Propagating large open quantum systems towards their steady states: cluster implementation of the time-evolving block decimation scheme

Many-body quantum systems are subjected to the Curse of Dimensionality: The dimension of the Hilbert space $\mathcal{H}$, where these systems live in, grows exponentially with systems' 'size' (number of their components, "bodies"). It means that, in order to specify a state of a quantum system, we need a description whose length grows exponentially with the system size. However, with some systems it is possible to escape the curse by using low-rank tensor approximations known as `matrix-product state/operator (MPS/O) representation' in the quantum community and `tensor-train decomposition' among applied mathematicians. Motivated by recent advances in computational quantum physics, we consider chains of $N$ spins coupled by nearest-neighbor interactions. The spins are subjected to an action coming from the environment. Spatially disordered interaction and environment-induced decoherence drive systems into non-trivial asymptotic states. The dissipative evolution is modeled with a Markovian master equation in the Lindblad form. By implementing the MPO technique and propagating system states with the time-evolving block decimation (TEBD) scheme (which allows to keep the length of the state descriptions fixed), it is in principle possible to reach the corresponding steady states. We propose and realize a cluster implementation of this idea. The implementation on four nodes allowed us to resolve steady states of the model systems with $N = 128$ spins

Circulating tumor cells in breast cancer: functional heterogeneity, pathogenetic and clinical aspects

Each patient has a unique history of cancer ecosystem development, resulting in intratumor heterogeneity. In order to effectively kill the tumor cells by chemotherapy, dynamic monitoring of driver molecular alterations is necessary to detect the markers for acquired drug resistance and find the new therapeutic targets. To perform the therapeutic monitoring, frequent tumor biopsy is needed, but it is not always possible due to small tumor size or its regression during the therapy or tumor inaccessibility in advanced cancer patients. Liquid biopsy appears to be a promising approach to overcome this problem, providing the testing of circulating tumor cells (CTC) and/or tumor-specific circulating nucleic acids. Their genomic characteristics make it possible to assess the clonal dynamics of tumors, comparing it with the clinical course and identification of driver mutation that confer resistance to therapy. The main attention in this review is paid to CTC. The biological behavior of the tumor is determined by specific cancer-promoting molecular and genetic alterations of tumor cells, and by the peculiarities of their interactions with the microenvironment that can result in the presence of wide spectrum of circulating tumor clones with various properties and potentialities to contribute to tumor progression and response to chemotherapy and prognostic value. Indeed, data on prognostic or predictive value of CTC are rather contradictory, because there is still no standard method of CTC identification, represented by different populations manifesting various biological behavior as well as different potency to metastasis. Circulating clasters of CTC appear to have essentially greater ability to metastasize in comparison with single CTC, as well as strong association with worse prognosis and chemoresistance in breast cancer patients. The Food and Drug Administration (USA) has approved the CTC-based prognostic test for clinical application in patients with advanced breast cancer. Prospective clinical trials have demonstrated that measuring changes in CTC numbers during treatment is useful for monitoring therapy response in breast cancer patients. Molecular and genetic analysis of CTC gives the opportunity to have timely information on emergence of resistant tumor clones and may shed light on the new targets for pathogenetic antitumor therapy

The molecular aspects of personalized anticancer treatment

Only 25% of cancer patients, on average, benefit from therapy. Even in the cases of complete clinical response the tumor progression is an event of high level expectation. The main reasons for tumor progression are: intratumor heterogeneity resulted from clonal evolution, drug resistance, and tumor-promoting microenvironment. The reprogramming of microenvironmental stromal-inflammatory components is expected to allow tumor phenotype reversion. So, to find the new effective markers of tumor progression, drug response and targets for therapy, it could be promising to take into account the tumor-microenvironment heterogeneity and tumor clonal evolution

Premalignant changes in the bronchial epithelium are prognostic factors of distant metastasis in non-small cell lung cancer patients

Background: The study assessed the possibility of dividing patients into groups based on the assessment of morphological changes in the epithelium of small-caliber bronchi located near the primary tumor in order to predict high and low risks of distant metastasis of non-small cell lung cancer. Methods: In 171 patients with non-small cell lung cancer (T1-4N0-3M0) in small-caliber bronchi taken at a distance of 3–5 cm from the tumor, various variants of morphological changes in the bronchial epithelium (basal cell hyperplasia (BCH), squamous cell metaplasia (SM), and dysplasia (D)) were assessed. Long-term results of treatment, namely, distant metastasis, were assessed after 2 and 5 years. Results: During the follow-up period, distant metastases were found in 35.1% (60/171) of patients. Most often, they were observed in patients of the high-risk group: BCH+SM−D−(51.6%, 40/95) and BCH−SM+D+ (54.4%, 6/11). Less often, distant metastases were observed in low-risk group patients: BCH+SM+D− (6.7%, 3/45) and BCH−SM−D−(10.0%, 2/20). Tumor size, grade, and stage were significant predictors of metastasis only in the high-risk group. The 5-year metastasis-free survival was better in the low-risk group of distant metastases. Conclusions: Isolated BCH or dysplasia in small bronchi distant from foci of tumor isassociated with a high-risk distant metastasis and less 5-year metastasis-free survival

Cancer invasion: patterns and mechanisms

Cancer invasion and the ability of malignant tumor cells for directed migration and metastasis have remained a focus of research for many years. Numerous studies have confirmed the existence of two main patterns of cancer cell invasion: collective cell migration and individual cell migration, by which tumor cells overcome barriers of the extracellular matrix and spread into surrounding tissues. Each pattern of cell migration displays specific morphological features and the biochemical/molecular genetic mechanisms underlying cell migration. Two types of migrating tumor cells, mesenchymal (fibroblast-like) and amoeboid, are observed in each pattern of cancer cell invasion. This review describes the key differences between the variants of cancer cell migration, the role of epithelial-mesenchymal, collective-amoeboid, mesenchymal-amoeboid, and amoeboid- mesenchymal transitions, as well as the significance of different tumor factors and stromal molecules in tumor invasion. The data and facts collected are essential to the understanding of how the patterns of cancer cell invasion are related to cancer progression and therapy efficacy. Convincing evidence is provided that morphological manifestations of the invasion patterns are characterized by a variety of tissue (tumor) structures. The results of our own studies are presented to show the association of breast cancer progression with intratumoral morphological heterogeneity, which most likely reflects the types of cancer cell migration and results from different activities of cell adhesion molecules in tumor cells of distinct morphological structures

INTERLEUKIN-17 IS A NEW TARGET FOR ANTI-CYTOKINE THERAPY OF IMMUNE INFLAMMATORY RHEUMATIC DISEASES

As of now, there have been notable advances in treating immune inflammatory rheumatic diseases, which are associated with the interpretation of basic pathogenetic mechanisms of their development. The most well studied therapeutic targets are tumor necrosis factor-α, interleukin (IL)-6 and IL-1; inhibition of these cytokines with genetically engineered biological agents is not always clinically effective and rarely gives rise to remission. The new promising treatment of rheumatoid arthritis (RA) and other inflammatory arthritides is linked to the inhibition of IL-17A, a proinflammatory cytokine, involved in the development of inflammation and in the destruction of bone tissue. The paper summarizes new evidence for the prospects of using anti-interleukin-17 monoclonal antibodies to treat RA

The influence of cisplatin on transcriptional profile of tumor-associated macrophages of breast cancer and colon cancer

In the present study we demonstrated the whole transcriptome analysis of model tumor-associate