搜索结果：Molecular cancer

Cancers are characterized by remarkable heterogeneity and diverse prognosis. Accurate cancer classification is essential for patient stratification and clinical decision-making. Although digital pathology has been advancing cancer diagnosis and prognosis, the paradigm in cancer pathology has shifted from purely relying on histology features to incorporating molecular markers. There is an urgent need for digital pathology methods to meet the needs of the new paradigm. We introduce a novel digital pathology approach to jointly predict molecular markers and histology features and model their interactions for cancer classification. Firstly, to mitigate the challenge of cross-magnification information propagation, we propose a multi-scale disentangling module, enabling the extraction of multi-scale features from high-magnification (cellular-level) to low-magnification (tissue-level) whole slide images. Further, based on the multi-scale features, we propose an attention-based hierarchical multi-task multi-instance learning framework to simultaneously predict histology and molecular markers. Moreover, we propose a co-occurrence probability-based label correlation graph network to model th

Cancer data, particularly cancer incidence and mortality, are fundamental to understand the cancer burden, to set targets for cancer control and to evaluate the evolution of the implementation of a cancer control policy. However, the complexity of data collection, classification, validation and processing result in cancer incidence figures often lagging two to three years behind the calendar year. In response, national or regional population-based cancer registries (PBCRs) are increasingly interested in methods for forecasting cancer incidence. However, in many countries there is an additional difficulty in projecting cancer incidence as regional registries are usually not established in the same year and therefore cancer incidence data series between different regions of a country are not harmonised over time. This study addresses the challenge of forecasting cancer incidence with incomplete data at both regional and national levels. To achieve this, we propose the use of multivariate spatio-temporal shared component models that jointly model mortality data and available cancer incidence data. We evaluate the performance of these multivariate models using lung cancer incidence dat

Cancer is recognized as a complex group of diseases, contributing to the highest global mortality rates, with increasing prevalence and a trend toward affecting younger populations. It is characterized by uncontrolled proliferation of abnormal cells, invasion of adjacent tissues, and metastasis to distant organs. Garcinia cowa, a traditional medicinal plant widely used in Southeast Asia, including Vietnam, is employed to treat fever, cough, indigestion, as a laxative, and for parasitic diseases. Numerous xanthone compounds isolated from this species exhibit a broad spectrum of biological activities, with some showing promise as anti cancer and antimalarial agents. Network pharmacology analysis successfully identified key bioactive compounds Rubraxanthone, Garcinone D, Norcowanin, Cowanol, and Cowaxanthone alongside their primary protein targets (TNF, CTNNB1, SRC, NFKB1, and MTOR), providing critical insights into the molecular mechanisms underlying their anti-cancer effects. The Graph Attention Network algorithm demonstrated superior predictive performance, achieving an R2 of 0.98 and an RMSE of 0.02 after data augmentation, highlighting its accuracy in predicting pIC50 values for

Although cancer is known to be characterized by several unifying biological hallmarks, systems biology has had limited success in identifying molecular signatures present in in all types of cancer. The current availability of rich data sets from many different cancer types provides an opportunity for thorough computational data mining in search of such common patterns. Here we report the identification of 18 "pan-cancer" molecular signatures resulting from analysis of data sets containing values from mRNA expression, microRNA expression, DNA methylation, and protein activity, from twelve different cancer types. The membership of many of these signatures points to particular biological mechanisms related to cancer progression, suggesting that they represent important attributes of cancer in need of being elucidated for potential applications in diagnostic, prognostic and therapeutic products applicable to multiple cancer types.

Embryology has long played a foundational role in shaping our scientific understanding of animal evolution. In recent decades, growing evidence has also highlighted its role in cancer. Despite the indisputable similarities between embryonic development and cancer, there has been limited discussion on the profound embryological implications for the disease. This article explores the understanding of cancer as an embryological and evolutionary phenomenon, offering a fresh perspective on the disease and discussing immediate consequences in the search for therapeutic approaches

An endogenous molecular-cellular network for both normal and abnormal functions is assumed to exist. This endogenous network forms a nonlinear stochastic dynamical system, with many stable attractors in its functional landscape. Normal or abnormal robust states can be decided by this network in a manner similar to the neural network. In this context cancer is hypothesized as one of its robust intrinsic states. This hypothesis implies that a nonlinear stochastic mathematical cancer model is constructible based on available experimental data and its quantitative prediction is directly testable. Within such model the genesis and progression of cancer may be viewed as stochastic transitions between different attractors. Thus it further suggests that progressions are not arbitrary. Other important issues on cancer, such as genetic vs epigenetics, double-edge effect, dormancy, are discussed in the light of present hypothesis. A different set of strategies for cancer prevention, cure, and care, is therefore suggested.

