Inhibition of Tumor Growth by Recognition Factors

Luzio, N. R. Di; McNamee, Rose B.; Olcay, I.; Kitahama, Akio; Miller, Rita H.

doi:10.3181/00379727-145-37800

Cited by 21 publications

(4 citation statements)

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“…Recent findings from this laboratory and others have accentuated the importance of opsonin protein or so-called humoral recognition factor (HRF) in the control of RE cell phagocytosis, especially hepatic clearance activity (Allen, Saba and Molnar, 1973;DiLuzio et al, 1974b;Saba, 1975). Opsonic protein has been isolated and is a heat-labile, large molecular weight, alpha-2-acid glycoprotein, unrelated to complement and highly dependent on heparin for expression of its phagocytosis stimulating capacity (Allen et at., 1973;Saba, 1970bSaba, , 1975.…”

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confidence: 99%

“…Determinations of opsonin levels by bioassay have demonstrated a decline following colloid induced RE blockade, major surgery, burn injury and traumatic shock (Saba, 1970a(Saba, , b, 1972Saba and DiLuzio, 1969). Moreover, Pisano et al (1972) have demonstrated opsonin or recognition factor depletion in patients with advanced malignant disease and a precipitate fraction of plasma containing HRF or opsonin will inhibit tumor growth in experimental animals (DiLuzio et al, 1974b).…”

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confidence: 99%

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Humoral mediated macrophage response during tumour growth

Saba¹,

Antikatzides²

1975

Br J Cancer

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confidence: 99%

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confidence: 99%

Humoral mediated macrophage response during tumour growth

Saba¹,

Antikatzides²

1975

Br J Cancer

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“…Macrophage discrimination between foreign matter (non-self), altered endogenous tissue (altered self) and healthy indigenous tissue (self) (Saba, 1970) (Di Luzio, 1975;Pisano et al, 1972;Saba, 1970 (Biozzi et al, 1958;Di Luzio et al, 1974;Hibbs et al, 1972a,b;Keller, 1975;Keller & Hess, 1972;Old et al, 1961 Additionally, phagocytosis is greatest in inbred mice manifesting the lowest incidence of spontaneous tumours, whilst mice with the greatest incidence of spontaneous tumours have lower basal levels of RE activity (Stern et al, 1967;Stern, 1960).…”

Section: Discussionmentioning

confidence: 99%

Circulating immunoreactive and bioassayable opsonic plasma fibronectin during experimental tumour growth

Saba¹,

Gregory²,

Blumenstock³

1980

Br J Cancer

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Immunoreactive and bioassayable plasma fibronectin (opsonic α 2 surface-binding (SB) glycoprotein) was measured during experimental Sarcoma-180 tumour growth in mice. Male C57BL/6 mice were challenged s.c. with 2 × 10 6 viable Sarcoma-180 tumour cells and evaluated sequentially in parallel with saline-injected controls over a 21-day experimental period. Before challenge, immunoreactive plasma fibronectin was 1050-1150 μg/ml. Minimal tumour growth occurred until 6 days after tumour challenge. There was then a rapid increase in primary tumour size, especially over the 7-14-day interval, with a plateau of growth over the 18-21-day interval. Immunoreactive plasma fibronectin was significantly ( P < 0·05) raised at 3 and 7 days after tumour challenge. A rapid rise ( P < 0·001) to 2816·6 ± 158·9 μg/ml was observed at 14 days followed by a modest decline at 21 days. Bioassayable opsonic activity increased ( P < 0·5) with the rise in immunoreactive fibronectin 3 and 7 days after tumour challenge, but the rapid rise in immunoreactive fibronectin over the 7-14-day interval was associated with a significant ( P < 0·5) fall in bioassayable opsonic activity. Thus, the rapid rise in immunoreactive plasma fibronectin parallels the rapid rate of tumour growth, but is associated with a fall in opsonically active plasma fibronectin. Dissociation between immunoreactive and opsonically active plasma fibronectin may be mediated by inhibition and/or alteration of circulating fibronectin during rapid tumour growth. Alternatively, it may reflect increased release of antigenically related protein (i.e. cell-surface fibronectin) during rapid tumour growth, which may have limited biological opsonic activity. Images Fig. 2

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“…Recent findings by Mansell et al (1975), utilizing the alpha-2-globulin opsonic protein or so-called recognition factor (RF) protein (Di Luzio, 1975;Di Luzio et al, 1974), have documented the ability for this protein (especially in conjunction with glucan, a macrophage activator) to induce necrosis of malignant lesions in patients (Mansell et al, 1975). Additionally, opsonin depletion has been documented in animals following the i.v.…”

Section: Discussionmentioning

confidence: 99%

Decreased resistance to intravenous tumour-cell challenge during reticuloendothelial depression following surgery1

Saba¹,

Antikatzides²

1976

Br J Cancer

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17*9 ± 0-8 days, while animals challenged during the period of RE depression survived 7.9 ± 0-4 days. An increased incidence of respiratory distress and nasal discharge was observed in the animals with impaired survival. Thus, surgical manipulation may transiently compromise RES systemic host defence and may be reflected in an increment in the pulmonary localization of blood-borne tumour cells. The relationship of this altered pattern of tumour cell distribution to the impaired survival remains to be determined, and warrants investigation.

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Inhibition of Tumor Growth by Recognition Factors

Cited by 21 publications

References 0 publications

Humoral mediated macrophage response during tumour growth

Humoral mediated macrophage response during tumour growth

Circulating immunoreactive and bioassayable opsonic plasma fibronectin during experimental tumour growth

Decreased resistance to intravenous tumour-cell challenge during reticuloendothelial depression following surgery1

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