Mathematical approach to predict the drug effects on cancer stem cell models
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This is a presentation on "Mathematical Approach to Predict the Drug Effects on Cancer Stem Cell Models" article doi:10.1016/j.entcs.2011.09.033
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Give background information concerning EMT and include what is known.pdf
Give background information concerning EMT and include what is known about EMT in normal
development as well as in neoplasms. What are strategies that could be used to overcome drug
resistance in cancer cells by targeting EMT (minimum four paragraphs).
Solution
Answer:
Cancer stem cell (CSC) hypothesis: This hypothesis elucidating that the CSC are the
subpopulation and able to exert higher resistance associated with explicit capability to self-renew
finally to differentiate into different offspring of cancer cells to generate a tumor. This
hypothesis is based on the cellular mechanisms exclusively developed inside the CSC to exert
resistance such pathways are mainly through Wnt signaling, Notch signaling. There are other
targets to regulate proliferation and differentiation through ABC transporter system and receptor
tyrosine kinases. These targets are the future stem cells anti-cancer therapies in regulating the
proliferation & differentiation of cancer cells as CSCs have a potential relationship with
epithelial-mesenchymal transition (EMT).
Metastasis has many steps. The main cancer cell morphological features that support invasion,
intravasation, and extravasation are epithelial-mesenchymal transition via cell -adhesion
molecules. Invasion is mainly due to presence of cell adhesion molecules such as integrins on the
cancer cells finally promote the movement of cancer cells to another region. This process is
going to connect adjacent cells to tumor cells finally undergo epithelial-mesenchymal transition
(EMT) result in formation of \"continuously dividing neoplasms\" with higher drug resistence to
cure compared to normal cells
Strategies that could be used to overcome drug resistance in cancer cells by targeting EMT:
\"A combination therapy of neutraceuticals & chemotherapeutic agents\" are most promising
strategies to overcome drug resistance in cancer cells by targeting EMTs, cancer stem cells
(CSC) &
Modulation of microRNAs do promote effective strategy to overcome drug resistance in cancer
cells
Oligonucletodie deliver: Another strategy could be used to overcome drug resistance in cancer
cells by targeting EMT. In this method, synthesized microRNAs are going to make in the form of
\"nanoparticle or microsomal\" formulation finally used to target microRNAs in cancer cells
result in \"complete destruction of pre-mRNA\" finally there will no translation mechanism to
synthesize \"cell survival proteins\" to proliferate.
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Similar to Mathematical approach to predict the drug effects on cancer stem cell models
Anticancer drug screening
The document describes screening methods for new anticancer drugs. It discusses how cancer arises from genetic mutations and different cancer types. Current treatments include chemotherapy, surgery and radiation. There is a need for more selective anticancer agents due to drug resistance and side effects. Various in vitro and in vivo screening assays are described to test compounds for cytotoxicity against cancer cells and tumors in animal models. The goal is to develop more effective and safer anticancer drugs.
Give background information concerning EMT and include what is known.pdf
Give background information concerning EMT and include what is known about EMT in normal
development as well as in neoplasms. What are strategies that could be used to overcome drug
resistance in cancer cells by targeting EMT (minimum four paragraphs).
Solution
Answer:
Cancer stem cell (CSC) hypothesis: This hypothesis elucidating that the CSC are the
subpopulation and able to exert higher resistance associated with explicit capability to self-renew
finally to differentiate into different offspring of cancer cells to generate a tumor. This
hypothesis is based on the cellular mechanisms exclusively developed inside the CSC to exert
resistance such pathways are mainly through Wnt signaling, Notch signaling. There are other
targets to regulate proliferation and differentiation through ABC transporter system and receptor
tyrosine kinases. These targets are the future stem cells anti-cancer therapies in regulating the
proliferation & differentiation of cancer cells as CSCs have a potential relationship with
epithelial-mesenchymal transition (EMT).
Metastasis has many steps. The main cancer cell morphological features that support invasion,
intravasation, and extravasation are epithelial-mesenchymal transition via cell -adhesion
molecules. Invasion is mainly due to presence of cell adhesion molecules such as integrins on the
cancer cells finally promote the movement of cancer cells to another region. This process is
going to connect adjacent cells to tumor cells finally undergo epithelial-mesenchymal transition
(EMT) result in formation of \"continuously dividing neoplasms\" with higher drug resistence to
cure compared to normal cells
Strategies that could be used to overcome drug resistance in cancer cells by targeting EMT:
\"A combination therapy of neutraceuticals & chemotherapeutic agents\" are most promising
strategies to overcome drug resistance in cancer cells by targeting EMTs, cancer stem cells
(CSC) &
Modulation of microRNAs do promote effective strategy to overcome drug resistance in cancer
cells
Oligonucletodie deliver: Another strategy could be used to overcome drug resistance in cancer
cells by targeting EMT. In this method, synthesized microRNAs are going to make in the form of
\"nanoparticle or microsomal\" formulation finally used to target microRNAs in cancer cells
result in \"complete destruction of pre-mRNA\" finally there will no translation mechanism to
synthesize \"cell survival proteins\" to proliferate.
