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Documents  92C50 | enregistrements trouvés : 6

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Breast cancer is the most common type of cancer among women and despite recent advances in the medical field, there are still some inherent limitations in the currently used screening techniques. The radiological interpretation of X-ray mammograms often leads to over-diagnosis and, as a consequence, to unnecessary traumatic and painful biopsies. First we use the 1D Wavelet Transform Modulus Maxima (WTMM) method to reveal changes in skin temperature dynamics of women breasts with and without malignant tumor. We show that the statistics of temperature temporal fluctuations about the cardiogenic and vasomotor perfusion oscillations do not change across time-scales for cancerous breasts as the signature of homogeneous monofractal fluctuations. This contrasts with the continuous change of temperature fluctuation statistics observed for healthy breasts as the hallmark of complex multifractal scaling. When using the 2D WTMM method to analyze the roughness fluctuations of X-ray mammograms, we reveal some drastic loss of roughness spatial correlations that likely results from some deep architectural change in the microenvironment of a breast tumor. This local breast disorganisation may deeply affect heat transfer and related thermomechanics in the breast tissue and in turn explain the loss of multifractal complexity of temperature temporal fluctuations previously observed in mammary glands with malignant tumor. These promising findings could lead to the future use of combined wavelet-based multifractal processing of dynamic IR thermograms and X-ray mammograms to help identifying women with high risk of breast cancer prior to more traumatic examinations. Besides potential clinical impact, these results shed a new light on physiological changes that may precede anatomical alterations in breast cancer development.

Keywords: breast cancer - X-ray mammography - infrared thermography - multifractal analysis - wavelet transform - wavelet transform modulus maxima method
Breast cancer is the most common type of cancer among women and despite recent advances in the medical field, there are still some inherent limitations in the currently used screening techniques. The radiological interpretation of X-ray mammograms often leads to over-diagnosis and, as a consequence, to unnecessary traumatic and painful biopsies. First we use the 1D Wavelet Transform Modulus Maxima (WTMM) method to reveal changes in skin ...

92-08 ; 92C50 ; 92C55

Il sera exposé divers exemples de modélisation en médecine (biologie du cancer, pharmacologie, imagerie fonctionnelle) pouvant donner lieu à des activités pédagogiques reposant de manières essentielles sur l'utilisation de l'informatique.

92C50 ; 65C20

Il sera exposé divers exemples de modélisation en médecine (biologie du cancer, pharmacologie, imagerie fonctionnelle) pouvant donner lieu à des activités pédagogiques reposant de manières essentielles sur l'utilisation de l'informatique.

92C50 ; 65C20

The post-surgical development of metastases (secondary tumors spread from a primary one) represents the major cause of death from a cancer disease. Mathematical models may have the potential to further assist in estimating metastatic risk, particularly when paired with in vivo tumor data that faithfully represent all stages of disease progression.
In this talk I will first describe a modeling approach that uses data from clinically relevant mouse models of spontaneous metastasis developing after surgical removal of orthotopically implanted primary tumors. Both presurgical (primary tumor) and postsurgical (metastatic) growth was quantified using bioluminescence. The model was able to fit and predict pre-/post-surgical data at the level of the individual as well as the population. Importantly, our approach also enabled retrospective analysis of clinical data describing the probability of metastatic relapse as a function of primary tumor size, where inter-individual variability was quantified by a key parameter of intrinsic metastatic potential. Critically, our analysis identified a highly nonlinear relationship between primary tumor size and postsurgical survival, suggesting possible threshold limits for the utility of tumor size as a predictor of metastatic recurrence.
In the second part of my talk, I will focus on some very intriguing phenomenon concerning systemic interactions between tumors within the organisms, termed "concomitant resistance", by which, in the presence of two tumors, one inhibits the growth of the other. This has important clinical consequences as it can lead to post-surgery metastatic acceleration. Based on experimental data involving the simultaneous growth of two tumor implants, we will test biological theories underlying this process and establish a biologically relevant and minimally parameterized mathematical model.
These findings represent a novel use of clinically relevant models to assess the impact of surgery on metastatic potential and may guide optimal timing of treatments in neoadjuvant (presurgical) and adjuvant (postsurgical) settings to maximize patient benefit.
The post-surgical development of metastases (secondary tumors spread from a primary one) represents the major cause of death from a cancer disease. Mathematical models may have the potential to further assist in estimating metastatic risk, particularly when paired with in vivo tumor data that faithfully represent all stages of disease progression.
In this talk I will first describe a modeling approach that uses data from clinically relevant ...

92C50 ; 65C20 ; 92C37

Multi angle  Non-genetic cancer cell plasticity
Pisco, Angela (Auteur de la Conférence) | CIRM (Editeur )

Therapy resistance and tumour relapse after drug therapy are commonly explained by Darwinian selection of pre-existing drug-resistant, often stem-like cancer cells resulting from random mutations. However, the ubiquitous nongenetic heterogeneity and plasticity of tumour cell phenotype raises the question: are mutations really necessary and sufficient to promote cell phenotype changes during tumour progression? Tumorigenesis is a dynamic biological process that involves distinct cancer cell subpopulations proliferating at different rates and interconverting between them. Cancer therapy inevitably spares some cancer cells, even in the absence of resistant mutants. Accumulating observations suggest that the non-killed, residual tumour cells actively acquire a new phenotype simply by exploiting their developmental potential. These surviving cells are stressed by the cytotoxic treatment, and owing to phenotype plasticity, exhibit a variety of responses. By entering such stem-like, stress-response states, the surviving cells strengthen their capacity to cope with future noxious agents. Considering nongenetic cell state dynamics and the relative ease with which surviving but stressed cells can be tipped into latent attractors of the gene regulatory network provides a foundation for exploring new therapeutic approaches that seek not only to kill cancer cells but also to avoid promoting resistance and relapse that are inherently linked to the attempts to kill them.

Keywords: cancer attractor, epigenetic landscape, multi-drug resistance
Therapy resistance and tumour relapse after drug therapy are commonly explained by Darwinian selection of pre-existing drug-resistant, often stem-like cancer cells resulting from random mutations. However, the ubiquitous nongenetic heterogeneity and plasticity of tumour cell phenotype raises the question: are mutations really necessary and sufficient to promote cell phenotype changes during tumour progression? Tumorigenesis is a dynamic ...

92C50 ; 92C37 ; 92C40

Multi angle  From metronomic to... chaotic therapy ?
André, Nicolas (Auteur de la Conférence) | CIRM (Editeur )

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