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Journal articles on the topic '111201 Cancer Cell Biology'

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Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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1

Muffly, Lori S., Qian Li, Elysia Alvarez, Justine M. Kahn, Lena E. Winestone, Rosemary Cress, Dolly Penn, and Theresa H. M. Keegan. "Hematopoietic Cell Transplantation in First Remission Amongst Adolescent and Young Adult Acute Lymphoblastic Leukemia: A Population-Level Analysis across the United States." Blood 132, Supplement 1 (November 29, 2018): 3965. http://dx.doi.org/10.1182/blood-2018-99-111205.

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Abstract Background: The optimal role of allogeneic hematopoietic cell transplantation (HCT) for adolescents and young adults (AYA) with acute lymphoblastic leukemia (ALL) is an area of clinical debate. In this population-based evaluation of AYA ALL patients across the United States (US), we sought to describe recent patterns of care and outcomes regarding HCT in first complete remission (CR1) amongst AYAs with ALL. Methods: Data were abstracted from the National Cancer Institute Surveillance, Epidemiology, and End Results (SEER) Patterns of Care (POC) study focused on AYA cancers. AYAs (15-39 years) with ALL newly diagnosed between January 1, 2012 through December 31, 2013 and registered in the SEER program were included. Allogeneic HCT in CR1 was defined as occurrence of HCT without relapse/progression prior to the HCT date; HCT was considered a time-dependent variable in survival models. Multivariable logistic regression was used to evaluate associations with HCT in CR1; cox proportional hazards regression was used to evaluate associations with survival. Results: Three-hundred and ninety-nine AYAs (15-39 years) with newly diagnosed ALL between 2012-2013 were included; median follow-up for survival was 19 months (range, 0-35 months). The median age was 24 years; 85% had B-cell ALL, 27% had high risk ALL cytogenetics. One-third of AYA ALL patients received care from pediatric oncologists while two-thirds were treated by adult hematologist/oncologists; a majority (86%) received care at a teaching hospital. Fifty-eight percent received an asparaginase-containing ALL front-line regimen, 32% received hyperCVAD; 5.9% and 4.5% received another/unknown regimens, respectively. One-hundred and two (29%) AYAs underwent allogeneic HCT in CR1. Excluding patients with relapse/progression or death within three months of diagnosis (n=32), older age, high-risk ALL cytogenetics, treatment by an adult hematologist/oncologist, and front-line therapy with hyperCVAD were variables significantly associated (all P< 0.05) with increased odds of HCT in CR1 in univariate analysis, while Hispanic ethnicity and public or no/other insurance were associated with significantly lower odds of HCT in CR1. In multivariate adjusted analysis, only high-risk cytogenetics (odds ratio (OR) 4.84, 95% confidence interval (CI) 2.99-7.83) and receipt of hyperCVAD (OR 1.84, 95% CI 1.07-3.16) retained significant associations with HCT in CR1. The two-year cumulative incidence of relapse, relapse-free survival (RFS), and overall survival (OS) of the entire cohort were 28.3% (95% CI 23.4%-33.4%), 69.3% (95% CI, 63.6%-74.3%), and 84.1% (95% CI 79.7%-87.5%), respectively. Two-year cumulative incidence of relapse was significantly lower in patients receiving HCT in CR1 as opposed to those not receiving HCT in CR1 (15.1%, 95% CI 8.1%-24.1% vs 32.8%, 95% CI 26.9%-38.9%). This translated into a significant improvement in 2-year RFS (83.6%, 95% CI 72.6%-90.5% vs 64.3%, 95% CI 57.5%-70.3%), but no statistically significant differences in 2-year OS (88.9%, 95% CI 80.8%-93.7% vs 82.5%, 95% CI 77.2%-86.7%). Among all patients, receipt of care at a non-teaching hospital (hazard ratio (HR) 2.14, 95% CI 1.22-3.75) and use of another/unknown regimen (HR 9.08, 95% CI, 4.83-17.06) were significantly associated with inferior OS. Conclusions: In the US, allogeneic HCT in CR1 is most commonly administered to AYA ALL with high risk cytogenetics and as consolidation therapy for those who receive front-line hyperCVAD, as opposed to asparaginase-containing ALL regimens. Consistent with prior studies, AYA ALL patients treated at non-teaching hospitals have inferior survival. Although the landscape of ALL therapy is changing, these data provide an important snapshot of the modern state of HCT in CR1 for AYA ALL. Disclosures Muffly: Shire Pharmaceuticals: Research Funding; Adaptive Biotechnologies: Research Funding.
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2