Cancer Res-2015-Cassidy-0008-5472.CAN-15-0727
This review discusses how patient-derived tumor xenograft (PDX) models can capture some aspects of tumor heterogeneity found in human cancers, but have limitations. PDX models retain genetic and epigenetic heterogeneity within tumors as well as distinct cellular clones that can drive treatment resistance. However, PDXs may not fully represent stromal and immune contributions to tumor progression and response to therapy. The review proposes strategies to improve PDX models to better maintain the diverse sources of heterogeneity in human malignancies.
REVIEWCancer stem cells a new framework for the designo.docx
REVIEW
Cancer stem cells: a new framework for the design
of tumor therapies
Boyan K. Garvalov & Till Acker
Received: 14 July 2010 /Revised: 27 August 2010 /Accepted: 16 September 2010
# Springer-Verlag 2010
Abstract Modern tumor therapy has achieved considerable
progress, but many tumors remain refractory to treatment or
relapse following initial remission. Recent evidence points
to one possible reason for this limited therapeutic efficiency:
that the design of anticancer agents so far may not have been
aimed at the right target. While conventional tumor therapies
have targeted the main mass of tumor cells, there is now
compelling evidence that tumor initiation and progression are
driven by a subpopulation of tumor cells that possess stem cell
properties and are resistant to traditional cancer treatments—
the cancer stem cells (CSCs). CSCs have been identified in
most types of cancer and can be separated from the rest of the
tumor cells using appropriate markers. CSCs are regulated by
molecular mechanisms and specific, perivascular, and hypox-
ic microenvironments, which largely overlap with those
controlling stem cells from normal tissues. Our improved
understanding of CSC biology has already provided a number
of novel targets and drug discovery platforms for the design of
specific therapies that aim to eradicate the CSC subpopula-
tion. Therapeutic approaches can be targeted either at
eliminating the CSCs themselves or at disrupting the niches
in which CSCs reside. Moreover, the importance of CSCs for
tumor growth, resistance, and progression implies that clinical
trials and preclinical studies of anticancer therapies should
include as a key element an assessment of the abundance and
persistence of CSCs. Thus, CSC research holds great promise
for providing important new impetus to the fields of tumor
biology and clinical oncology.
Keywords Cancer stem cell . Hypoxia .
Microenvironment . Angiogenesis . Antitumor therapy.
Metastasis
The hierarchy model and cancer stem cells (CSCs)
The classical view of tumor formation is based on the
“stochastic” or “clonal evolution” model [1, 2]. It perceives
the tumor as a mass of hyperproliferative cells with similar
potential for driving tumor growth. Tumor heterogeneity
and progression are seen as the result of variations in the
tumor microenvironment and genetic mutations in individ-
ual cells, followed by selection of those that are best
adapted to support the further growth of the tumor (Fig. 1a).
An alternative concept that has been gaining increasing
experimental support is the “hierarchy” or “cancer stem
cell” model [3]. This model posits that tumors are generated
and maintained in a manner similar to the physiological
stem cell system operating in normal tissues, i.e., by cells
with stem cell-like properties, which self-renew and
differentiate into the distinct cellular subtypes of the tumor
(Fig. 1b). The key novel features of this model are that only
a limited population of tumor cell ...
Chemosensitivity Testing of Circulating Epithelial Tumor Cells (CETC) in Vitr...
ABSTRACT
Background: Chemotherapy is a mainstay of tumor therapy, however, it is predominantly applied according to empiri- cally developed recommendations derived from statistical relapse rates occurring years after the treatment in the adju- vant situation and from progression-free interval data in the metastatic situation, without any possibility of individually determining the efficacy in the adjuvant situation and with loss of time and quality of life in the metastatic situation if the drugs chosen are not effective. Here, we present a method to determine the efficiency of chemotherapeutic drugs using tumor cells circulating in blood as the part of the tumor actually available in the patient’s body for chemosensitiv- ity testing. Methodology/Principal Findings: After only red blood cell lysis, omitting any enrichment (analogous to other blood cell enumeration methods, including rare CD34 cells), the white cells comprising the circulating epithelial tumor cells (CETC) are exposed to the drugs in question in different concentrations and for different periods of time. Staining with a fluorescence-labeled anti-epithelial antibody detects both vital and dying tumor cells, distinguishing vital from dying cells through membrane permeability and nuclear staining with propidium iodide. Increasing percent- ages of dying tumor cells are observed dependent on time and concentration. The sensitivity can vary during therapy and was correlated with decrease or increase in CETC and clinical outcome. Conclusions/Significance: Thus, we are able to show that chemosensitivity testing of circulating tumor cells provides real-time information about the sensitivity of the tumor present in the patient, even at different times during therapy, and correlates with treatment success.
