Transformation Of Normal Cells Research Articles

BIOLOGY OF THE CANCER CELL

Our organism is a collection of a big number of cells, each of them an organism in its own being and which lives its own complicated life but is constantly interacting with all the other cells from this collection by adequately responding to signals from them and, in its turn, send signals. Thanks to this complex social behavior of each cell from the millions and trillions of cells helping each other and also that every cell executes its functions and has a certain location in the organism for doing so, it reproduces only when necessary and finally the cells unite with each other in the making of the multicellular organism. Despite this, cells with altered social behavior appear in the organism: these cells, to one or another degree, remain ‘deaf” to the signals from other cells of the organism. These ‘deaf’ cells reproduce regardless of the signals sent by other cells and pervade into territory occupied by other tissues. These changes in separate cells are inheritable: the ‘anti-social’ behavior of these cells could be transferred in cell division to the daughter cells, this process repeating infinitely many times. In the last years, the study of the process of transformation of normal cells in cancerous ones has led to even more intriguing and unexpected result: in normal cells has been found a system for interaction with certain proteins named ‘system for guarding the genes’. This system protects the cells and the organism from mutations in the gene. A key role plays a protein called p53.

Phenome-Wide Scan Finds Potential Orofacial Risk Markers for Cancer

Cancer is a disease caused by a process that drives the transformation of normal cells into malignant cells. The late diagnosis of cancer has a negative impact on the health care system due to high treatment cost and decreased chances of favorable prognosis. Here, we aimed to identify orofacial conditions that can serve as potential risk markers for cancers by performing a phenome-wide scan (PheWAS). From a pool of 6,100 individuals, both genetic and epidemiological data of 1,671 individuals were selected: 350 because they were previously diagnosed with cancer and 1,321 to match to those individuals that had cancer, based on age, sex, and ethnicity serving as a comparison group. Results of this study showed that when analyzing the individuals affected by cancer separately, tooth loss/edentulism is associated with SNPs in AXIN2 (rs11867417 p = 0.02 and rs2240308 p = 0.02), and leukoplakia of oral mucosa is associated with both AXIN2 (rs2240308 p = 0.03) and RHEB (rs2374261 p = 0.03). These phenotypes did not show the same trends in patients that were not diagnosed with cancer, allowing for the conclusion that these phenotypes are unique to cases with higher cancer risk.

Targeting Circulating SINEs and LINEs with DNase I Provides Metastases Inhibition in Experimental Tumor Models

Tumor-associated cell-free DNAs (cfDNAs) are found to play some important roles at different stages of tumor progression; they are involved in the transformation of normal cells and contribute to tumor migration and invasion. DNase I is considered a promising cancer cure, due to its ability to degrade cfDNAs. Previous studies using murine tumor models have proved the high anti-metastatic potential of DNase I. Later circulating cfDNAs, especially tandem repeats associated with short-interspersed nuclear elements (SINEs) and long-interspersed nuclear elements (LINEs), have been found to be the enzyme’s main molecular targets. Here, using Lewis lung carcinoma, melanoma B16, and lymphosarcoma RLS40 murine tumor models, we reveal that tumor progression is accompanied by an increase in the level of SINE and LINEs in the pool of circulating cfDNAs. Treatment with DNase I decreased in the number and area of metastases by factor 3–10, and the size of the primary tumor node by factor 1.5–2, which correlated with 5- to 10-fold decreasing SINEs and LINEs. We demonstrated that SINEs and LINEs from cfDNA of tumor-bearing mice are able to penetrate human cells. The results show that SINEs and LINEs could be important players in metastasis, and this allows them to be considered as attractive new targets for anticancer therapy.