Osman, Afaf, Brian Yu, Nancy Glavin, Tamar S. Polonsky, James K. Liao, and Richard A. Larson. "ABL Tyrosine Kinase Inhibitors (TKIs) Are Associated with Increased Rho-Associated Kinase (ROCK) Activity That May Contribute to Vascular Toxicity in Patients with Chronic Myeloid Leukemia (CML)." Blood 132, Supplement 1 (November 29, 2018): 1739. http://dx.doi.org/10.1182/blood-2018-99-111201.

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Abstract Introduction The use of 2nd or 3rd generation ABL TKIs in patients with CML is associated with vascular toxicity, including peripheral arterial occlusive disease and cardiovascular and cerebrovascular events. However, Imatinib, a 1st generation TKI, has not been shown to increase risk of cardiovascular events (Douxfils J et al. JAMA Oncol 2016;2:625). Therefore, there is a need to identify risk factors and predictors of vascular toxicity for patients receiving these TKIs. In mice, inhibition of the Abl kinases results in activation of Rho and its downstream target Rho kinase (ROCK) (Zandy et al. Proc Natl Acad Sci USA 2007;104:17686). Growing evidence suggests that elevated ROCK activity plays a central role in the pathogenesis of cardiovascular disease and stroke in both animal and clinical studies. TKIs used in CML are potent inhibitors of ABL1 and ABL2 kinases. We hypothesized that CML patients receiving 2nd or 3rd generation BCR/ABL1 TKIs have higher ROCK activity than patients not receiving these TKIs, providing a putative mechanism for the vascular toxicity observed in clinical studies. Methods We measured leukocyte ROCK activity in CML patients and analyzed results based on their last TKI dose. We isolated fresh peripheral blood leukocytes from 38 patients (17 females, 21 males) with a median age of 53 years (range, 24-90 years). 4 patients had newly diagnosed untreated CML at the start of the study. One male was receiving Dasatinib for Ph+ ALL and was also included. ROCK activity was assessed in leukocytes by measuring the ratio of phospho-myosin-binding subunit (p-MBS) on myosin light-chain phosphatase, a downstream target of ROCK, to total MBS using an automated Western blotting system (Wes, ProteinSimple, San Jose, CA) (Hata T et al. Atherosclerosis 2011; 214:117). Each patient had 1-6 measurements of leukocyte ROCK activity over 1 - 18 months (n=78 measurements). Information about cardiovascular risk factors, concomitant medications, CML status, and total duration of TKI therapy was collected. For patients with multiple samples over time, ROCK activity was calculated as the mean of all samples taken while receiving the same TKI. Patients in treatment-free remission (TFR) were considered off-TKI, but those in TFR < 1 month were excluded from the analysis to reduce potential confounding effects. Results We analyzed blood samples from 4 untreated CML patients, 8 while in TFR, and 31 who were actively receiving one of the 5 TKIs (7 Imatinib, 12 Dasatinib, 9 Nilotinib, 2 Ponatinib, 1 Bosutinib). 3 patients developed acute coronary syndrome during the study and required coronary revascularization for myocardial infarction. We found no significant difference in ROCK activity when comparing all patients receiving TKIs to those not receiving TKIs. However, we found higher leukocyte ROCK activity when comparing all patients receiving 2nd and 3rd generation TKIs to those not receiving any TKI (Welch's t test, mean leukocyte ROCK activity 1.00 ± 0.06 vs 0.80 ± 0.06; p=0.03). We also found higher leukocyte ROCK activity when comparing patients receiving Dasatinib to patients receiving Imatinib (mean leukocyte ROCK activity 1.05 ± 0.09 vs 0.75 ± 0.10; p=0.04). The comparison of Imatinib to all 2nd and 3rd generation TKIs was not significant (p=0.06). Conclusions We found that patients on 2nd and 3rd generation TKIs have higher leukocyte ROCK activity compared to those not receiving TKIs, and higher leukocyte ROCK activity in patients on Dasatinib compared with patients receiving Imatinib. These results are consistent with the known lower-risk of cardiovascular side-effects observed with Imatinib in comparison to the next generation ABL TKIs. Limitations include small sample size and heterogeneity in the patient population in terms of age, cardiovascular risk factors, specific TKI used, and total duration and sequencing of TKI agents. The study continues to accrue CML subjects in order to follow individual patients over time on TKI therapy. Disclosures Larson: Ariad/Takeda: Consultancy, Research Funding; BristolMyers Squibb: Consultancy, Research Funding; Novartis: Consultancy, Research Funding; Pfizer: Consultancy, Research Funding.
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3

