Sustainable Production of Aquatic and Wetland Plants
Namrita Lall in Aquatic Plants, 2020
Numerous species remain dormant (even after overcoming primary dormancy) unless ideal environmental conditions necessary to overcome secondary dormancy are present. This is a mechanism that allows germination to be scattered through time, enhancing the genetic pool of the seed bank and improving a species’ chance of persistence under changing climatic conditions. Numerous mechanisms of dormancy exist from physical to physiological and morphological dormancies. Particular conditions are required to overcome dormancy. These conditions often imitate natural processes. For example, mechanical scarification imitates trampling/pecking to overcome physical dormancy, and cold conditions imitates overwintering to facilitate physiological development and overcome physiological dormancy, while time is necessary to complete the development of naturally underdeveloped embryos of morphologically dormant seed (Finch-Savage and Leubner-Metzger 2006). It is well known that before germination is initiated in ideal conditions to avoid secondary dormancy, certain conditions or treatments are necessary to overcome primary dormancy. The selected dormancy mechanism is quite species-specific. Since it is generally difficult to predict the presence or type of dormancy based on physical characteristics of the seed, a few strategies are commonly used to overcome primary dormancy. Dormancy breaking treatments include scarification, imbibition with water, smoke solution, gibberellic acid, and/or cold or warm treatments (Finch-Savage and Leubner-Metzger 2006).
In Situ Cultivation of Artemisia annua
Tariq Aftab, M. Naeem, M. Masroor, A. Khan in Artemisia annua, 2017
Early germination has been observed after covering Artemisia seeds with polythene material. This might help in maintaining adequate moisture, warmth, and humidity levels in the soil, which are essential for their germination. Dormancy of some seeds is reported to be inhibited when soil temperatures are too warm. They therefore germinate only at high temperatures (Nicolas, 2003). Similarly, germination depends on weakening the seed coat by heating, thus providing the optimum temperature for influencing the rate of enzyme-controlled reactions (Taylor, 1997; Style, 2008). This physiology contributes to the maintenance of dormancy by impeding water and gas to and from the embryo; chemically, by inhibiting germination and mechanically, by restricting the growth of the embryo (Mott and Groves, 1981; Farouk et al., 2008; Style, 2008). This eventually serves as a barrier that restricts water uptake by the impermeable outer part of the epidermal layer of Malphigian cells, thus restraining expansion of the radicle and manifestation of germination (Bewley and Black, 1994).
A Pathologist's View of Tumor Dormancy
Thomas H. M. Stewart, E. Frederick Wheelock in Cellular Immune Mechanisms and Tumor Dormancy, 2017
The factors involved in dormancy are the same as those in spontaneous regression, as outlined by Everson and Cole and Sindelar and Ketcharn.12,17 These are immunologic, hormonal, trauma, irradiation, infections, drugs, elimination of carcinogen and psychologic factors. To these should be added induction of maturation and angiogenesis. Tumors must develop a blood supply or remain very small, the rate of cell necrosis and loss balancing the rate of cell acquisition. Although it is not understood what initiates the angiogenic activity, Weidner et al have shown that lesions with little angiogenesis do not tend to metastasize, whereas those with greater neovascularization do tend to metastasize.18
Research progress on therapeutic targeting of quiescent cancer cells
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2019
Jinhua Zhang, Jing Si, Lu Gan, Cuixia Di, Yi Xie, Chao Sun, Hongyan Li, Menghuan Guo, Hong Zhang
Moreover, dormant colorectal cancer cells are reported to respond to itraconazole, which suppresses the Wnt pathway through non-canonical Hedgehog signaling. Itraconazole treatment initially caused a proliferative burst, forcing dormant cells to cycle briefly and subsequently enter irreversible G1 cell cycle arrest and senescence [31,48]. Furthermore, tubeimoside-1 potently suppressed the growth of human prostate cancer cells via inducing oxidative stress-mediated apoptosis and G0/G1 phase arrest [49]. Arctigenin, the active component of burdock root, enhanced p27Kip1 protein levels through inhibition of Akt and stimulation of FOXO3a activity, in turn, suppressing CDK2 kinase activity and finally inducing overall inhibition of HSC proliferation and G0/G1 phase arrest [50]. Altogether, our findings suggest that dormancy can be effectively sustained through inhibition of proliferative signaling, activation of dormant pathways or delivering the components of dormant niches.