NEPHRECTOMY BY PAPILAR CARCINOMA OF TRANSITIONAL CELLS (UROTELIAL) HIGH GRADE NOT INVASIVE CASE STUDY

Cancer is one of the main causes of morbidity and mortality worldwide, it is produced by the transformation of normal cells into tumor cells in a multiple stages process that can progress to a precancerous lesion to a malignant tumor that can spread through the blood and lymphatic system causing metastasis. The incidence of kidney cancer seems to be increasing, in adults, it begins in the kidneys and can spread to the entire urinary tract that surrounds distant organs or places, renal cell carcinoma is the most common type of kidney cancer and represents approximately 90 percent of cancers tumors.
 The present study evidences the case of a patient who comes to medical services when the problem shows symptoms.
 Objective - To describe the renal cancer case of a patient with papillary transitional cell carcinoma who was operated to remove a kidney tumor in order to prevent it from triggering in severe states.
 Method - The literature on cancer and cancer patients has been reviewed, in the urinary system the data of a case that generated kidney tumor surgery performed in a 63-year-old female patient has been reviewed.
 Result - High-grade, non-invasive papillary transitional cell carcinoma (UROTELIAL) can occur, in patients altering the quality of life of people, if it is detected and treated in time complications can be avoided
 Conclusion - It is essential to identify the risk factors and possible causes that can trigger this type of pathology, the information collected is expected to be useful to professionals and to contribute as an alert to detect health problems in patients early.

Transformation of normal cells by aberrant activation of YAP via cMyc with TEAD

YAP (also known as YAP1 or YAP65) is a transcriptional coactivator that interacts with a number of transcription factors including RUNX and TEAD and plays a pivotal role in controlling cell growth. YAP is classified as a proto-oncogene. However, the mechanism by which activated YAP induces cancerous changes is not well known. Here we demonstrate that overexpression of YAP in NIH3T3 cells was sufficient for inducing tumorigenic transformation of cells. Mechanistically, YAP exerts its function in cooperation with the TEAD transcription factor. Our data also show that cMYC is a critical factor that acts downstream of the YAP/TEAD complex. Furthermore, we also found that aberrant activation of YAP is sufficient to drive tumorigenic transformation of non-immortalized mouse embryonic fibroblasts. Together our data indicate that YAP can be categorized as a new type of proto-oncogene distinct from typical oncogenes, such as H-RAS, whose expression in non-immortalized cells is tightly linked to senescence.

EARLY DETECTION OF BREAST CANCER USING ULTRA WIDE BAND SLOT ANTENNA

Breast cancer is the transformation of normal cells in the breast area into a malignant tumor, which is the second largest disease as a cause of death for women. Early detection is one way to avoid significant risks in breast cancer. X-ray mammography and magnetic resonance imaging (MRI) techniques are used to detect breast cancer. However, those techniques have several limitations. Ultra-wideband (UWB) microwave imaging, approved by The Federal Communications Commission (FCC) in the United States, has promising capabilities in detecting breast cancer. Microwave imaging uses a microstrip antenna that has the advantage of convenience, potentially low cost, and is a non-ionized and safe alternative. In this paper, the ultra-wideband microstrip antenna for breast cancer detection is proposed. The antenna was designed by adding some rectangular slots on a rectangular patch to meet the UWB specifications. The antenna works well at 8.41 GHz to 10.29 GHz with directivity of 6.451 dBi and SAR value of 1.6 W / kg. The antenna was simulated with breast phantom. The tumor sizes of 6 mm and 10 mm are added to evaluate the E/H fields and current density with and without tumor. The highest E-Field value of 928.8 V / m was obtained at 10 GHz with a 10 mm tumor size. The highest H-Field value of 4.06 V / m was achieved at 10 GHz with a 6 mm tumor size. From the simulation, the E/H-field and current density are higher if there is a tumor in the breast compared to the breast without the tumor.

Measuring Clonal Evolution in Cancer with Genomics.

Cancers originate from somatic cells in the human body that have accumulated genetic alterations. These mutations modify the phenotype of the cells, allowing them to escape the homeostatic regulation that maintains normal cell number. Viewed through the lens of evolutionary biology, the transformation of normal cells into malignant cells is evolution in action. Evolution continues throughout cancer growth, progression, treatment resistance, and disease relapse, driven by adaptation to changes in the cancer's environment, and intratumor heterogeneity is an inevitable consequence of this evolutionary process. Genomics provides a powerful means to characterize tumor evolution, enabling quantitative measurement of evolving clones across space and time. In this review, we discuss concepts and approaches to quantify and measure this evolutionary process in cancer using genomics.

