Does extirpation of the primary breast tumor give boost to growth of metastases? Evidence revealed by mathematical modeling

Hanin, Leonid; Korosteleva, Olga

doi:10.1016/j.mbs.2009.11.006

Cited by 26 publications

(51 citation statements)

References 23 publications

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“…Volumes of all tumors were measured through laborious reading of the whole body PET/CT scans. In particular, , and one soft tissue tumor with the volume 11.41 cm 3 [56]. The researchers revealed also 20 and 15 secondary bone tumors in two other breast cancer patients 5.5 years and 9 months after primary resection, respectively.…”

Section: The Hypothesis Of Genome Intrusionmentioning

confidence: 91%

“…The researchers revealed also 20 and 15 secondary bone tumors in two other breast cancer patients 5.5 years and 9 months after primary resection, respectively. Besides they found the inception of the first secondary tumor occurred 29.5 years prior to the primary diagnosis, and resection of the primary tumor was followed by a 32-fold increase in the rate of secondary tumors growth [56]. This may mean the growth of all populations of a cancer is under control performed by their own united physiological mechanism which maintains the whole structure of cancer within its genetically predetermined size.…”

Section: The Hypothesis Of Genome Intrusionmentioning

confidence: 99%

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Functions of hereditary immunity and xenogamy in cancer origin and pandemic spread

Rumyantsev¹

2011

OJI

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The efficacy of means exploited currently for cancer prevention and treatment appeared to be very low. New insights into the origin of the disease are sorely needed. The present article synthesizes the results from integrative reconsideration of actual data on cancer from the viewpoint of recent developments in pathology, epidemiology, immunology, genetics, and evolution. In contrast to the 80 years old hypothesis of somatic mutative origin of carcinogenesis, the revealed set of evidence showed the origin of cancerous clones is based on inherent constitutional incongruence between the regulators of cell physiology and their targets realized in inherent immunity of cancerous cells to normal regulation of cell replication and tissue growth. The incongruence arises out of both genome mutations which led to interethnic differences in the regulator-receptor structures and intercourse between ethnoses, the regulator-receptor evolution of which has been processed to deal with different ecologic conditions. The current pandemic spread of cancer is brought about growing expansion of interethnic xenogamy favored by growing industrialization, urbanization, globalization, and migration. The proposed hypothesis of genome intrusion in the origin of cancer induces new research ideas and proposals for cancer prevention and therapy.

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Section: The Hypothesis Of Genome Intrusionmentioning

confidence: 91%

Section: The Hypothesis Of Genome Intrusionmentioning

confidence: 99%

Functions of hereditary immunity and xenogamy in cancer origin and pandemic spread

Rumyantsev¹

2011

OJI

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“…Measurement of the primary tumor's volume typically involves a signi fi cant error due to uncertainty in determination of the tumor boundary. However, neither this error nor the possible deviation of the cell volume from the "standard" value c = 10 −9 cm 3 assumed in the studies [ 7,52,55 ] have a signi fi cant impact on parameter estimation, because the primary tumor size S appears in formulas ( 12.11 ) under the sign of logarithm.…”

Section: If > a M Thenmentioning

confidence: 99%

“…A more general functional form, g ( x ) = a 1 x q , was explored in [ 52 ] , and the resulting model was used to reconstruct the natural history of the disease in one case of metastatic breast cancer; however, the model did not account for an effect of surgery on the rate of growth of metastases. An extension of the model accounting for such an effect was designed in [ 54 ] , which was applied to clinical data on the same patient in [ 55 ] . Importantly, this led to a considerable improvement in the model fi t to the volumes of detected bone metastases.…”

Section: T V T W T M V T G S F T S S T G S F W T M S S T W T M (127)mentioning

confidence: 99%

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Seeing the Invisible: How Mathematical Models Uncover Tumor Dormancy, Reconstruct the Natural History of Cancer, and Assess the Effects of Treatment

Hanin

2012

Advances in Experimental Medicine and Biology

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The hypothesis of early metastasis was debated for several decades. Dormant cancer cells and surgery-induced acceleration of metastatic growth were first observed in clinical studies and animal experiments conducted more than a century ago; later, these findings were confirmed in numerous modern studies.In this primarily methodological work, we discuss critically important, yet largely unobservable, aspects of the natural history of cancer, such as (1) early metastatic dissemination; (2) dormancy of secondary tumors; (3) treatment-related interruption of metastatic dormancy, induction of angiogenesis, and acceleration of the growth of vascular metastases; and (4) the existence of cancer stem cells. The hypothesis of early metastasis was debated for several decades. Dormant cancer cells and surgery-induced acceleration of metastatic growth were first observed in clinical studies and animal experiments conducted more than a century ago; later, these findings were confirmed in numerous modern studies.We focus on the unique role played by very general mathematical models of the individual natural history of cancer that are entirely mechanistic yet, somewhat paradoxically, essentially free of assumptions about specific nature of the underlying biological processes. These models make it possible to reconstruct in considerable detail the individual natural history of cancer and retrospectively assess the effects of treatment. Thus, the models can be used as a tool for generation and validation of biomedical hypotheses related to carcinogenesis, primary tumor growth, its metastatic dissemination, growth of metastases, and the effects of various treatment modalities. We discuss in detail one such general model and review the conclusions relevant to the aforementioned aspects of cancer progression that were drawn from fitting a parametric version of the model to data on the volumes of bone metastases in one breast cancer patient and 12 prostate cancer patients.

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A mixed radiotherapy and chemotherapy model for treatment of cancer with metastasis

Ghaffari

Bahmaie

Nazari

2016

Math Methods in App Sciences

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In this paper, a mathematical model of cancer treatment, in the form of a system of ordinary differential equations, by chemotherapy and radiotherapy where there is metastasis from a primary to a secondary site has been proposed and analyzed. The interaction between immune cells and cancer cells has been examined, and the chemotherapy agent has been considered as a predator on both normal and cancer cells. The metastasis may be time delayed. For better investigation of the treatment process and based on physical investigation, the immanent effects of inputs on cancer dynamic have been investigated. It is supposed that the interaction between NK cells and tumor cells changes during the chemotherapy. Thisnovel approach is useful not only to gain a broad understanding of the specific system dynamics but also to guide the development of combination therapies. The analysis is carried out both analytically (where possible) and numerically. By considering such immanent effects, the tumor-free equilibrium point will be stable at the end of treatment, and the tumor can not recur again, and the patient will totally recover. So, the present analysis suggests that a proper treatment method should change the dynamics of the cancer instead of only reducing the population of cancer cells.

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Does extirpation of the primary breast tumor give boost to growth of metastases? Evidence revealed by mathematical modeling

Cited by 26 publications

References 23 publications

Functions of hereditary immunity and xenogamy in cancer origin and pandemic spread

Functions of hereditary immunity and xenogamy in cancer origin and pandemic spread

Seeing the Invisible: How Mathematical Models Uncover Tumor Dormancy, Reconstruct the Natural History of Cancer, and Assess the Effects of Treatment

A mixed radiotherapy and chemotherapy model for treatment of cancer with metastasis

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