Relevant bibliographies by topics / Cancer cell fitness

Contents

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

Academic literature on the topic 'Cancer cell fitness'

Author: Grafiati
Published: 30 November 2024

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Cancer cell fitness.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Cancer cell fitness"

1

Bittman, Kevin S. "Immune Cell Metabolic Fitness for Life." Antibodies 11, no. 2 (April 30, 2022): 32. http://dx.doi.org/10.3390/antib11020032.

Full text
Abstract:
Adoptive cell therapy holds great promise for treating a myriad of diseases, especially cancer. Within the last decade, immunotherapy has provided a significant leap in the successful treatment of leukemia. The research conducted throughout this period to understand the interrelationships between cancer cells and infiltrating immune cells winds up having one very common feature, bioenergetics. Cancer cells and immune cells both need ATP to perform their individual functions and cancer cells have adopted means to limit immune cell activity via changes in immune cell bioenergetics that redirect immune cell behavior to encourage tumor growth. Current leading strategies for cancer treatment super-charge an individual’s own immune cells against cancer. Successful Chimeric Antigen Receptor T Cells (CAR T) target pathways that ultimately influence bioenergetics. In the last decade, scientists identified that mitochondria play a crucial role in T cell physiology. When modifying T cells to create chimeras, a unique mitochondrial fitness emerges that establishes stemness and persistence. This review highlights many of the key findings leading to this generation’s CAR T treatments and the work currently being done to advance immunotherapy, to empower not just T cells but other immune cells as well against a variety of cancers.
APA, Harvard, Vancouver, ISO, and other styles
2

Derbal, Youcef. "Cell Adaptive Fitness and Cancer Evolutionary Dynamics." Cancer Informatics 22 (January 2023): 117693512311546. http://dx.doi.org/10.1177/11769351231154679.

Full text
Abstract:
Genome instability of cancer cells translates into increased entropy and lower information processing capacity, leading to metabolic reprograming toward higher energy states, presumed to be aligned with a cancer growth imperative. Dubbed as the cell adaptive fitness, the proposition postulates that the coupling between cell signaling and metabolism constrains cancer evolutionary dynamics along trajectories privileged by the maintenance of metabolic sufficiency for survival. In particular, the conjecture postulates that clonal expansion becomes restricted when genetic alterations induce a sufficiently high level of disorder, that is, high entropy, in the regulatory signaling network, abrogating as a result the ability of cancer cells to successfully replicate, leading to a stage of clonal stagnation. The proposition is analyzed in the context of an in-silico model of tumor evolutionary dynamics to illustrate how cell-inherent adaptive fitness may predictably constrain clonal evolution of tumors, which would have significant implications for the design of adaptive cancer therapies.
APA, Harvard, Vancouver, ISO, and other styles
3

Skums, Pavel, Viachaslau Tsyvina, and Alex Zelikovsky. "Inference of clonal selection in cancer populations using single-cell sequencing data." Bioinformatics 35, no. 14 (July 2019): i398—i407. http://dx.doi.org/10.1093/bioinformatics/btz392.

Full text
Abstract:
Abstract Summary Intra-tumor heterogeneity is one of the major factors influencing cancer progression and treatment outcome. However, evolutionary dynamics of cancer clone populations remain poorly understood. Quantification of clonal selection and inference of fitness landscapes of tumors is a key step to understanding evolutionary mechanisms driving cancer. These problems could be addressed using single-cell sequencing (scSeq), which provides an unprecedented insight into intra-tumor heterogeneity allowing to study and quantify selective advantages of individual clones. Here, we present Single Cell Inference of FItness Landscape (SCIFIL), a computational tool for inference of fitness landscapes of heterogeneous cancer clone populations from scSeq data. SCIFIL allows to estimate maximum likelihood fitnesses of clone variants, measure their selective advantages and order of appearance by fitting an evolutionary model into the tumor phylogeny. We demonstrate the accuracy our approach, and show how it could be applied to experimental tumor data to study clonal selection and infer evolutionary history. SCIFIL can be used to provide new insight into the evolutionary dynamics of cancer. Availability and implementation Its source code is available at https://github.com/compbel/SCIFIL.
APA, Harvard, Vancouver, ISO, and other styles
4

Giannarelli, Chiara. "Loss of TET2 boosts cell fitness." Science Translational Medicine 12, no. 553 (July 22, 2020): eabd3619. http://dx.doi.org/10.1126/scitranslmed.abd3619.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

George, Bijesh, P. Mukundan Pillai, Aswathy Mary Paul, Revikumar Amjesh, Kim Leitzel, Suhail M. Ali, Oleta Sandiford, et al. "Cellular Fitness Phenotypes of Cancer Target Genes from Oncobiology to Cancer Therapeutics." Cells 10, no. 2 (February 18, 2021): 433. http://dx.doi.org/10.3390/cells10020433.