MicroRNA expression in melanocytes and melanoma cells

Diagnostic biomarkers cancer diagnostics at preclinical stage seem to be a very promising strategy to increase effectiveness of anti-cancer treatment. Currently there are no such biomarkers available for daily routine practice. However, there are some candidate molecules in research that possibly can be used as biomarkers for early diagnosis, one of them is microRNA. MicroRNA is a small, 20–25 bp, non-coding RNA that is highly involved into epigenetic regulation of gene expression. These molecules participate in malignant transformation of normal cells into cancer cells including melanoma. And moreover, definite expression level of some microRNAs are essential for normal differentiation and function of human cells. Changes in microRNA profile are one of the reasons for malignant tumor development. Identification of these changes may help to develop diagnostic systems to start anti-cancer treatment at early stages.

Basic Concepts in Tumor Angiogenesis

The transformation of normal cells into cancer encompasses a complex series of events, such as genetic disorders, aberrant cell cycles, changes in the phenotype and in cell adhesion, inhibition of apoptosis and generation of new blood vessels. This process is controlled by factors that promote and which factors inhibit it, and the balance between these factors determines their advancement, aggressiveness and prognosis. This review shows basics in the process of tumor angiogenesis.

IKBKE inhibits TSC1 to activate the mTOR/S6K pathway for oncogenic transformation.

IKBKE (IKKε) has emerged as a key modulator of multiple substrates, controlling oncogenic pathways in various malignancies. mTOR signaling, required for cellular growth, proliferation, and vascular angiogenesis in cancer, is potentially one of the pathways regulated by IKKε. Upon activation by various stimuli, PI3K/AKT or similar effectors can relieve the inhibitory effect of the TSC1/TSC2 complex through their phosphorylation to favor mTOR/S6K activation in the downstream. Therefore, any activity that interferes with PI3K/AKT or their downstream targets, such as TSC1/2 or GSK3α/β, may activate the mTOR/S6K pathway for oncogenic transformation in normal cells. Previous studies have shown that PI3K/AKT can be directly phosphoregulated by IKKε. Here, we propose a new regulatory function for IKKε in the mTOR/S6K pathway through its direct interaction with TSC1, leading to TSC1 phosphorylation, which is vital to suppress its inhibitory role in mTOR activation. Experimentally, upon IKKε deficiency in colorectal cancer cells, we observed that S6K activity was diminished while TSC1 levels were found to be stabilized. We hypothesized that these observations may result from direct interaction between IKKε and TSC1. Indeed, the interaction of these two proteins involves the phosphoregulation of TSC1 in various cell lines. Therefore, we propose a mechanism where IKKε, through regulating TSC1 stability in cancer cells, may create an alternative regulatory loop for the activation of mTOR signaling. These results can potentially be important for the development of novel therapeutic strategies targeting mTOR signaling.

Toksisitas Senyawa Tembaga(II)Klorida Dihidrat Terhadap Sel Kanker Payudara T74D Secara in vitro

Cancer is a transformation of normal cells in the body into malignancy due to the induction of carcinogens. Breast cancer is the second leading cause of death in Indonesia. The field of treatment with inorganic compounds has been widely developed and shows better anticancer activity than organic compounds. This research aims to know the toxicity level of copper value of 29.021 μg/ml. The value of IC 50 obtained <100 μg/ml so that the copper Cancer is a transformation of normal cells in the body into malignancy due to the induction ofcarcinogens. Breast cancer is the second leading cause of death in Indonesia. The field oftreatment with inorganic compounds has been widely developed and shows better anticanceractivity than organic compounds. This research aims to know the toxicity level ofcoppervalue of 29.021 μg/ml. The value of IC50obtained<100 μg/ml so that the copper

Cold Atmospheric Plasma for the treatment of Oral Lichen Planus as intraoral precancerous lesion