Zelenkova, N. P. "Cancer cell biology." Kazan medical journal 43, no. 6 (October 19, 2021): 74–76. http://dx.doi.org/10.17816/kazmj83368.

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4

Bebber, Christina M., Fabienne Müller, Laura Prieto Clemente, Josephine Weber, and Silvia von Karstedt. "Ferroptosis in Cancer Cell Biology." Cancers 12, no. 1 (January 9, 2020): 164. http://dx.doi.org/10.3390/cancers12010164.

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A major hallmark of cancer is successful evasion of regulated forms of cell death. Ferroptosis is a recently discovered type of regulated necrosis which, unlike apoptosis or necroptosis, is independent of caspase activity and receptor-interacting protein 1 (RIPK1) kinase activity. Instead, ferroptotic cells die following iron-dependent lipid peroxidation, a process which is antagonised by glutathione peroxidase 4 (GPX4) and ferroptosis suppressor protein 1 (FSP1). Importantly, tumour cells escaping other forms of cell death have been suggested to maintain or acquire sensitivity to ferroptosis. Therefore, therapeutic exploitation of ferroptosis in cancer has received increasing attention. Here, we systematically review current literature on ferroptosis signalling, cross-signalling to cellular metabolism in cancer and a potential role for ferroptosis in tumour suppression and tumour immunology. By summarising current findings on cell biology relevant to ferroptosis in cancer, we aim to point out new conceptual avenues for utilising ferroptosis in systemic treatment approaches for cancer.
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5

Colaco, Camilo A. L. S. "Cancer immunotherapy: simply cell biology?" Trends in Molecular Medicine 9, no. 12 (December 2003): 515–16. http://dx.doi.org/10.1016/j.molmed.2003.10.006.

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6

Ray, L. B. "Cancer Cell Vulnerability." Science Signaling 4, no. 202 (December 6, 2011): ec338-ec338. http://dx.doi.org/10.1126/scisignal.4202ec338.

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7

Kroemer, Guido. "Tetraploid cancer cell precursors." Nature Reviews Molecular Cell Biology 11, no. 8 (June 23, 2010): 539. http://dx.doi.org/10.1038/nrm2924.

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8

Momeny, Majid, Tiina Arsiola, and Jukka Westermarck. "Cancer stem cell phosphatases." Biochemical Journal 478, no. 14 (July 28, 2021): 2899–920. http://dx.doi.org/10.1042/bcj20210254.

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Cancer stem cells (CSCs) are involved in the initiation and progression of human malignancies by enabling cancer tissue self-renewal capacity and constituting the therapy-resistant population of tumor cells. However, despite the exhausting characterization of CSC genetics, epigenetics, and kinase signaling, eradication of CSCs remains an unattainable goal in most human malignancies. While phosphatases contribute equally with kinases to cellular phosphoregulation, our understanding of phosphatases in CSCs lags severely behind our knowledge about other CSC signaling mechanisms. Many cancer-relevant phosphatases have recently become druggable, indicating that further understanding of the CSC phosphatases might provide novel therapeutic opportunities. This review summarizes the current knowledge about fundamental, but yet poorly understood involvement of phosphatases in the regulation of major CSC signaling pathways. We also review the functional roles of phosphatases in CSC self-renewal, cancer progression, and therapy resistance; focusing particularly on hematological cancers and glioblastoma. We further discuss the small molecule targeting of CSC phosphatases and their therapeutic potential in cancer combination therapies.
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9

Ray, L. B. "Fueling the Cancer Cell." Science Signaling 3, no. 122 (May 18, 2010): ec153-ec153. http://dx.doi.org/10.1126/scisignal.3122ec153.