Full text
Abstract:
To define the growing significance of cellular targets and/or effectors of cancer drugs, we examined the fitness dependency of cellular targets and effectors of cancer drug targets across human cancer cells from 19 cancer types. We observed that the deletion of 35 out of 47 cellular effectors and/or targets of oncology drugs did not result in the expected loss of cell fitness in appropriate cancer types for which drugs targeting or utilizing these molecules for their actions were approved. Additionally, our analysis recognized 43 cellular molecules as fitness genes in several cancer types in which these drugs were not approved, and thus, providing clues for repurposing certain approved oncology drugs in such cancer types. For example, we found a widespread upregulation and fitness dependency of several components of the mevalonate and purine biosynthesis pathways (currently targeted by bisphosphonates, statins, and pemetrexed in certain cancers) and an association between the overexpression of these molecules and reduction in the overall survival duration of patients with breast and other hard-to-treat cancers, for which such drugs are not approved. In brief, the present analysis raised cautions about off-target and undesirable effects of certain oncology drugs in a subset of cancers where the intended cellular effectors of drug might not be good fitness genes and that this study offers a potential rationale for repurposing certain approved oncology drugs for targeted therapeutics in additional cancer types.
APA, Harvard, Vancouver, ISO, and other styles
6

Ferrari, Adam James, Ronny Drapkin, and Rajan Gogna. "Cell Fitness: More Than Push-Ups." International Journal of Molecular Sciences 22, no. 2 (January 7, 2021): 518. http://dx.doi.org/10.3390/ijms22020518.

Full text
Abstract:
Cell competition (CC) is a feature that allows tumor cells to outcompete and eliminate adjacent cells that are deemed less fit. Studies of CC, first described in Drosophila melanogaster, reveal a diversity of underlying mechanisms. In this review, we will discuss three recent studies that expand our understanding of the molecular features governing CC. In particular, we will focus on a molecular fitness fingerprint, oncogenic pathways, and the importance of cell junction stability. A fitness fingerprint, mediated by flower (hFWE) protein isoforms, dictates that cells expressing the flower-win isoforms will outcompete adjacent flower-loss-expressing cells. The impact of the flower protein isoforms is seen in cancer progression and may have diagnostic potential. The yes-associated protein (YAP) and TAZ transcription factors, central mediators of the oncogenic Hippo pathway, elevate peritumoral fitness thereby protecting against tumor progression and provide a suppressive barrier. Similarly, COL17A1 is a key component in hemidesmosome stability, and its expression in epidermal stem cells contributes to fitness competition and aging characteristics. The contributions of these pathways to disease development and progression will help define how CC is hijacked to favor cancer growth. Understanding these features will also help frame the diagnostic and therapeutic possibilities that may place CC in the crosshairs of cancer therapeutics.
APA, Harvard, Vancouver, ISO, and other styles
7

Lawlor, Katerina, Salvador Pérez-Montero, Ana Lima, and Tristan A. Rodríguez. "Transcriptional versus metabolic control of cell fitness during cell competition." Seminars in Cancer Biology 63 (June 2020): 36–43. http://dx.doi.org/10.1016/j.semcancer.2019.05.010.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Nunney, Leonard, and Kevin Thai. "Determining cancer risk: the evolutionary multistage model or total stem cell divisions?" Proceedings of the Royal Society B: Biological Sciences 287, no. 1941 (December 16, 2020): 20202291. http://dx.doi.org/10.1098/rspb.2020.2291.