Background Carcinogenesis of head and neck tumor is a multiphase process that leads from the initial transformation of normal cells to a clinically manifest cancer with a latency of month to decades. Oral lichen planus (OLP) is one of the common immune-mediated mucocutaneous disease characterized by chronic inflammatory process, in which an immune response attacks the lining epithelium. Several prospective and retrospective studies reported malignant transformation rates of OLP ranging from 0 to 10%. In this clinical study, we examined the therapeutic potential of Cold Atmospheric Plasma (CAP) for the treatment of OLP as intraoral precancerous lesions. Material & Methods For preclinical in-vitro investigations, tissue samples have been collected from healthy and diseased mucosal regions from 10 patients suffering from OLP. For detection of CAP-related cell death, investigation of DNA fragmentation using the TUNEL-assay has been performed after CAP treatment. Supernatant culture medium of tissue samples were analyzed for 13 different cytokines. Furthermore, white cell populations were stained in CAP-treated tissue samples. Saliva was collected for quantification of inflammatory markers. In addition, five patients suffering from intraoral leukoplakia of the cheek have undergone an in-vivo treatment using the plasma jet kINPen MED. Intraoral treatments have been performed for a period of 1 min/cm2 and with a continuous exhausting of gas and salivary. Results No significant enlargement of apoptotic cells could be detected after plasma exposure within the tissue. At the time this abstract was completed no final data concerning changes in cytokines as well as white cell population were available. The in-vivo treatment of OLP tissue revealed a reduction of pain and local inflammation. Especially the treatment of a therapy-resistant erosive OLP of the cheek could achieve pain reduction and a cure of mucosal ulcers. Conclusion Previous studies were primarily concerned with plasma effects on cancer cells and its value in cancer treatment. This is the second report about plasma treatment of intraoral precancerous lesions. It has been shown that CAP could be useful in the treatment of intraoral mucosa diseases, especially OLP as precancerous lesion. The treatment of precancerous lesions could prevent the development of cancer and obviate the need for cancer treatment. A larger number of cases, investigation of long-term effects, and clinical studies are needed to further qualify plasma for treatment of precancerous lesions. Download : Download high-res image (424KB) Download : Download full-size image Figure shows the right cheek of a multimorbid patient suffering from a therapy-resistant erosive OLP before (left), during (middle), and after (right) CAP treatment. All volunteers gave written and informed consent to participate in the laboratory and clinical study.

Head and Neck Carcinogenesis

Cancer is caused by mutation(s) in driver gene(s), leading to the transformation of normal cell into malignant one, followed by rapid proliferation. Head and neck cancers (HNCs) comprise epithelial malignancies of the mucosal lining in upper aero-digestive tract. These cancers are heterogeneous in nature. Carcinogenesis therein is correlated with the use of tobacco, chewing of areca nut (betel quid), alcohol consumption and infection with the human papillomavirus (HPV). These factors in conjunction with molecular variations contribute to tumour development, pathology and response to treatment. Thus, the carcinogenesis of head and neck cancers comprise a complex system of gene-gene and geneenvironment interactions.

Abstract 5729: Loss of USP10 and p14ARF protein expression is associated with poor prognosis patients with small intestinal adenocarcinoma

Abstract Ubiquitin Specific Peptidase 10 (USP10) is a member of the ubiquitin-specific protease family and its related pathways are apoptosis, autophagy and DNA damage. P14ARF is encoded by an alternative reading frame within the INK4a/ARF locus at chromosome 9p21, which is related with cell cycle arrest and apoptosis. Recently, ablation of USP10 prevented c-myc induced cellular senescence by destabilization of p14ARF and p53, and accelerated hyper-proliferation and transformation of normal cells, suggesting USP10 have a crucial role in oncogenes induced senescence by keeping the stability of p14ARF and p53, key regulator of cellular senescence. However, knowledge on the clinical and prognostic significance of USP10 and p14ARF expression in patients with small intestine adenocarcinoma is limited. In the present study, we investigated the prognostic significance of USP10 and p14ARF by immunohistochemistry. 195 of resected small intestine adenocarcinomas were retrieved from 22 South Korean institutions by Korean Small Intestinal Cancer Study Group. Tissue microarrays were constructed using formalin-fixed paraffin-embedded specimen. 70 (35.9 %) out of 195 patients showed immunoreactivity for USP10 and 124 (63.6 %) showed loss of immunoreactivity for USP10. 120 (61.5 %) of 195 patients were immunopositive for p14ARF and 75 (38.5 %) patients showed loss of immunoreactivity for p14ARF. Loss of USP 10 was correlated with male predominancy (p=0.014), higher pT stage (p=0.044), presence of lymphatic invasion (p=0.033), absences of sporadic adenoma (p=0.024) and absences of peritumoral dyplasia (p=0.019). On multivariate survival analysis, loss of USP10 expression was independent poor prognostic factor ( HR=3.04, 95% CI= 1.79-5.18, p &amp;lt; 0.001) and also both loss of USP10 and p14ARF expressions showed similar result ( HR=3.76, 95% CI= 1.93-7.23, p &amp;lt; 0.001) while loss of p14ARF was not an independent prognostic factor ( p= 0.587). Our findings indicate that loss of USP10, associated with loss of p14ARF protein expression, could be poor prognostic factors in small intestine adenocarcinoma. Citation Format: Joon Seon Song, Hanbyoul Cho, Joon-Yong Chung, Ilseon Hwang, Hee Jin Lee, Seung-Mo Hong, Stephen M. Hewitt. Loss of USP10 and p14ARF protein expression is associated with poor prognosis patients with small intestinal adenocarcinoma [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 5729. doi:10.1158/1538-7445.AM2017-5729