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10

Nishino, Hiroshi. "Interleukin-6 affects cancer cell biology." Journal of Japan Society of Immunology & Allergology in Otolaryngology 34, no. 1 (2016): 13–18. http://dx.doi.org/10.5648/jjiao.34.13.

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11

Haake, Scott, and W. Kimryn Rathmell. "The Biology of Renal Cell Cancer." Emerging Cancer Therapeutics 2, no. 1 (April 1, 2011): 1–19. http://dx.doi.org/10.5003/2151-4194.2.1.1.

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12

Johnson, Bruce E., and Michael J. Kelley. "Biology of small cell lung cancer." Lung Cancer 12 (June 1995): S5—S16. http://dx.doi.org/10.1016/s0169-5002(10)80014-5.

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13

Carney, D. N. "Biology of small-cell lung cancer." Lancet 339, no. 8797 (April 1992): 843–46. http://dx.doi.org/10.1016/0140-6736(92)90286-c.

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14

Vega, Francisco M., and Anne J. Ridley. "Rho GTPases in cancer cell biology." FEBS Letters 582, no. 14 (May 5, 2008): 2093–101. http://dx.doi.org/10.1016/j.febslet.2008.04.039.

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15

Whiteside, Theresa L., and Christine Odoux. "Dendritic cell biology and cancer therapy." Cancer Immunology, Immunotherapy 53, no. 3 (March 1, 2004): 240–48. http://dx.doi.org/10.1007/s00262-003-0468-6.

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16

Campisi, Judith. "Aging and cancer cell biology, 2007." Aging Cell 6, no. 3 (June 2007): 261–63. http://dx.doi.org/10.1111/j.1474-9726.2007.00292.x.

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17

Campisi, Judith. "Aging and cancer cell biology, 2008." Aging Cell 7, no. 3 (June 2008): 281–84. http://dx.doi.org/10.1111/j.1474-9726.2008.00383.x.

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18

Campisi, Judith, and Paul Yaswen. "Aging and cancer cell biology, 2009." Aging Cell 8, no. 3 (May 26, 2009): 221–25. http://dx.doi.org/10.1111/j.1474-9726.2009.00475.x.

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19

Gazdar, Adi F. "Cell biology and molecular biology of small cell and non-small cell lung cancer." Current Opinion in Oncology 2, no. 2 (April 1990): 321–27. http://dx.doi.org/10.1097/00001622-199004000-00013.

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20

Borovski, Tijana, Louis Vermeulen, Martin R. Sprick, and Jan Paul Medema. "One renegade cancer stem cell?" Cell Cycle 8, no. 6 (March 15, 2009): 803–8. http://dx.doi.org/10.4161/cc.8.6.7935.

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21

Myung, Kyungjae. "Targeting the cancer cell state." Cell Cycle 14, no. 15 (July 7, 2015): 2385–86. http://dx.doi.org/10.1080/15384101.2015.1063294.

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22

Tang, Bor Luen, and Ee Ling Ng. "Rabs and cancer cell motility." Cell Motility and the Cytoskeleton 66, no. 7 (July 2009): 365–70. http://dx.doi.org/10.1002/cm.20376.

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23

Xia, Pu, and Da-Hua Liu. "Cancer stem cell markers for liver cancer and pancreatic cancer." Stem Cell Research 60 (April 2022): 102701. http://dx.doi.org/10.1016/j.scr.2022.102701.

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24

Morrison, Sean J. "Stem cell self-renewal, cancer cell proliferation, and aging." Developmental Biology 295, no. 1 (July 2006): 330. http://dx.doi.org/10.1016/j.ydbio.2006.04.031.