Full text
Abstract:
A recent hypothesis proposed that the total number of stem cell divisions in a tissue (TSCD model) determine its intrinsic cancer risk; however, a different model—the multistage model—has long been used to understand how cancer originates. Identifying the correct model has important implications for interpreting the frequency of cancers. Using worldwide cancer incidence data, we applied three tests to the TSCD model and an evolutionary multistage model of carcinogenesis (EMMC), a model in which cancer suppression is recognized as an evolving trait, with natural selection acting to suppress cancers causing a significant mean loss of Darwinian fitness. Each test supported the EMMC but contradicted the TSCD model. This outcome undermines results based on the TSCD model quantifying the relative importance of ‘bad luck' (the random accumulation of somatic mutations) versus environmental and genetic factors in determining cancer incidence. Our testing supported the EMMC prediction that cancers of large rapidly dividing tissues predominate late in life. Another important prediction is that an indicator of recent oncogenic environmental change is an unusually high mean fitness loss due to cancer, rather than a high lifetime incidence. The evolutionary model also predicts that large and/or long-lived animals have evolved mechanisms of cancer suppression that may be of value in preventing or controlling human cancers.
APA, Harvard, Vancouver, ISO, and other styles
9

Jiang, Xiaowei, and Ian P. M. Tomlinson. "Why is cancer not more common? A changing microenvironment may help to explain why, and suggests strategies for anti-cancer therapy." Open Biology 10, no. 4 (April 2020): 190297. http://dx.doi.org/10.1098/rsob.190297.

Full text
Abstract:
One of the great unsolved puzzles in cancer biology is not why cancers occur, but rather explaining why so few cancers occur compared with the theoretical number that could occur, given the number of progenitor cells in the body and the normal mutation rate. We hypothesized that a contributory explanation is that the tumour microenvironment (TME) is not fixed due to factors such as immune cell infiltration, and that this could impair the ability of neoplastic cells to retain a high enough fitness to become a cancer. The TME has implicitly been assumed to be static in most cancer evolution models, and we therefore developed a mathematical model of spatial cancer evolution assuming that the TME, and thus the optimum cancer phenotype, changes over time. Based on simulations, we show how cancer cell populations adapt to diverse changing TME conditions and fitness landscapes. Compared with static TMEs, which generate neutral dynamics, changing TMEs lead to complex adaptations with characteristic spatio-temporal heterogeneity involving variable fitness effects of driver mutations, subclonal mixing, subclonal competition and phylogeny patterns. In many cases, cancer cell populations fail to grow or undergo spontaneous regression, and even extinction. Our analyses predict that cancer evolution in a changing TME is challenging, and can help to explain why cancer is neither inevitable nor as common as expected. Should cancer driver mutations with effects dependent of the TME exist, they are likely to be selected. Anti-cancer prevention and treatment strategies based on changing the TME are feasible and potentially effective.
APA, Harvard, Vancouver, ISO, and other styles
10

Rozhok, Andrii I., and James DeGregori. "Toward an evolutionary model of cancer: Considering the mechanisms that govern the fate of somatic mutations." Proceedings of the National Academy of Sciences 112, no. 29 (July 21, 2015): 8914–21. http://dx.doi.org/10.1073/pnas.1501713112.

Full text
Abstract:
Our understanding of cancer has greatly advanced since Nordling [Nordling CO (1953) Br J Cancer 7(1):68–72] and Armitage and Doll [Armitage P, Doll R (1954) Br J Cancer 8(1):1–12] put forth the multistage model of carcinogenesis. However, a number of observations remain poorly understood from the standpoint of this paradigm in its contemporary state. These observations include the similar age-dependent exponential rise in incidence of cancers originating from stem/progenitor pools differing drastically in size, age-dependent cell division profiles, and compartmentalization. This common incidence pattern is characteristic of cancers requiring different numbers of oncogenic mutations, and it scales to very divergent life spans of mammalian species. Also, bigger mammals with larger underlying stem cell pools are not proportionally more prone to cancer, an observation known as Peto’s paradox. Here, we present a number of factors beyond the occurrence of oncogenic mutations that are unaccounted for in the current model of cancer development but should have significant impacts on cancer incidence. Furthermore, we propose a revision of the current understanding for how oncogenic and other functional somatic mutations affect cellular fitness. We present evidence, substantiated by evolutionary theory, demonstrating that fitness is a dynamic environment-dependent property of a phenotype and that oncogenic mutations should have vastly different fitness effects on somatic cells dependent on the tissue microenvironment in an age-dependent manner. Combined, this evidence provides a firm basis for understanding the age-dependent incidence of cancers as driven by age-altered systemic processes regulated above the cell level.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "Cancer cell fitness"

1

Rutledge, Samuel Drew. "Investigating aneuploidy's role in cancer cell fitness under various conditions of stress." Thesis, Virginia Tech, 2015. http://hdl.handle.net/10919/56481.