Protection from Cr(VI)-induced malignant cell transformation and tumorigenesis of Cr(VI)-transformed cells by luteolin through Nrf2 signaling

Cr(VI) is a well known environmental carcinogen, but its mechanism of action and the measures required to mitigate its effects remain to be investigated. Our previous studies showed that exposure of human bronchial epithelial (BEAS-2B) cells to Cr(VI) caused malignant transformation, that these transformed cells progressed through tumorigenesis, and that luteolin, a natural compound, inhibited both of these processes. The present study investigates the underlying mechanisms by which luteolin protects cells against Cr(VI)-induced transformation and tumorigenesis. The present study shows that luteolin activates inducible Nrf2 to inhibit Cr(VI)-generated reactive oxygen species (ROS) in normal BEAS-2B cells. The decreased ROS level is likely responsible for the protective effect of luteolin against Cr(VI)-induced malignant cell transformation in normal cells. By contrast, in cells that have been transformed by Cr(VI), Nrf2 is constitutively activated, and its target proteins, heme oxygenase 1 (HO-1), NAD(P)H:quinone oxidoreductase 1 (NQO1), and superoxide dismutase 1/2 (SOD1/SOD2) are all constitutively activated, and ROS levels are low. Bcl-2, an anti-apoptotic protein and target protein of Nrf2 is elevated. Cr(VI)-transformed BEAS-2B cells develop apoptosis resistance, increasing the survival of these transformed cells. Luteolin decreases interactions between Nrf2 and the antioxidant response element sites of its target anti-apoptotic and antioxidant proteins, Bcl-2, Bcl-XL, and HO-1, which results in decreased constitutive Nrf2 activation. The decreased constitutive Nrf2 activation, decrease in Nrf2 target proteins and consequent apoptosis resistance by luteolin are possible mechanisms that mediate the protective effect of luteolin in Cr(VI)-transformed cells.

Radiation oxidative stress in cancer induction and prevention

Exposure of cells to ionizing radiation causes generation of intracellular reactive oxygen species (ROS) which are implicated in the mechanism of carcinogenesis. Molecular steps involved in the transformation of normal cells to cancer cells have been enigmatic but generally believed to arise from aberration in cellular redox homeostasis. In normal cell function, a delicate balance is maintained between ROS generated in the metabolic process and level of endogenous antioxidant defense. ROS are known to regulate various cellular functions, such as cell division, signal transduction, and apoptosis. Cells experience oxidative stress when excess production of ROS occurs inside a cell upon exposure to external stressor agents. This redox imbalance affects the cellular functions due to DNA strand breaks, chromosomal aberrations, gene mutations, alteration in signal transduction, and inhibition of apoptosis leading to induction of cancer and other diseases. Radiation-induced ROS are involved in initiation and promotion of carcinogenesis. Therefore, detoxification of ROS by exogenous antioxidants including dietary polyphenols offers an important strategy for cancer prevention. Recent research results have shown that resistance of cancer stem cells to therapies is linked to low level of ROS. Interestingly, in vitro and in vivo experiments have reported that radiotherapy- and chemotherapy-induced ROS in cytosol sensitize the tumor cells to death, resulting in tumor growth retardation. This review is an attempt to delineate mechanisms of ROS in carcinogenesis and prevention by dietary compounds. Natural polyphenols and dietary antioxidants hold potential to prevent cancer. Interventions in ROS-mediated signal alteration, apoptosis activation, and modulation of epigenetic processes may offer effective cancer prevention strategy.