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25

Zahn, L. M. "Cancer at Single-Cell Resolution." Science Signaling 7, no. 331 (June 24, 2014): ec174-ec174. http://dx.doi.org/10.1126/scisignal.2005613.

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26

Prabakaran, S. "BMP2 decides cancer cell fate." Science Signaling 8, no. 408 (December 22, 2015): ec379-ec379. http://dx.doi.org/10.1126/scisignal.aaf1131.

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27

Onuma, Michiko, Jeffrey D. Bub, Thomas L. Rummel, and Yoshiki Iwamoto. "Prostate Cancer Cell-Adipocyte Interaction." Journal of Biological Chemistry 278, no. 43 (August 5, 2003): 42660–67. http://dx.doi.org/10.1074/jbc.m304984200.

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28

Fu, Ping, Julian A. Thompson, and Leon A. Bach. "Promotion of Cancer Cell Migration." Journal of Biological Chemistry 282, no. 31 (May 22, 2007): 22298–306. http://dx.doi.org/10.1074/jbc.m703066200.

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29

Kan, Jean S., Gregory S. DeLassus, Kenneth G. D'Souza, Stanley Hoang, Rajeev Aurora, and George L. Eliceiri. "Modulators of cancer cell invasiveness." Journal of Cellular Biochemistry 111, no. 4 (July 30, 2010): 791–96. http://dx.doi.org/10.1002/jcb.22794.

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30

Ford, Heide L., and Arthur B. Pardee. "Cancer and the cell cycle." Journal of Cellular Biochemistry 75, S32 (1999): 166–72. http://dx.doi.org/10.1002/(sici)1097-4644(1999)75:32+<166::aid-jcb20>3.0.co;2-j.

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31

Zheng, Yinan, Yusha Sun, Gonzalo Torga, Kenneth Pienta, and Robert Austin. "Game Theory Cancer Models of Cancer Cell-Stromal Cell Dynamics using Interacting Particle Systems." Biophysical Reviews and Letters 15, no. 03 (August 8, 2020): 171–93. http://dx.doi.org/10.1142/s1793048020500058.

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We describe an evolutionary game theory model that has been used to predict the population dynamics of interacting cancer and stromal cells. We first consider the mean field case assuming homogeneous and nondiscrete populations. Interacting Particle Systems (IPS) are then presented as a discrete and spatial alternative to the mean field approach. Finally, we discuss cases where IPS gives results different from the mean field approach.
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32

Leal-Esteban, Lucia C., and Lluis Fajas. "Cell cycle regulators in cancer cell metabolism." Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease 1866, no. 5 (May 2020): 165715. http://dx.doi.org/10.1016/j.bbadis.2020.165715.

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33

Liu, Hai G., Jie You, Yi F. Pan, Xiao Q. Hu, Du P. Huang, and Xiao Hua Zhang. "Cancer Stem Cell Hierarchy." Stem Cell Reviews and Reports 5, no. 2 (January 7, 2009): 174. http://dx.doi.org/10.1007/s12015-008-9049-6.

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34

Yamasaki, Lili, and Michele Pagano. "Cell cycle, proteolysis and cancer." Current Opinion in Cell Biology 16, no. 6 (December 2004): 623–28. http://dx.doi.org/10.1016/j.ceb.2004.08.005.

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35

Trajkovska, Maria. "Macropinocytosis supports cancer cell proliferation." Nature Cell Biology 15, no. 7 (July 2013): 729. http://dx.doi.org/10.1038/ncb2809.

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36

de Sousa e Melo, Felipe, and Louis Vermeulen. "Wnt Signaling in Cancer Stem Cell Biology." Cancers 8, no. 7 (June 27, 2016): 60. http://dx.doi.org/10.3390/cancers8070060.

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37

Al-Marsoummi, Sarmad, Emilie E. Vomhof-DeKrey, and Marc D. Basson. "Schlafens: Emerging Proteins in Cancer Cell Biology." Cells 10, no. 9 (August 29, 2021): 2238. http://dx.doi.org/10.3390/cells10092238.