Full text
Abstract:
The gain or loss of whole chromosomes, known as aneuploidy, is a distinguishing feature of cancer cells. The rapid gain or loss of hundreds of genes dramatically alters a cell's genomic landscape and is typically detrimental to cell survival under normal conditions. However, cancer cells display enhanced proliferation and overcome multiple conditions of stress, suggesting aneuploidy may increase cellular fitness. Furthermore, distinct patterns of aneuploidy are found in cancers from different anatomical sites. Despite these observations, scant research has sought to examine the role of aneuploidy in cancer, or determine whether aneuploidy is a driver or passenger mutation, or why certain aneuploidies appear to be selected for and others against. To investigate the role of aneuploidy in cancer cell fitness, we utilized the diploid colorectal cancer (CRC) cell line DLD1 and two trisomic variants carrying an extra copy of either chromosome 7 or chromosome 13, two trisomies frequently seen in colorectal cancer. To assess fitness, we compared proliferation, anchorage-independence, and invasiveness in aneuploid CRC cells versus their diploid counterpart when grown under various culture conditions, including regular media, serum-free media, cytotoxic drug-containing media, and hypoxia. We found that aneuploid cells proliferated better than diploid cells under all but standard culture conditions. Moreover, regardless of growth condition, we found that aneuploid CRC cells formed larger and more numerous colonies in soft agar (anchorage-independent growth), and displayed greater invasiveness (assessed by matrigel invasion assay). Taken together, these results indicate that aneuploidy enhances the fitness of CRC cells under stressful conditions that are likely to occur in the tumor microenvironment.
Master of Science
APA, Harvard, Vancouver, ISO, and other styles
2

Thareja, Gaurav. "Mapping the adaptive landscape of cancer cells using a multiomics approach." Electronic Thesis or Diss., université Paris-Saclay, 2024. http://www.theses.fr/2024UPASL075.

Full text
Abstract:
Le cancer est considéré principalement comme une maladie de la cellule. Certaines cellules cancéreuses acquièrent un avantage adaptatif sous la pression sélective d’un microenvironnement dynamique qui leur permet de surpasser les autres cellules cancéreuses, favorisant leur expansion. Par conséquent, ce travail de thèse vise à cartographier le paysage adaptatif des cellules cancéreuses à l’aide d’une approche multiomique.L’étude d’association pangénomique a montré l’effet des mutations germinales sur les niveaux d’expression 64 protéines cancéreuses listées dans OncoKB et a permis l’identification de 17 oncogènes thérapeutiquement exploitables. J'ai en outre démontré que différentes conditions de co-culture conduisait à l'activation et à l'inhibition de voies de signalisation dans la cellule cancéreuse qui les aident à s’adapter à des niches spécifiques. Enfin, ces cellules cancéreuses peuvent moduler des signaux extrinsèques dans les ganglions sentinelles qui conduisent à l'acquisition de nouvelles propriétés métastatiques. Ces études montrent globalement le caractère adaptatif et la trajectoire évolutive des cellules cancéreuses
Cancer is considered primarily a disease of the cell. Some cancer cells gain an adaptive advantage under the selective pressure of a dynamic microenvironment that allows them to outcompete other cancer cells, promoting their expansion. Therefore, this thesis aims to map cancer cells' adaptive landscape using a multiomics approach. The genome-wide association study showed the effect of germline mutations on the expression levels of 64 cancer proteins listed in OncoKB and allowed the identification of 17 therapeutically exploitable oncogenes. I further demonstrated that different co-culture conditions led to activating and inhibiting signaling pathways in the cancer cells that help them adapt to specific niches. Finally, these cancer cells can modulate extrinsic signals in sentinel lymph nodes that lead to the acquisition of new metastatic properties. These studies generally show the adaptive nature and evolutionary trajectory of cancer cells
APA, Harvard, Vancouver, ISO, and other styles
3