Cells of patients with Down syndrome—a model to study mechanisms of oncogenesis and hypersensitivity to genotoxicants and antimutagenesis

Several molecular and genetic features of cells from Down syndrome patients are considered in comparison to those of healthy donors, as is the possibility of using these cells to study mechanisms of the transformation of normal cells to malignant ones, based on the study of the expression of the genes controlling these processes. The role of microRNAs in the regulation of gene activity is estimated. These investigations make it possible to detect the genes for a hereditary predisposition to oncogenesis. The application of antimutagens-anticancerogens provides a new approach to the prophylaxis of this and other human pathologies. In addition, the data on the hypersensitivity of Down syndrome cells to genotoxicants (radiation and others) and the possibility of correcting these disturbances with antimutagens are presented. A special section is devoted to specific changes in cells typical for Down syndrome and Alzheimer disease; the commonality of several elements of the pathogenesis of these diseases is emphasized. The research on Down syndrome cells in terms of an imbalance in the entire genome under this pathology opens new means for the prophylaxis and treatment of several human pathologies.

CD147 overexpression promotes tumorigenicity in Chinese hamster ovary cells.

CD147 overexpresses in many epithelium-originated tumors and plays an important role in tumor migration and invasion. Most studies aim at the role of CD147 in tumor progression using tumor cell models. However, the influence of abnormal overexpression of CD147 on neoplastic transformation of normal cells is unknown. Here, the role of CD147 in malignant phenotype transformation in CHO cells was investigated. Three CHO cell lines that stably overexpressed CD147 (CHO-CD147), EGFP-CD147 (CHO-EGFP-CD147), and EGFP (CHO-EGFP) were generated by transfection of plasmids containing human CD147, EGFP-human CD147, and EGFP genes into CHO cells. Cell migration and invasion were detected by wound healing and transwell matrix penetration assay. Trypan blue exclusion, MTT, cell cycle analysis, and BrdU cell proliferation assay were used to detect cell viability and cell proliferation. Annexin V-FITC analysis was performed to detect apoptosis. We found that CD147 overexpression promoted the migration and invasion of CHO cells. CD147 accelerated the G1 to S phase transition and enhanced the CHO cell proliferation. Overexpression of CD147 inhibited both early- and late-stages of apoptosis of CHO-CD147 cells, which is caused by serum deprivation. CHO-EGFP-CD147 cells showed an increased anchorage-independent growth compared with CHO-EGFP cells as detected by soft-agar colony formation assay. The tumors formed by CHO-CD147 cells in nude mice were larger and coupled with higher expression of proliferating cell nuclear antigen and Ki-67 than that of CHO cells. In conclusion, human CD147 overexpression induces malignant phenotype in CHO cells.

Editorial: Cancer-Associated Defects in the DNA Damage Response: Drivers for Malignant Transformation and Potential Therapeutic Targets.

Transformation of normal cells into cancer cells almost invariably goes along with increased levels of DNA damage. An important source of DNA damage is the enhanced activity of growth-promoting transcription factors, such as MYC. Oncogenic activation of these transcription factors aberrantly stimulates DNA replication, which leads to replication stress and ensuing DNA breaks. Cells respond to this type of stress by activation of the DNA damage response (DDR). The DDR is a complex signaling network, displaying multiple levels of cross-talk and feed-back control. Its kinase-driven signaling axes ensure rapid responses to DNA lesions, which is complemented by its transcriptional axis that warrants maintained signaling. Ultimately, activation of the DDR prevents further proliferation and thus provides time to repair genotoxic lesions, and in case of excessive levels of DNA damage promotes permanent cell cycle exit (senescence) or programmed cell death (apoptosis). Activation of the DDR thus prevents the outgrowth of incipient tumor cells, early during tumorigenesis.

Multiscale modeling of tumor growth induced by circadian rhythm disruption in epithelial tissue.

We propose a multiscale chemo-mechanical model of cancer tumor development in epithelial tissue. The model is based on the transformation of normal cells into a cancerous state triggered by a local failure of spatial synchronization of the circadian rhythm. The model includes mechanical interactions and a chemical signal exchange between neighboring cells, as well as a division of cells and intercalation that allows for modification of the respective parameters following transformation into the cancerous state. The numerical simulations reproduce different dephasing patterns--spiral waves and quasistationary clustering, with the latter being conducive to cancer formation. Modification of mechanical properties reproduces a distinct behavior of invasive and localized carcinoma.