In recent years, cancer genome sequencing and other high-throughput studies of cancer genomes have generated many notable discoveries. In this review, Novel genomic alteration mechanisms, such as chromothripsis (chromosomal crisis) and kataegis (mutation storms), and their implications for cancer are discussed. Genomic alterations spur cancer genome evolution. Thus, the relationship between cancer clonal evolution and cancer stems cells is commented. The key question in cancer biology concerns how these genomic alterations support cancer development and metastasis in the context of biological functioning. Thus far, efforts such as pathway analysis have improved the understanding of the functional contributions of genetic mutations and DNA copy number variations to cancer development, progression and metastasis. However, the known pathways correspond to a small fraction, plausibly 5-10%, of somatic mutations and genes with an altered copy number. To develop a comprehensive understanding of the function of these genomic alterations in cancer, an integrative network framework is proposed and discussed. Finally, the challenges and the directions of studying cancer omic data using an in

There is a widening recognition that cancer cells are products of complex developmental processes. Carcinogenesis and metastasis formation are increasingly described as systems-level, network phenomena. Here we propose that malignant transformation is a two-phase process, where an initial increase of system plasticity is followed by a decrease of plasticity at late stages of carcinogenesis as a model of cellular learning. We describe the hallmarks of increased system plasticity of early, tumor initiating cells, such as increased noise, entropy, conformational and phenotypic plasticity, physical deformability, cell heterogeneity and network rearrangements. Finally, we argue that the large structural changes of molecular networks during cancer development necessitate a rather different targeting strategy in early and late phase of carcinogenesis. Plastic networks of early phase cancer development need a central hit, while rigid networks of late stage primary tumors or established metastases should be attacked by the network influence strategy, such as by edgetic, multi-target, or allo-network drugs. Cancer stem cells need special diagnosis and targeting, since their dormant and rapid

Breast cancer screening plays a pivotal role in early detection and subsequent effective management of the disease, impacting patient outcomes and survival rates. This study aims to assess breast cancer screening rates nationwide in the United States and investigate the impact of social determinants of health on these screening rates. Data on mammography screening at the census tract level for 2018 and 2020 were collected from the Behavioral Risk Factor Surveillance System. We developed a large dataset of social determinants of health, comprising 13 variables for 72337 census tracts. Spatial analysis employing Getis-Ord Gi statistics was used to identify clusters of high and low breast cancer screening rates. To evaluate the influence of these social determinants, we implemented a random forest model, with the aim of comparing its performance to linear regression and support vector machine models. The models were evaluated using R2 and root mean squared error metrics. Shapley Additive Explanations values were subsequently used to assess the significance of variables and direction of their influence. Geospatial analysis revealed elevated screening rates in the eastern and northern U

Cancer is increasingly perceived as a systems-level, network phenomenon. The major trend of malignant transformation can be described as a two-phase process, where an initial increase of network plasticity is followed by a decrease of plasticity at late stages of tumor development. The fluctuating intensity of stress factors, like hypoxia, inflammation and the either cooperative or hostile interactions of tumor inter-cellular networks, all increase the adaptation potential of cancer cells. This may lead to the bypass of cellular senescence, and to the development of cancer stem cells. We propose that the central tenet of cancer stem cell definition lies exactly in the indefinability of cancer stem cells. Actual properties of cancer stem cells depend on the individual "stress-history" of the given tumor. Cancer stem cells are characterized by an extremely large evolvability (i.e. a capacity to generate heritable phenotypic variation), which corresponds well with the defining hallmarks of cancer stem cells: the possession of the capacity to self-renew and to repeatedly re-build the heterogeneous lineages of cancer cells that comprise a tumor in new environments. Cancer stem cells rep

