Tumor stasis factor (TSF): A possible mechanism for the regulation of tumor cell proliferation

Jack A. Roth, Darrell Davidson, Robert S. Ames, Philip D. Schneider

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

A new class of factors that regulates tumor cell division in vitro can be isolated from fresh and cultured tumor cells by 3 M KCl extraction. Tumor stasis factors (TSF) inhibiting cultured tumor cell proliferation were extracted from 8 of 11 fresh human tumors and 2 cultured tumor cell lines. TSF inhibited [3H]Tdr incorporation by allogeneic and autologous cultured tumor cells in a dose-dependent manner. Extracts of normal human tissues and benign tumors did not demonstrate inhibition with the exception of liver. The mechanism of inhibition was cytostatic and not cytotoxic as demonstrated with trypan blue exclusion by tumor cells following TSF treatment, maintenance of intact tumor cell monolayers following addition of TSF, and lack of inhibition of Con A-mediated lymphocyte proliferation by TSF. TSF activity could be reversed by washing for up to 48 hr of incubation and was resistant to heat, pH alterations, reducing agents, proteases, and glycosidases. However, the active moiety bound to lentil lectin and could be purified 80-fold by preparative isoelectric focusing. These factors may represent a novel regulatory mechanism for tumor cell proliferation.

Original languageEnglish (US)
Pages (from-to)298-309
Number of pages12
JournalJournal of Surgical Research
Volume35
Issue number4
DOIs
StatePublished - 1983
Externally publishedYes

Fingerprint

Cell Proliferation
Cultured Tumor Cells
Neoplasms
Trypan Blue
Glycoside Hydrolases
Reducing Agents
Cytostatic Agents
Isoelectric Focusing
Tumor Cell Line
Cell Division
Peptide Hydrolases
Hot Temperature
Maintenance
Lymphocytes
Liver

ASJC Scopus subject areas

  • Surgery

Cite this

Tumor stasis factor (TSF) : A possible mechanism for the regulation of tumor cell proliferation. / Roth, Jack A.; Davidson, Darrell; Ames, Robert S.; Schneider, Philip D.

In: Journal of Surgical Research, Vol. 35, No. 4, 1983, p. 298-309.

Research output: Contribution to journalArticle

Roth, Jack A. ; Davidson, Darrell ; Ames, Robert S. ; Schneider, Philip D. / Tumor stasis factor (TSF) : A possible mechanism for the regulation of tumor cell proliferation. In: Journal of Surgical Research. 1983 ; Vol. 35, No. 4. pp. 298-309.
@article{e40a6bffdf5546f3af94f3751a647937,
title = "Tumor stasis factor (TSF): A possible mechanism for the regulation of tumor cell proliferation",
abstract = "A new class of factors that regulates tumor cell division in vitro can be isolated from fresh and cultured tumor cells by 3 M KCl extraction. Tumor stasis factors (TSF) inhibiting cultured tumor cell proliferation were extracted from 8 of 11 fresh human tumors and 2 cultured tumor cell lines. TSF inhibited [3H]Tdr incorporation by allogeneic and autologous cultured tumor cells in a dose-dependent manner. Extracts of normal human tissues and benign tumors did not demonstrate inhibition with the exception of liver. The mechanism of inhibition was cytostatic and not cytotoxic as demonstrated with trypan blue exclusion by tumor cells following TSF treatment, maintenance of intact tumor cell monolayers following addition of TSF, and lack of inhibition of Con A-mediated lymphocyte proliferation by TSF. TSF activity could be reversed by washing for up to 48 hr of incubation and was resistant to heat, pH alterations, reducing agents, proteases, and glycosidases. However, the active moiety bound to lentil lectin and could be purified 80-fold by preparative isoelectric focusing. These factors may represent a novel regulatory mechanism for tumor cell proliferation.",
author = "Roth, {Jack A.} and Darrell Davidson and Ames, {Robert S.} and Schneider, {Philip D.}",
year = "1983",
doi = "10.1016/0022-4804(83)90005-7",
language = "English (US)",
volume = "35",
pages = "298--309",
journal = "Journal of Surgical Research",
issn = "0022-4804",
publisher = "Academic Press Inc.",
number = "4",

}

TY - JOUR

T1 - Tumor stasis factor (TSF)

T2 - A possible mechanism for the regulation of tumor cell proliferation

AU - Roth, Jack A.

AU - Davidson, Darrell

AU - Ames, Robert S.

AU - Schneider, Philip D.

PY - 1983

Y1 - 1983

N2 - A new class of factors that regulates tumor cell division in vitro can be isolated from fresh and cultured tumor cells by 3 M KCl extraction. Tumor stasis factors (TSF) inhibiting cultured tumor cell proliferation were extracted from 8 of 11 fresh human tumors and 2 cultured tumor cell lines. TSF inhibited [3H]Tdr incorporation by allogeneic and autologous cultured tumor cells in a dose-dependent manner. Extracts of normal human tissues and benign tumors did not demonstrate inhibition with the exception of liver. The mechanism of inhibition was cytostatic and not cytotoxic as demonstrated with trypan blue exclusion by tumor cells following TSF treatment, maintenance of intact tumor cell monolayers following addition of TSF, and lack of inhibition of Con A-mediated lymphocyte proliferation by TSF. TSF activity could be reversed by washing for up to 48 hr of incubation and was resistant to heat, pH alterations, reducing agents, proteases, and glycosidases. However, the active moiety bound to lentil lectin and could be purified 80-fold by preparative isoelectric focusing. These factors may represent a novel regulatory mechanism for tumor cell proliferation.

AB - A new class of factors that regulates tumor cell division in vitro can be isolated from fresh and cultured tumor cells by 3 M KCl extraction. Tumor stasis factors (TSF) inhibiting cultured tumor cell proliferation were extracted from 8 of 11 fresh human tumors and 2 cultured tumor cell lines. TSF inhibited [3H]Tdr incorporation by allogeneic and autologous cultured tumor cells in a dose-dependent manner. Extracts of normal human tissues and benign tumors did not demonstrate inhibition with the exception of liver. The mechanism of inhibition was cytostatic and not cytotoxic as demonstrated with trypan blue exclusion by tumor cells following TSF treatment, maintenance of intact tumor cell monolayers following addition of TSF, and lack of inhibition of Con A-mediated lymphocyte proliferation by TSF. TSF activity could be reversed by washing for up to 48 hr of incubation and was resistant to heat, pH alterations, reducing agents, proteases, and glycosidases. However, the active moiety bound to lentil lectin and could be purified 80-fold by preparative isoelectric focusing. These factors may represent a novel regulatory mechanism for tumor cell proliferation.

UR - http://www.scopus.com/inward/record.url?scp=0021086426&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0021086426&partnerID=8YFLogxK

U2 - 10.1016/0022-4804(83)90005-7

DO - 10.1016/0022-4804(83)90005-7

M3 - Article

C2 - 6621026

AN - SCOPUS:0021086426

VL - 35

SP - 298

EP - 309

JO - Journal of Surgical Research

JF - Journal of Surgical Research

SN - 0022-4804

IS - 4

ER -