+ Site Statistics
References:
54,258,434
Abstracts:
29,560,870
PMIDs:
28,072,757
+ Search Articles
+ Subscribe to Site Feeds
Most Shared
PDF Full Text
+ PDF Full Text
Request PDF Full Text
+ Follow Us
Follow on Facebook
Follow on Twitter
Follow on LinkedIn
+ Translate
+ Recently Requested

Host response in tumor growth and progression



Host response in tumor growth and progression



Invasion and Metastasis 16(4-5): 235-246



Tumor growth and progression result from complex controls that appear to be facilitated by the growth factors (GFs) which emerge from the tumor and find responsive targets both within the tumor and in the surrounding host. For example, basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF) are both angiogenic signals which appear to emerge from upregulated genetic messages in the proliferating rim of a solid tumor in response to tumor-wide hypoxia. If these signals are generated in response to unfavorable environmental conditions, i.e. a tumor-wide decrease in oxygen tension, then the tumor may be playing a role in manipulating its own environment. Two questions are raised in this paper: (1) How does the host respond to such signals? (2) Is there a linkage between the host's response and the ultimate growth of the tumor? To answer these questions, we have idealized these adaptive signals within a mathematical model of tumor growth. The host response is characterized by a function which represents the host's carrying capacity for the tumor. If the function is constant, then environmental control is strictly limited to tumor shape and mitogenic signal processing. However, if we assume that the response of the local stroma to these signals is an increase in the host's ability to support an ever larger tumor, then the model describes a positive feedback controller. In this paper, we summarize our previous results and ask the question: What form of host response is reasonable, and how will it affect ultimate tumor growth? We examine some specific candidate response functions, and analyze them for system stability. In this model, unstable states correspond to 'infinite' tumor growth. We will also discuss countervailing negative feedback signals and their roles in maintaining tumor stability.

(PDF emailed within 1 workday: $29.90)

Accession: 046274909

Download citation: RISBibTeXText

PMID: 9311388


Related references

Tumor progression, biology, and host response in melanoma. Current Opinion in Oncology 4(2): 351-356, 1992

Cancer growth and progression vol 4 influence of the host on tumor development. Herberman, Rd. . Cancer Growth And Progression, Vol. 4. Influence Of The Host On Tumor Development. X . Kluwer Academic Publishers: Dordrecht, Netherlands; Boston, Massachusetts, Usa. Illus. X 191p, 1988

Cancer growth and progression vol 3 influence of tumor development on the host. Liotta, Ld. . Cancer Growth And Progression, Vol. 3. Influence Of Tumor Development On The Host. X 240p. Kluwer Academic Publishers: Dordrecht, Netherlands; Boston, Massachusetts, Usa. Illus. X 240p, 1988

Role of immune response as determinant of tumor progression in function of host age in the B16 melanoma. Mechanisms of Ageing & Development 80(2): 121-137, 1995

Metastatic variants derived following in vivo tumor progression of an in vitro transformed squamous cell carcinoma line acquire a differential growth advantage requiring tumor-host interaction. Clinical & Experimental Metastasis 15(5): 527-537, 1997

Tumor and host-mediated pathways of resistance and disease progression in response to antiangiogenic therapy. Clinical Cancer Research 15(16): 5020-5025, 2009

Fibroblast growth factor-2-induced host stroma reaction during initial tumor growth promotes progression of mouse melanoma via vascular endothelial growth factor A-dependent neovascularization. Cancer Science 98(4): 541-548, 2007

Tissue transglutaminase is expressed as a host response to tumor invasion and inhibits tumor growth. Laboratory Investigation; a Journal of Technical Methods and Pathology 79(12): 1679-1686, 2000

Host's immune state and kinetics of local tumor growth control--progression of postoperative lung metastasis. Recent Results in Cancer Research. Fortschritte der Krebsforschung. Progres Dans les Recherches sur le Cancer 75: 20-28, 1980

Biopsychosocial studies on cutaneous malignant melanoma: psychosocial factors associated with prognostic indicators, progression, psychophysiology and tumor-host response. Social Science and Medicine 20(8): 833-840, 1985

A validated mathematical model of tumor growth including tumor-host interaction, cell-mediated immune response and chemotherapy. Bulletin of Mathematical Biology 76(11): 2884-2906, 2016

Myeloid cells in cancer progression: unique subtypes and their roles in tumor growth, vascularity, and host immune suppression. Cancer Microenvironment 4(1): 1-11, 2010

Local gene delivery of tumor necrosis factor alpha can impact primary tumor growth and metastases through a host-mediated response. Clinical and Experimental Metastasis 24(7): 521-531, 2007

Enhanced cell surface expression of matrix metalloproteinases and their inhibitors, and tumor-induced host response in progression of human gastric carcinoma. Digestive Diseases and Sciences 49(10): 1621-1630, 2004