine ovarian cancer, and B16 mouse melanoma. Viability was by MTT and proteins by immunoblot. We challenged NSG mice (n = 5 per group) with RT4 (SQ) and treated with cefepime (200 mg/kg), rabusertib (2.5 mg/kg), vehicle, or combination daily.ResultsCefepime at pharmacologically relevant concentrations depletes tumor PD-L1 and phenocopies genetic tumor PD-L1 depletion by decreasing Chk2 protein and increasing DNA damage (γH2AX) (figure 1). Chk2 is depleted by cefepime in CTRL cells, but not in PD-L1KO or PD-L1 overexpressing cells, and sensitizes PD-L1+ tumor cells to Chk1 inhibitors in vitro in a PD-L1-dependent manner (figures 1 and 2). Combining cefepime with rabusertib in vivo significantly prolonged severely immunodeficient NSG mice survival in RT4 challenge versus cefepime alone while rabusertib alone was not effective (figure 3). Antimicrobial mechanisms, reported to influence tumor treatment responses,6 are unlikely in NSG mice. To test β-lactam contributions to cefepime efficacy, we found that ceftazidime, a structurally related cephalosporin, also depletes tumor PD-L1 and Chk2 protein and sensitizes tumors to rabusertib in a PD-L1 dependent manner (figures 4 and 5). Structurally-unrelated β-lactam antibiotics did not sensitize tumors to rabusertib. Both cefepime and ceftazidime activate tumor STING, suggesting they could augment immunotherapies by increasing tumor immunogenicity (figure 6).ConclusionsAs genetic PD-L1 depletion is not yet clinically feasible, we provide pharmacologic means to deplete tumor PD-L1 to improve clinical treatment efficacy as a rapidly translated approach. Cefepime is the prototype agent, but ceftazidime is structurally similar with significant activity, suggesting important structure activity relationships to explore. Pharmacologic tumor PD-L1 depletion could augment other standard of care approaches, including immunotherapy, and deserves further investigation.ReferencesDong H, Strome SE, Salomao DR, Tamura H, Fumiya H, Flies DB, et al. Tumor-associated B7-H1 promotes T-cell apoptosis: a potential mechanism of immune evasion. Nat Med 2002;8:793–800.Clark CA, Gupta HB, Gangadhara S, Pandeswara S, Lao S, Yuan B, et al. Tumor-Intrinsic PD-L1 signals regulate cell growth, pathogenesis, and autophagy in Ovarian Cancer and Melanoma. Cancer Res 2016;76(23):6964–6974.3. Gupta HB, Clark CA, Yuan B, Sareddy G, Pandeswara S, Padron AS, et al. Tumor cell-intrinsic PD-L1 promotes tumor-initiating cell generation and functions in melanoma and ovarian cancer. Signal Transduct Target Ther 2016;1.Kornepati AV, Zhang D, Hambright HG, Kari SC, Deng Y, Clark CA, et al. Cell-intrinsic programmed death ligand-1 (PD-L1) inhibits cytotoxic chemo, promotes DNA damage repair, and enhances ATM/ATR signaling following exposure to DNA damaging agents in bladder, melanoma, and ovarian cancer cells. J Immunol 2019;202(1):195.17.Gehrke N, Mertens C, Zillinger T, Wenzel J, Bald T, Zahn S, et al. Oxidative damage of DNA confers resistance to cytosolic nuclease TREX1 degradation and potentiates STING-dependent immune sensing. Immunity 2013;39(3):482–495.Gopalakrishnan V, Spencer CN, Nezi L, Reuben A, Andrews MC, Karpinets TV, et al. Gut microbiome modulates response to anti-PD-1 immunotherapy in melanoma patients. Science 2018;359(6371):97–103.Ethics ApprovalThis protocol was approved by the UTHSCSA IACUC.Abstract 755 Figure 1Cefepime depletes tumor PD-L1 and Chk2 and induces γH2AXAbstract 755 Figure 2Cefepime sensitizes tumors to Chk1 inhibitors in a PD-L1 dependent mannerAbstract 755 Figure 3Cefepime combined with Chk1 inhibitors in vivo prolongs NSG mouse survivalAbstract 755 Figure 4Ceftazidime depletes tumor PD-L1 and Chk2Abstract 755 Figure 5Ceftazidime, but not other B-lactam antibiotics, sensitizes RT4 to Chk1 inhibitors in a PD-L1 dependent mannerAbstract 755 Figure 6Cefepime and ceftazidime induce STING and p-TBK1
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Szatanek, Rafał, and Monika Baj-Krzyworzeka. "CD44 and Tumor-Derived Extracellular Vesicles (TEVs). Possible Gateway to Cancer Metastasis." International Journal of Molecular Sciences 22, no. 3 (February 2, 2021): 1463. http://dx.doi.org/10.3390/ijms22031463.