Pituitary carcinomas: review of the current literature and report of atypical case
Published in British Journal of Neurosurgery, 2020
Alexandre B. Todeschini, André Beer-Furlan, Alaa S. Montaser, Ali O. Jamshidi, Luma Ghalib, Jesus A. Chavez, Norman L. Lehman, Daniel M. Prevedello
Cancer dormancy refers to the asymptomatic period of time after initial treatment in which residual viable cells persist in the body in a latent state retaining the potential to initiate growth.37 There are 2 mechanisms to explain tumour dormancy: (1) growth arrest from lack of an adequate vascular supply and (2) cell development arrest in the G0/G1 phase due to the absence of adequate extrinsic or intrinsic signals from the cells’ micro-environment.38,39,41 The escape from dormancy is poorly understood. One of the theories to explain this ‘awakening’ is a sudden peak of angiogenic factors, such as fibroblast growth factor (FGF) or vascular endothelial growth factor (VEGF), which can alter the micro-environment of the dormant cells and provide the necessary vascular supply.42 The dormancy period may also be required for a cell to develop the required random mutations that leads to a malignant or aggressive disease. Currently, research in cancer dormancy mechanisms have not led to a clinical application, but future studies may possibly take advantage of this phenomenon to control cases of disseminated cancer, by artificially returning the cells to a dormant state, or to identify and eradicate these dormant cells, preventing late metastasis.38
The hepatic microenvironment essentially determines tumor cell dormancy and metastatic outgrowth of pancreatic ductal adenocarcinoma
Published in OncoImmunology, 2018
Lennart Lenk, Maren Pein, Olga Will, Beatriz Gomez, Fabrice Viol, Charlotte Hauser, Jan-Hendrik Egberts, Jan-Paul Gundlach, Ole Helm, Sanjay Tiwari, Ralf Weiskirchen, Stefan Rose-John, Christoph Röcken, Wolfgang Mikulits, Patrick Wenzel, Günter Schneider, Dieter Saur, Heiner Schäfer, Susanne Sebens
While a profound influence of inflammatory processes on primary PDAC development is well appreciated, the impact of the hepatic microenvironment on regulation of survival and growth behavior of disseminated PDECs is insufficiently understood. Several studies on other tumor entities support the view that disseminated tumor cells (DTCs) can persist in secondary sites in a viable but non-dividing state thereby remaining clinically unobtrusive and undetectable for extended time periods.19,20 This reversible state of quiescence is termed dormancy in which tumor mass dormancy can be distinguished from cellular dormancy, the latter implying a reversible growth arrest of solitary cells. Hallmarks of cellular dormancy are a flattened cell morphology, Ki67-negativity, reduced ratio of phosphorylated ERK (p-ERK) to phosphorylated p38 (p-p38) and increased p21 expression.19,20,21 All these features are also characteristics of senescent cells, which additionally exhibit an elevated senescence-associated β-galactosidase (SABG) activity.20,22 The acquisition of further mutations (e.g., in P53) as well as microenvironmental alterations may induce reawakening of dormant cells leading to local relapse and/or outgrowth of metastases even after curative therapy.23 A recent study strongly supports the role of inflammation in escape from tumor latency.24 However, underlying mechanisms leading to such microenvironmental alterations and favoring dormancy reversal in PDAC are poorly understood.
Related Knowledge Centers
- Heart Rate
- Mortality Rate
- Photoperiodism
- Physiology
- Thermoregulation
- Metabolism
- Genotype
- Adipose Tissue
- Biological Life Cycle
- Embryonic Diapause