Hayes, Sandra C. "Exercise, functional capacity and quality of life in peripheral blood stem cell transplant patients." Thesis, Queensland University of Technology, 2001. https://eprints.qut.edu.au/36758/7/36758_Digitised%20Thesis.pdf.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Books on the topic "Cancer cell fitness"

1

Blagosklonny, Mikhail V. Cell cycle checkpoints and cancer. Georgetown, Tex: Landes Bioscience, 2001.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
2

1936-, Waxman Samuel, Rossi G. B, Takaku Fumimaro, Conference on Differentiation Therapy (2nd : 1987 : Bermuda Islands), and Conference on Differentiation Therapy (4th : 1990 : Chiba-ken, Japan), eds. The Status of differentiation therapy of cancer. New York: Raven Press, 1988.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
3

Agnew, Karen L. Skin cancer. Oxford: Health Press, 2005.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
4

Maldonado, Jonathon G., and Mikayla K. Cervantes. Small cell carcinomas: Causes, diagnosis and treatment. New York: Nova Biomedical Books, 2009.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
5

MD, Giordano Antonio, and Soprano Kenneth J, eds. Cell cycle inhibitors in cancer therapy: Current strategies. Totowa, N.J: Humana Press, 2003.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
6

H, Goldfarb Ronald, ed. Fundamental aspects of cancer. Dordrecht: Kluwer Academic Publishers, 1989.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
7

Raghavan, Derek. Germ cell tumors. Hamilton [Ont.]: BC Decker, 2003.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
8

Parker, James N., and Philip M. Parker. The official patient's sourcebook on plasma cell neoplasms. San Diego, Calif: ICON Health Publications, 2003.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
9

Karen, Bellenir, ed. Cancer sourcebook: Basic consumer health information about major forms and stages of cancer, featuring facts about head and neck cancers, lung cancers, gastrointestinal cancers, genitourinary cancers, lymphomas, blood cell cancers, endocrine cancers, skin cancers, bone cancers, metastatic cancers, and more; along with facts about cancer treatments, cancer risks and prevention, a glossary of related terms, statistical data, and a directory of resources for additional information. 5th ed. Detroit, MI: Omnigraphics, 2007.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
10

Parker, Philip M., and James N. Parker. Basal cell carcinoma: A medical dictionary, bibliography, and annotated research guide to internet references. San Diego, CA: ICON Health Publications, 2004.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Book chapters on the topic "Cancer cell fitness"

1

Szturz, Petr, and Jan B. Vermorken. "Systemic Treatment Sequencing and Prediction of First-line Therapy Outcomes in Recurrent or Metastatic Head and Neck Cancer." In Critical Issues in Head and Neck Oncology, 199–215. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-23175-9_13.