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Schlafens (SLFN) are a family of genes widely expressed in mammals, including humans and rodents. These intriguing proteins play different roles in regulating cell proliferation, cell differentiation, immune cell growth and maturation, and inhibiting viral replication. The emerging evidence is implicating Schlafens in cancer biology and chemosensitivity. Although Schlafens share common domains and a high degree of homology, different Schlafens act differently. In particular, they show specific and occasionally opposing effects in some cancer types. This review will briefly summarize the history, structure, and non-malignant biological functions of Schlafens. The roles of human and mouse Schlafens in different cancer types will then be outlined. Finally, we will discuss the implication of Schlafens in the anti-tumor effect of interferons and the use of Schlafens as predictors of chemosensitivity.
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38

Kranenburg, Onno, Benjamin L. Emmink, Jaco Knol, Winan J. van Houdt, Inne HM Borel Rinkes, and Connie R. Jimenez. "Proteomics in studying cancer stem cell biology." Expert Review of Proteomics 9, no. 3 (June 2012): 325–36. http://dx.doi.org/10.1586/epr.12.24.

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39

Kuo, Joe Chin-Hun, Jay G. Gandhi, Roseanna N. Zia, and Matthew J. Paszek. "Physical biology of the cancer cell glycocalyx." Nature Physics 14, no. 7 (July 2018): 658–69. http://dx.doi.org/10.1038/s41567-018-0186-9.

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40

Zafiropoulos, Alexandros, and George N. Tzanakakis. "Decorin-Mediated Effects in Cancer Cell Biology." Connective Tissue Research 49, no. 3-4 (January 2008): 244–48. http://dx.doi.org/10.1080/03008200802147746.

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41

Fahed, Elie, Donna E. Hansel, Derek Raghavan, David I. Quinn, and Tanya B. Dorff. "Small Cell Bladder Cancer: Biology and Management." Seminars in Oncology 39, no. 5 (October 2012): 615–18. http://dx.doi.org/10.1053/j.seminoncol.2012.08.009.

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42

Gough, Nancy R. "Focus Issue: Cell biology meets cancer therapy." Science Signaling 9, no. 415 (February 16, 2016): eg2-eg2. http://dx.doi.org/10.1126/scisignal.aaf3386.

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43

Yamada, Yasuhiro. "Dissecting cancer biology with iPS cell technology." Proceedings for Annual Meeting of The Japanese Pharmacological Society WCP2018 (2018): SY46–4. http://dx.doi.org/10.1254/jpssuppl.wcp2018.0_sy46-4.

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44

Stahel, Rolf A., and Erich Weber. "Small cell lung cancer: The new biology." Seminars in Radiation Oncology 5, no. 1 (January 1995): 11–18. http://dx.doi.org/10.1016/s1053-4296(05)80004-9.

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45

Chakravarti, Deboki, and Wilson W. Wong. "Synthetic biology in cell-based cancer immunotherapy." Trends in Biotechnology 33, no. 8 (August 2015): 449–61. http://dx.doi.org/10.1016/j.tibtech.2015.05.001.

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46

Xie, Nan, and Marie-Odile Parat. "Opioid Analgesic Agents and Cancer Cell Biology." Current Anesthesiology Reports 5, no. 3 (September 2015): 278–84. http://dx.doi.org/10.1007/s40140-015-0118-5.

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47

Donaldson, Timothy D., and Robert J. Duronio. "Cancer Cell Biology: Myc Wins the Competition." Current Biology 14, no. 11 (June 2004): R425—R427. http://dx.doi.org/10.1016/j.cub.2004.05.035.

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48

Mills, Anthony D., and Lesley Morris. "From basic cell biology to cancer screening." Trends in Cell Biology 9, no. 10 (October 1999): 418. http://dx.doi.org/10.1016/s0962-8924(99)01623-2.

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49

Sánchez-García, Isidro. "Understanding telomerase in cancer stem cell biology." Cell Cycle 11, no. 8 (April 15, 2012): 1479–80. http://dx.doi.org/10.4161/cc.20108.

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50

Smyth, John F. "Cancer Genetics and Cell and Molecular Biology." Chest 109, no. 5 (May 1996): 125S—129S. http://dx.doi.org/10.1378/chest.109.5_supplement.125s.

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