Nanorobots are a promising development in targeted drug delivery and the treatment of neurological disorders, with potential for crossing the blood-brain barrier (BBB). These small devices leverage advancements in nanotechnology and bioengineering for precise navigation and targeted payload delivery, particularly for conditions like brain tumors, Alzheimer's disease, and Parkinson's disease. Recent progress in artificial intelligence (AI) and machine learning (ML) has improved the navigation and effectiveness of nanorobots, allowing them to detect and interact with cancer cells through biomarker analysis. This study presents a new reinforcement learning (RL) framework for optimizing nanorobot navigation in complex biological environments, focusing on cancer cell detection by analyzing the concentration gradients of surrounding biomarkers. We utilize a computer simulation model to explore the behavior of nanorobots in a three-dimensional space with cancer cells and biological barriers. The proposed method uses Q-learning to refine movement strategies based on real-time biomarker concentration data, enabling nanorobots to autonomously navigate to cancerous tissues for targeted drug d

We present a general computational theory of cancer and its developmental dynamics. The theory is based on a theory of the architecture and function of developmental control networks which guide the formation of multicellular organisms. Cancer networks are special cases of developmental control networks. Cancer results from transformations of normal developmental networks. Our theory generates a natural classification of all possible cancers based on their network architecture. Each cancer network has a unique topology and semantics and developmental dynamics that result in distinct clinical tumor phenotypes. We apply this new theory with a series of proof of concept cases for all the basic cancer types. These cases have been computationally modeled, their behavior simulated and mathematically described using a multicellular systems biology approach. There are fascinating correspondences between the dynamic developmental phenotype of computationally modeled {\em in silico} cancers and natural {\em in vivo} cancers. The theory lays the foundation for a new research paradigm for understanding and investigating cancer. The theory of cancer networks implies that new diagnostic methods

Prostate cancer (PCa) is the most prevalent cancer among men in the United States, accounting for nearly 300,000 cases, 29\% of all diagnoses and 35,000 total deaths in 2024. Traditional screening methods such as prostate-specific antigen (PSA) testing and magnetic resonance imaging (MRI) have been pivotal in diagnosis, but have faced limitations in specificity and generalizability. In this paper, we explore the potential of enhancing PCa gland segmentation using a novel MRI modality called synthetic correlated diffusion imaging (CDI$^s$). We employ several state-of-the-art deep learning models, including U-Net, SegResNet, Swin UNETR, Attention U-Net, and LightM-UNet, to segment prostate glands from a 200 CDI$^s$ patient cohort. We find that SegResNet achieved superior segmentation performance with a Dice-Sorensen coefficient (DSC) of $76.68 \pm 0.8$. Notably, the Attention U-Net, while slightly less accurate (DSC $74.82 \pm 2.0$), offered a favorable balance between accuracy and computational efficiency. Our findings demonstrate the potential of deep learning models in improving prostate gland segmentation using CDI$^s$ to enhance PCa management and clinical support.

Background Precise prediction of cancer types is vital for cancer diagnosis and therapy. Important cancer marker genes can be inferred through predictive model. Several studies have attempted to build machine learning models for this task however none has taken into consideration the effects of tissue of origin that can potentially bias the identification of cancer markers. Results In this paper, we introduced several Convolutional Neural Network (CNN) models that take unstructured gene expression inputs to classify tumor and non-tumor samples into their designated cancer types or as normal. Based on different designs of gene embeddings and convolution schemes, we implemented three CNN models: 1D-CNN, 2D-Vanilla-CNN, and 2D-Hybrid-CNN. The models were trained and tested on combined 10,340 samples of 33 cancer types and 731 matched normal tissues of The Cancer Genome Atlas (TCGA). Our models achieved excellent prediction accuracies (93.9-95.0%) among 34 classes (33 cancers and normal). Furthermore, we interpreted one of the models, known as 1D-CNN model, with a guided saliency technique and identified a total of 2,090 cancer markers (108 per class). The concordance of differential e

The primary activation of the epidermal growth factor receptor (EGFR) has become a prominent target for molecular therapies against several forms of cancer. But despite considerable progress during the last years, many of its aspects remain poorly understood. Experiments on lateral spreading of receptor activity into ligand-free regions challenge the current standard models of EGFR activation. Here, we propose and study a theoretical model, which explains spreading into ligand-free regions without introducing any new, unknown kinetic parameters. The model exhibits bistability of activity, induced by a generic reaction mechanism, which consists of activation via dimerization and deactivation via a Michaelis-Menten reaction. It possesses slow propagating front solutions and faster initial transients. We analyze relevant experiments and find that they are in quantitative accordance with the fast initial modes of spreading, but not with the slow propagating front. We point out that lateral spreading of activity is linked to pathological levels of persistent receptor activity as observed in cancer cells and exemplify uses of this link for the design and quick evaluation of molecular the