Full text
Abstract:
AbstractIn the palliative management of patients with recurrent and/or metastatic squamous cell carcinoma of the head and neck who are not candidates for a complete resection or full-dose radiotherapy, systemic treatment has seen important advances over the past several decades. In general, there are six major factors impacting on the decision-making process. Four of them belong to a class of continuous functions and include overall health status (from fitness to frailty), disease burden (from high to low), pace of the disease (from fast to slow), and expression of programmed-death ligand 1 (PD-L1, from high to low). In addition, there are two categorical variables including disease site (e.g., locoregional recurrence versus metastatic) and platinum-sensitivity or resistance depending on disease-free interval after previous platinum-based therapy with a usual cut-off of 6 months. Taking into account these six factors and local drug policies, healthcare professionals opt either for 1) chemotherapy with or without cetuximab or 2) immunotherapy with or without chemotherapy. In platinum-sensitive cases, level I evidence based on data from the EXTREME and Keynote-048 randomized trials supports the use of the following three regimens. Biochemotherapy combining platinum, 5-fluorouracil, and cetuximab (the so-called EXTREME regimen) is suitable for fit patients with low PD-L1 expression measured as combined positive score (CPS). Higher CPS is predictive for improved overall survival when replacing cetuximab with the immune checkpoint inhibitor pembrolizumab, an anti-PD-1 antibody (immunochemotherapy regimen). Further, Keynote-048 demonstrated activity of single-agent pembrolizumab in patients with high CPS values. The latter (third) treatment retained its efficacy in the elderly, suggesting possible advantage in less fit patients who otherwise receive best supportive care only or single-agent cytotoxic chemotherapy with dubious impact on survival. In selected patients, the TPEx regimen consisting of cisplatin, docetaxel, and cetuximab represents an alternative to EXTREME. Treatment choice can also be influenced by disease extension (site). Compared with disseminated cancer cases, presence of locoregional recurrence without distant metastases may have a negative predictive value for immune checkpoint inhibitors, while favouring biochemotherapy. If the tumour is deemed platinum-resistant, the only evidence-based systemic approach is monotherapy with either pembrolizumab or nivolumab, another anti-PD-1 antibody. Alternatively, being especially pertinent to resource-limited countries, a taxane with or without cetuximab can be prioritized. Obviously, the list of different treatment schedules is longer, but the level of supporting evidence is proportionally lower. One of modern approaches to multidisciplinary management of SCCHN patients is treatment sequencing. It should be understood as a deliberate process of treatment planning typically starting in the locally advanced setting and reaching beyond several treatment failures. This has been enabled by a growing portfolio of effective anticancer modalities complemented by progress in supportive care. Finally, all therapeutic interventions impact somehow on quality of life, either in a positive or negative way, and the choice of anticancer agents should therefore not be reduced to a simple estimate of survival benefit but should contain an adequate appraisal and understanding of individual patient’s situation comprising emotional and spiritual dimensions, cultural and financial aspects, and environmental, social, and educational contexts.
APA, Harvard, Vancouver, ISO, and other styles
2

Falk, Stephen, and Chris Williams. "Treatment of non-small cell lung cancer." In Lung Cancer, 59–76. Oxford University PressOxford, 2009. http://dx.doi.org/10.1093/oso/9780199569335.003.0007.

Full text
Abstract:
Abstract The treatment is planned according to the extent of the disease and general fitness. The major curative treatment is surgery. Radiotherapy can cure lung cancer and also help the common symptoms. Chemotherapy either adds to radiotherapy or surgery for cure or is used to prolong the quantity and quality of life. Newer targeted treatments offer the hope of improving treatment outcomes with fewer side-effects.
APA, Harvard, Vancouver, ISO, and other styles
3

Hayward, Martin, and Davide Patrini. "Preoperative assessment and fitness for surgery: T2N0M0 left hilar squamous cell carcinoma in a female with severe COPD." In Oxford Case Histories in Lung Cancer, edited by Himender Makker, Adam Ainley, Sanjay Popat, Julian Singer, Martin Hayward, and Antke Hagena, 247–56. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198813033.003.0036.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Duncan, Larry, Shaotong Zhu, Mackenzi Pergolotti, Smith Giri, Hoda Salsabili, Miad Faezipour, Sarah Ostadabbas, and S. Abdollah Mirbozorgi. "Automated Camera-Based Assessment of Short Physical Performance Battery (SPPB) for Older Adults with Cancer." In Human Gait - Recent Findings and Research [Working Title]. IntechOpen, 2024. http://dx.doi.org/10.5772/intechopen.112899.

Full text
Abstract:
This chapter introduces a motorized camera system designed for monitoring and evaluating the tests of the Short Physical Performance Battery (SPPB). This system targets physical performance assessment for older patients undergoing cancer treatment. The device is self-contained, incorporating a small computer, three cameras, and two motors. The core algorithms utilize three object recognition techniques: template matching, Haar cascades, and Channel and Spatial Reliability Tracking. To facilitate user interaction, graphical user interfaces (GUIs) are developed on the small computer, enabling test execution and camera adjustments via cell phone and its hotspot. The system delivers precise results, with gait speed tests showing a range of 0.041–1.92 m/s and average speed and distance accuracies exceeding 95%. The standing balance and 5 times sit-stand (5TSS) tests achieve average time accuracies exceeding 97%. This novel camera-based device holds promise in enhancing evaluation of lower body extremity fitness for elderly people receiving cancer health care, offering a reliable and efficient solution for monitoring their progress and well-being.
APA, Harvard, Vancouver, ISO, and other styles
5

Silvertown, Jonathan. "Peas and justice." In Selfish Genes to Social Beings, 167–75. Oxford University PressOxford, 2024. http://dx.doi.org/10.1093/oso/9780198876397.003.0014.