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Cancer metastasis, the final stage of tumor progression, is a complex process governed by the interplay of multiple types of cells and the tumor microenvironment. One of the aspects of this interplay involves the release of various factors by the tumor cells alone or by forcing other cells to do so. As a consequence of these actions, tumor cells are prepared in favorable conditions for their dissemination and spread to other sites/organs, which guarantees their escape from immunosurveillance and further progression. Tumor-derived extracellular vesicles (TEVs) represent a heterogeneous population of membrane-bound vesicles that are being actively released by different tumors. The array of proteins (i.e., receptors, cytokines, chemokines, etc.) and nucleic acids (i.e., mRNA, miR, etc.) that TEVs can transfer to other cells is often considered beneficial for the tumor’s survival and proliferation. One of the proteins that is associated with many different tumors as well as their TEVs is a cluster of differentiation 44 in its standard (CD44s) and variant (CD44v) form. This review covers the present information regarding the TEVs-mediated CD44s/CD44v transfer/interaction in the context of cancer metastasis. The content and the impact of the transferred cargo by this type of TEVs also are discussed with regards to tumor cell dissemination.
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Torphy, Robert J., Zhen Wang, Aisha True-Yasaki, Keith E. Volmar, Naim Rashid, Benjamin Yeh, Julia S. Johansen, Michael A. Hollingsworth, Jen Jen Yeh, and Eric A. Collisson. "Stromal Content Is Correlated With Tissue Site, Contrast Retention, and Survival in Pancreatic Adenocarcinoma." JCO Precision Oncology, no. 2 (November 2018): 1–12. http://dx.doi.org/10.1200/po.17.00121.
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Purpose Desmoplastic stroma is a cardinal feature of primary pancreatic ductal adenocarcinoma (PDA), but its effects on the biology, prognosis, and therapeutic outcomes in the disease are not known. We developed an automated method to assess tumor stroma density (TSD) and investigated computed tomography (CT) correlates of stroma in PDA. Patients and Methods We collected PDA samples from rapid autopsy and resection series and digitally annotated samples to quantify TSD. A series of patients who had undergone resection also underwent preoperative multiphasic CT imaging. Results Automated and manual assessments of TSD were highly correlated (ρ = 0.65; P < .001). Solid organ metastases had a lower median TSD than primary tumors ( P < .001). Patients whose tumors had high TSD had prolonged recurrence-free survival (hazard ratio [HR] = 0.51; P = .003) and overall survival (HR = 0.57; P = .008). In another independent dataset, patients whose tumors had high TSD had decreased risk for recurrence (HR = 0.03; P = .003) and death (HR = 0.03; P = .003) at time of resection; however, the protective effect of high TSD diminished over time. Patients with a normalized portovenous phase CT tumor enhancement ratio ≥ 0.40 had a longer time to recurrence after resection ( P = .020). Normalized portovenous phase CT tumor enhancement ratio was significantly correlated with TSD ( P = .003). Conclusion Objective quantitative assessment of stroma in PDA revealed several clinically relevant observations. Stroma was less abundant in metastatic PDA, the primary cause of mortality associated with PDA. High stromal content correlated with favorable outcome in patients with resected tumors, implying a protective effect of stroma and suggesting careful consideration of active stromal depletion therapies. Standard, multiphase CT imaging correlated with stroma content and clinical outcome, indicating that noninvasive assessment of stroma is a feasible sensitivity enrichment approach in PDA.
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Pappo, A. S., W. M. Crist, J. Kuttesch, S. Rowe, R. A. Ashmun, H. M. Maurer, W. A. Newton, L. Asmar, X. Luo, and D. N. Shapiro. "Tumor-cell DNA content predicts outcome in children and adolescents with clinical group III embryonal rhabdomyosarcoma. The Intergroup Rhabdomyosarcoma Study Committee of the Children's Cancer Group and the Pediatric Oncology Group." Journal of Clinical Oncology 11, no. 10 (October 1993): 1901–5. http://dx.doi.org/10.1200/jco.1993.11.10.1901.