General principles in chemotherapy of cancer
This document provides an overview of general principles in cancer chemotherapy. It discusses that chemotherapy uses cytotoxic drugs to destroy malignant cells. Drugs can be cell cycle specific, killing dividing cells, or nonspecific, killing resting and dividing cells. Combination chemotherapy using multiple drugs with different mechanisms of action is now common to achieve total tumor cell kill. Careful scheduling of cell cycle specific and nonspecific drugs is important. Tumors can become resistant to repeated use of single drugs through selection of less responsive cells or mutations altering drug targets. The goal of chemotherapy is complete remission through use of maximum tolerated drug doses in combination regimens.
01-Ca Intro_2016.pdf pharmacy student ca
This document provides information about cancer treatment and chemotherapy. It discusses the types and characteristics of cancer cells, principles of chemotherapy including drug combinations and treatment cycles, methods for calculating chemotherapy doses, and types of chemotherapeutic drugs including antimetabolites like 5-FU and capecitabine. The document contains details on the mechanisms of action, administration methods, and side effects of specific chemotherapy drugs.
Using biomarkers to monitor the dynamics of tumor
This document discusses tumor markers and their use in monitoring tumor response to therapy. It provides information on different types of tumor markers including proteins, enzymes, hormones, genetic markers and circulating tumor cells. Ideal tumor markers are highly sensitive and specific, correlate with tumor stage and prognosis, and can be used for screening, diagnosis, prognosis, monitoring treatment and detecting recurrence. Examples discussed include CEA, AFP, PSA, CA125 and circulating tumor cells. The Oncotype DX 21-gene recurrence score test and tissue polypeptide specific antigen are also summarized.
PMED Opening Workshop - Regrowth Rates of Tumors after Radiation Vary Dependi...
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A simple immune system model of effector cells and regulator cells is coupled to a compartment model tuned to neuroblastoma xenograft data. Radiation is modeled as a raised death rate on a fixed day that reduces tumor size by transferring a fraction of cells into a compartment of “doomed” cells whose presence can be detected by effector cells, producing an immune response. The model predicts that the
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This document summarizes a study on monitoring the response of circulating epithelial tumor cells (CETCs) to adjuvant chemotherapy in breast cancer patients. The study found that CETCs can be quantified from blood samples of patients before, during, and after chemotherapy. Three typical response patterns were observed: a decrease of more than 10-fold in CETC numbers correlated with a good prognosis; marginal changes in CETC numbers correlated with a medium prognosis; and an increase of more than 10-fold in CETC numbers, even after an initial decrease, correlated with a poor prognosis and high risk of early relapse. Patients with increasing CETC numbers had a significantly worse relapse-free survival compared to the other groups. Therefore,
Staging an tumor markers
This document discusses tumor staging and biomarkers for oral cancer. It introduces the TNM staging system and its components for assessing tumor size, lymph node involvement, and metastasis. It also addresses limitations of staging and types of biomarkers that can be used, including commonly used ones like CD44, interleukin levels, and tissue polypeptide antigen. Biomarkers can help with screening, diagnosis, prognosis, and monitoring treatment response for oral cancer.
Metastatic Breast Cancer
The document summarizes research on the metastatic spread of breast cancer cells in mice. Key findings include:
- Line 4T1, a metastatic breast cancer cell line, primarily spreads through hematogenous metastasis to the lungs followed later by the liver. Necropsy found lung and liver nodules.
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cancer cell lines
In vitro models are crucial tools in cancer research because they assist researchers to identify carcinogens, developing cancer therapies, drug discovery, and study about the molecular pathways of tumour growth and spread. Cancer cells are an essential part of any in vitro tumour model. Cancer cell lines are simple to culture, allow for quick comparisons of experiments, and are commonly employed to research tumour cell biology molecular pathways. Tumour cell biology, 3D cell culture, tissue engineering, biomaterials, microfabrication, and microfluidics advancements have facilitated the dynamic development of in vitro tumour models.
25987109 tipos-infrecuentes-de-cancer-de-mama
This document reviews rare types of breast cancer. It summarizes information on 16 epithelial subtypes classified by the World Health Organization, including histopathology descriptions and clinical parameters. While rare cancers cannot be studied through large randomized trials, this review aims to provide clinicians an understanding to help determine optimal treatment approaches. It discusses cancers such as tubular carcinoma and mucinous carcinoma, which typically have a good prognosis and are often estrogen receptor positive with low lymph node involvement.
Cancer Stem Cell.pptx
This document discusses cancer stem cells (CSCs). It introduces CSCs and their properties of self-renewal and differentiation. CSCs have been identified in many cancers using cell surface markers and can mediate metastasis, treatment resistance, and relapse. CSCs are regulated by the tumor microenvironment through growth factors and cytokines. Several signaling pathways important in CSCs are discussed, including Hedgehog, Notch, and WNT, which are potential therapeutic targets. The relationship between epithelial-mesenchymal transition (EMT) and CSCs is also covered.
Clinical value of circulating tumor cells in metastatic breast cancer
1) Circulating tumor cells (CTCs) in patients with metastatic breast cancer provide important clinical information and can help guide treatment decisions. The number of CTCs before and during therapy correlates with progression-free and overall survival.
2) Molecular characterization of CTCs can reveal discordance between primary tumors and metastases, as well as heterogeneity within metastatic sites, helping to identify appropriate targeted therapies. Serial CTC analysis during treatment can detect emerging resistance mutations.
3) Monitoring changes in CTC counts during therapy provides an early indicator of treatment effectiveness compared to imaging, and may help determine when to switch treatments for better outcomes.
Cell survival curves
LQmodel, survival curve, factors affecting survival curve, alpha beta ratio, plating efficacy, surviving fractions
Li_Lee_Luo_SubclonalSwitchingBoard_scd.2012
This document discusses a new hypothesis that shifting dominance between cancer subclones is controlled by "subclonal switchboard signals" (SSS). The hypothesis posits that destroying the currently dominant subclone triggers the activation of dormant subclones through SSS, leading to cancer progression and recurrence after treatment. The authors argue that a new strategy should focus on eliminating these SSS to prevent dormant subclones from becoming dominant, rather than trying to destroy all cancer subclones. Understanding the mechanisms and pathways involved in SSS could provide insights for developing therapies to manage tumor growth.
ANNOTATION ON THE BASIC CONCEPT OF NEOPLASM..PPTX
This document provides an overview of neoplasms and cancer. It defines a neoplasm as abnormal cell growth and defines cancer as a genetic disease caused by mutations. It describes the components, classification, characteristics and molecular basis of cancers. It discusses the differences between benign and malignant tumors. It also covers cancer epidemiology in Bangladesh, noting that cervical cancer is most common in women and lung cancer is increasing in men. The document concludes by emphasizing the importance of early detection, timely treatment and raising awareness to reduce cancer mortality.
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- 1. An article presentation Mathematical Approach to Predict the Drug Effects on Cancer Stem cell Models M. Amin Ghavami Fall 95
- 3. Model structure Many cancers are driven by small groups of Cancer Stem Cells (CSCs) In normal tissues: CSCs are self-renewing Capable of tissue regeneration Rise to non-CSCs In our ODEs system we also account for the drug effect on the cancer in order to simulate the behavior of the cells, considering different drug concentrations.
- 4. Model structure Traditional view That the malignant tumor consists of a unique type of cell population characterized by the ability to divide without limit. New heterogeneity concept CSCs that can differentiate into heterogeneous cancer subpopulations Progenitor cells (PCs) Terminally differentiated cells (TCs)
- 6. Model structure Proliferation rate is: ω Differentiation rate is: η Ability of progenitor cells to acquire CSC phenotype: ϒ die rate: d NCSC, NPCi and NTC are the numbers of cancer stem cells Drug effects for each individual population i: Θi
- 10. Equilibrium analysis Z’= AZ matrix A contains the coefficients of the biological system vector Z refers to the variables
- 11. Equilibrium analysis Zi = Wi eλit Wi is the i − th eigenvector of A λi is its corresponding eigenvalue Our description of the dynamics of tumor progression builds on Zhu’s model
- 12. Equilibrium analysis This result confirms the key role of CSCs in tumor growth: all cell populations reach a steady state if and only if the proliferation of CSCs is kept under control PsyωCSC = d1 in real cases, instead, the control of the proliferation of CSCs depends also on differentiation, feedback, and drug treatments
- 13. Equilibrium analysis The difficulty of this task is mainly caused by the presence of the feedback effect which can be however overcome by following a step-by-step procedure we consider three variants of the model: Var1: corresponds to the system of ODEs with nine subpopulations but without the representation of the feedback var2: is the system of ODEs accounting only for the CSC and PC1 subpopulations, but with the representation of the feedback var3: is the whole system corresponding
- 14. Equilibrium analysis Var 1 PsyωCSC = d1 + η1 +Θ1
- 15. Equilibrium analysis Var2 It has to be balanced by the CSC surrogate production given by the feedback action that is proportional to the concentration of PC1
- 16. Equilibrium analysis Var3 solve a cubic polynomial The analytic solution of this polynomial is difficult to manage, hence we adopt a graphical approach to determine its roots
- 17. Results The model parameters are tuned by using experimental data; the resulting model setting is used to investigate several drug effects and their combination