Full text
Abstract:
Abstract An allele is present among offspring in proportion to its frequency among parents. This is ‘gene justice’, or Mendel’s First Law. The process of Mendelian inheritance is blind to the differences between alleles, as justice is said to be blind, and does not favour one allele over another. This kind of justice, enacted during meiosis, is a cornerstone of the evolution of cooperation among genes. But how did a genome of thousands of individual genes, any of which could defect, come to cooperate in the evolution of the system of gene justice enacted in meiosis? Or, to put it more succinctly, how did cooperation triumph over cheating? There are two parts to the answer, reflecting the two essential ingredients of team building that have echoed throughout this book: a community of interest among team members and a mechanism to control cheats. The community of interest among genes arises from the complexity of cellular processes. The functional interdependence of processes in the cell makes the success and fitness of the genes in the cell interdependent too. If the genome is imagined as a parliament of genes, they all vote for cooperation because it is in their individual interests to do so. And yet we know that mutation can produce defectors who will try to cheat, as in cancer. The reason that cheats are never successful for long is that they are outvoted by overwhelmingly superior numbers in the parliament of genes. That doesn’t stop the cheats trying though.
APA, Harvard, Vancouver, ISO, and other styles
6

Gilbert, Gregory S., and Ingrid M. Parker. "Types of plant diseases." In The Evolutionary Ecology of Plant Disease, 83–96. Oxford University PressOxford, 2023. http://dx.doi.org/10.1093/oso/9780198797876.003.0008.

Full text
Abstract:
Abstract Plant pathogens affect their hosts in diverse ways. Some deprive the host of carbon by parasitizing it or by reducing photosynthetic tissue, and some restrict access to water by disrupting the vascular system; either can slow the growth of the plant and reduce host fecundity. Other pathogens directly kill parts or all of the plant, and still other pathogens change growth patterns by manipulating host physiology or genetics. All plants can experience foliar diseases, developmental diseases caused by hormonal manipulation by the pathogen, stunting or dwarfing, damping off, vascular diseases, and root rot. Diseases of woody plant species include cankers and heart rot/butt rot. Some pathogens attack flowers and the reproductive organs of plants, including smut fungi on the anthers of flowers, fruit rot, and seed-decay fungi. All these impacts can reduce the fitness of the plants, altering population dynamics or driving down crop yields. Necrotrophs actively kill cells, causing chlorosis and necrosis, while biotrophs like rusts and viruses depend on live plant tissue to grow and reproduce. The life-history strategies of the pathogens, whether necrotrophs, biotrophs, or opportunistic saprotrophs, often strongly influence the impacts they have on their hosts as well as their level of host specificity.
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Cancer cell fitness"

1

Haase, T., A. Grosser, L. Rohrbacher, L. Weiss, K. Dorman, D. Zhang, C. Gießen-Jung, et al. "P04.03 Immuno-analytics of patients with gastric cancer: impact of systemic polychemotherapy on peripheral T-cell fitness and immunologic features of gastric cancer tissue." In iTOC10 - 10th Immunotherapy of Cancer Conference, March 21 – 23, 2024 – Munich, Germany. BMJ Publishing Group Ltd, 2024. http://dx.doi.org/10.1136/jitc-2024-itoc10.38.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Foust, Amber, Brent Dixon, John D. Powderly, and Renaud F. Warin. "429 Point of care (POC) manufacturing with warm chain production allows for higher immune cell recovery and fitness for cancer therapeutic applications." In SITC 39th Annual Meeting (SITC 2024) Abstracts, A488. BMJ Publishing Group Ltd, 2024. http://dx.doi.org/10.1136/jitc-2024-sitc2024.0429.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Azzi, Mathilde, David Debeaumont, Tristan Bonnevie, Bernard Aguilaniu, Damiano Cerasuolo, Fairuz Boujibar, Antoine Cuvelier, and Francis-Edouard Gravier. "Utility of the 3-minute chair rise test (3CRT) to assess cardiopulmonary fitness of patients with non-small cell lung cancer before lung resection." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.1724.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Francisco, Alice Aparecida Rodrigues Ferreira, and Pedro Lopez. "EXERCISE AS AN ADJUVANT THERAPY FOR FATIGUE AND CARDIORESPIRATORY FITNESS IN BREAST CANCER PATIENTS: A REVIEW OF CURRENT EVIDENCE." In XXIV Congresso Brasileiro de Mastologia. Mastology, 2022. http://dx.doi.org/10.29289/259453942022v32s1032.