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PURPOSE The prognostic value of tumor-cell DNA content (ploidy) was evaluated in children with unresectable, nonmetastic rhabdomyosarcoma of embryonal histology. PATIENTS AND METHODS Flow-cytometric techniques were used to estimate the ploidy of tumor specimens from 34 patients with embryonal rhabdomyosarcoma who were enrolled in the intergroup rhabdomyosarcoma study III (IRS III) from 1985 to 1991. Tumors were classified as diploid or hyperdiploid (DNA content, 1.1 to 1.8 times that of normal diploid cells). The influence of ploidy on clinical outcome was assessed by the Kaplan-Meier technique and Cox regression analysis with stepwise selection. RESULTS Twelve of the tumor specimens were diploid and 22 were hyperdiploid. The patient groups defined by diploid or hyperdiploid tumors had similar presenting characteristics (eg, age, tumor size, and anatomic site). Significantly more children with hyperdiploid tumors achieved a complete response than did children with diploid tumors (85% v 42%; P = .01). The probability of progression-free survival at 5 years (+/- SE) was 91% +/- 6% for the hyperdiploid group, compared with 17% +/- 11% for the diploid group (P < .001). Hyperdiploidy was also associated with a significantly higher overall survival rate at 5 years: 96% +/- 4% versus 50% +/- 14% (P = .004). Ploidy retained its prognostic significance after adjustment for tumor site in the Cox regression model. CONCLUSION Tumor-cell ploidy strongly correlates with outcome in children with nonmetastic, unresectable embryonal rhabdomyosarcoma. The two biologically distinct groups identified by this measure would benefit from further refinements in risk-directed therapy.
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Liebig, Marie, Dirk Dannenberger, Brigitte Vollmar, and Kerstin Abshagen. "n-3 PUFAs reduce tumor load and improve survival in a NASH-tumor mouse model." Therapeutic Advances in Chronic Disease 10 (January 2019): 204062231987211. http://dx.doi.org/10.1177/2040622319872118.
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Background: With 9.1% of all cancer deaths, hepatocellular carcinoma is the second leading cause of cancer deaths worldwide. Due to the increasing prevalence of metabolic syndrome, nonalcoholic fatty liver disease (NAFLD) has evolved into a major risk factor for hepatocellular carcinoma development. Herein, we investigated whether a dietary n-3 polyunsaturated fatty acid (PUFA) supplementation improves the outcome of progressive NAFLD. Methods: Feeding three high-fat diets, differing in n-3 and n-6 PUFA contents and ratios (n-3/n-6: 1:8, 1:1, 5:1), the impact of n-3 PUFAs and n-3/n-6 PUFA ratios on NAFLD-related liver fibrosis and tumorigenesis was analyzed in 12- and 20-week-old streptozotocin/high-fat diet (STZ/HFD)-treated mice. Results: Feeding of n-3 PUFA-rich diets (1:1 and 5:1) resulted in increased hepatic n-3 PUFA content and n-3/n-6 PUFA ratio with decreased hepatic lipid accumulation. In 20-week-old mice, n-3 PUFA-rich diets alleviated tumor load significantly, with reduced liver/body weight index, tumor size, and tumor number. Finally, these effects were accompanied by a significant improvement of survival of these mice. Conclusions: Herein, we showed that increased n-3 PUFA content and n-3/n-6 PUFA ratios lead to improved survival and attenuated tumor progression in STZ/HFD-treated mice. Thus, n-3 PUFAs could be the basis for new therapeutic options against NAFLD-related tumorigenesis.
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Song, Yu, Jing Li, Kai Yu Wang, Chun Mei Wang, Wen Yi Fu, and Rui Zhao. "The Anti-Oxidative Effect of CCCS from Acia Water Soluble Corn-Cob in Tumor-Bearing Mice." Applied Mechanics and Materials 675-677 (October 2014): 1674–79. http://dx.doi.org/10.4028/www.scientific.net/amm.675-677.1674.
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Objective To research the relationship between anti-tumor and of corn-cob sulfate polysaccharide in tumor-bearing mice .Methods Xanthosine oxidase and TBA colorimetryr methods were used to assay the contents of blood plasma SOD activities and MDA content. Results CCCS could increased the SOD activity (P<0.05) and decrease MDA (P<0.05) blood plasma of tumor – bearing mice .Conclusion The anti-tumor effect of CCCS may be due to enhanced anti-oxidative capacity in tumor-bearing mice.