Lung cancer is the primary cause of cancer-related mortality, claiming approximately 1.79 million lives globally in 2020, with an estimated 2.21 million new cases diagnosed within the same period. Among these, Non-Small Cell Lung Cancer (NSCLC) is the predominant subtype, characterized by a notably bleak prognosis and low overall survival rate of approximately 25% over five years across all disease stages. However, survival outcomes vary considerably based on the stage at diagnosis and the therapeutic interventions administered. Recent advancements in artificial intelligence (AI) have revolutionized the landscape of lung cancer prognosis. AI-driven methodologies, including machine learning and deep learning algorithms, have shown promise in enhancing survival prediction accuracy by efficiently analyzing complex multi-omics data and integrating diverse clinical variables. By leveraging AI techniques, clinicians can harness comprehensive prognostic insights to tailor personalized treatment strategies, ultimately improving patient outcomes in NSCLC. Overviewing AI-driven data processing can significantly help bolster the understanding and provide better directions for using such syste

With the advances in artificial intelligence (AI), data-driven algorithms are becoming increasingly popular in the medical domain. However, due to the nonlinear and complex behavior of many of these algorithms, decision-making by such algorithms is not trustworthy for clinicians and is considered a black-box process. Hence, the scientific community has introduced explainable artificial intelligence (XAI) to remedy the problem. This systematic scoping review investigates the application of XAI in breast cancer detection and risk prediction. We conducted a comprehensive search on Scopus, IEEE Explore, PubMed, and Google Scholar (first 50 citations) using a systematic search strategy. The search spanned from January 2017 to July 2023, focusing on peer-reviewed studies implementing XAI methods in breast cancer datasets. Thirty studies met our inclusion criteria and were included in the analysis. The results revealed that SHapley Additive exPlanations (SHAP) is the top model-agnostic XAI technique in breast cancer research in terms of usage, explaining the model prediction results, diagnosis and classification of biomarkers, and prognosis and survival analysis. Additionally, the SHAP mo

Tumor protein P53 is believed to be involved in over half of human cancers cases, the prediction of malignancies plays essential roles not only in advance detection for cancer, but also in discovering effective prevention and treatment of cancer, till now there isn't approach be able in prediction the mutated in tumor protein P53 which is caused high ratio of human cancers like breast, Blood, skin, liver, lung, bladder etc. This research proposed a new approach for prediction pre-cancer via detection malignant mutations in tumor protein P53 using bioinformatics tools like FASTA, BLAST, CLUSTALW and TP53 databases worldwide. Implement and apply this new approach of prediction pre-cancer through mutations at tumor protein P53 shows an effective result when used more specific parameters/features to extract the prediction result that means when the user increase the number of filters of the results which obtained from the database gives more specific diagnosis and classify, addition that the detecting pre-cancer via prediction mutated tumor protein P53 will reduces a person's cancers in the future by avoiding exposure to toxins, radiation or monitoring themselves at older ages by chang

Cancer is a fatal disease caused by a combination of genetic diseases and a variety of biochemical abnormalities. Lung and colon cancer have emerged as two of the leading causes of death and disability in humans. The histopathological detection of such malignancies is usually the most important component in determining the best course of action. Early detection of the ailment on either front considerably decreases the likelihood of mortality. Machine learning and deep learning techniques can be utilized to speed up such cancer detection, allowing researchers to study a large number of patients in a much shorter amount of time and at a lower cost. In this research work, we introduced a hybrid ensemble feature extraction model to efficiently identify lung and colon cancer. It integrates deep feature extraction and ensemble learning with high-performance filtering for cancer image datasets. The model is evaluated on histopathological (LC25000) lung and colon datasets. According to the study findings, our hybrid model can detect lung, colon, and (lung and colon) cancer with accuracy rates of 99.05%, 100%, and 99.30%, respectively. The study's findings show that our proposed strategy ou