Full text
Abstract:
Introduction: During primary breast cancer (BC) treatment, both systemic and local therapies are used to eliminate tumoral cells and reduce the risk of recurrence or disease progression. However, despite the efficacy and success of these treatments, most patients have their quality of life affected by some treatment-related side effects. Among them, fatigue and reductions in cardiorespiratory fitness are commonly observed in response to treatment toxicities during and even following primary treatment. To date, exercise has been considered an effective intervention to counteract these side effects. In the past few years, guidelines from the American Cancer Society, American College of Sports Medicine, and Exercise and Sport Science Australia were published highlighting the importance of being physically active before or after a cancer diagnosis. Recently, the Brazilian Clinical Oncology Society also started a new guideline in exercise and oncology. However, even with numerous studies demonstrating that exercise is effective, the relationship between its prescription variables and effects on these outcomes is unclear. Consequently, it is of great interest to understand the effects of different exercise modalities (e.g., resistance training, aerobic exercise or combined resistance, and aerobic exercise) and their effects on fatigue and cardiorespiratory fitness. Objective: The aim of this study was to describe the effects and moderators of exercise on fatigue and cardiorespiratory fitness in women with BC. Methods: This is a narrative literature review concerning the exercise effects and moderators of exercise response on fatigue and cardiorespiratory fitness in women with BC. The search was undertaken in PubMed using the following terms: “cancer” AND “exercise” AND (“fatigue” OR “cardiorespiratory fitness”) in November 2021. Given the specificity of the topic and outcomes of interest, we selected seven systematic reviews with meta-analysis to describe the exercise effects and moderators of exercise response on fatigue and cardiorespiratory fitness in BC patients. Results: In summary, the design of supervised exercise programs could benefit women with BC. In addition, exercise could result in greater effects in patients presenting higher levels of fatigue when compared to those who do not present. Some examples of supervised exercise programs are in studies from the Supervised Trial of Aerobic Versus Resistance Training (START), Combined Aerobic and Resistance Exercise (CARE), and Optimal Training Women with BC trials (OptiTrain). These studies prescribed resistance training, aerobic exercise, and combined resistance and aerobic exercise, 2–3 exercise sessions per week, 1–3 sets of 8–12 repetitions at 60–70% of one-repetition maximum (1RM) per resistance exercise, and 20–30 min of continuous or high-intensity interval aerobic exercise at 13–15 of the rated perceived exertion (RPE) scale. Regarding the exercise program prescription, supervised, high-intensity, or nonlinear schedule aerobic exercises are also associated with greater effects on cardiorespiratory fitness. The fact that supervised exercise results in greater benefits in cardiorespiratory fitness compared to unsupervised programs (supervised exercise, ES=0.34, 95%CI 0.28–0.40; unsupervised exercise, ES=0.19, 95%CI 0.07–0.32) is an important information. Conclusion: Sufficient evidence indicates that exercise promotes significant effects on fatigue and cardiorespiratory fitness in women with BC. In addition, specific subgroups of patients based on age and baseline levels appear to respond more favorably than others. Regarding contraindications, the exercise prescription should occur accordingly to and with the clearance of the oncologist and the medical team, respecting patients’ individualities, the feasible period for exercise, symptoms, and treatment course.
APA, Harvard, Vancouver, ISO, and other styles
5

Qian, Feng, Jianqun Liao, Anthony J. Miliotto, Katherine A. Collins, and Kunle Odunsi. "Abstract A35: Ovarian cancer stem cells subvert tumor-specific T cells by disrupting T cells’ metabolic fitness." In Abstracts: AACR Special Conference: Addressing Critical Questions in Ovarian Cancer Research and Treatment; October 1-4, 2017; Pittsburgh, PA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1557-3265.ovca17-a35.

Full text
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'Cancer cell fitness' for particular source types:
Journal articles Books
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography