The effect of isoprenaline on induction of tumours by methyl nitrosourea in the salivary and mammary glands of female wistar rats

Parkin, Rebecca; Neale, S.

doi:10.1038/bjc.1976.189

Cited by 9 publications

(16 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Since similar nodular proliferation was not observed in the controls, the proliferation may be eonsidered the result of the combined effeet of isoproterenol and X-irradiation. Enhancement of the neoplastic effeet of several agents ineluding X-irradiation by stimulating the target cells to proliferate has been reported by Cole & Nowell (1965) and by Parkin & Neale (1976).…”

Section: B Reparative and Proliferative Changesmentioning

confidence: 91%

Morphologic changes in rat parotid following isoproterenol administration and fractionated X‐irradiation

Nicolatou¹

1981

J Oral Pathology Medicine

View full text Add to dashboard Cite

The effects of fractionated X‐irradiation following isoproterenol (1PN) administration on rat parotid gland were studied 4, 8, and 12 weeks post‐irradiation. Degenerative and necrotic changes of the acinar cells were observed at all three time intervals as a result of the radiation. These changes were more obvious 4 and 8 weeks post‐irradiation and isoproterenol administration. The necrotic acinar cells were replaced by fibrous connective tissue, especially conspicuous at 12 weeks. Reparative changes were observed along with the degenerative and regressive phenomena of the gland. Enlarged acinar cells and nuclei were observed as early as 4 weeks post‐irradiation. This change was locally distributed at the 4–week interval but more widespread 8 and 12 weeks post‐irradiation. Mitochondria! hyperplasia with alteration of mitochondria! cristae was observed 12 weeks post‐irradiation. Proliferation of cells of ductal origin and nodular proliferation of ducts were observed 12 weeks after isoproterenol administration plus X‐irradiation. These proliferative phenomena may represent an early stage of tumor formation resulting from the combined effect of isoproterenol and X‐irradiation on rat parotid gland.

show abstract

Section: B Reparative and Proliferative Changesmentioning

confidence: 91%

Morphologic changes in rat parotid following isoproterenol administration and fractionated X‐irradiation

Nicolatou¹

1981

J Oral Pathology Medicine

View full text Add to dashboard Cite

show abstract

“…In fact, several studies have shown that adrenergic stimulation may suppress synthesis and secretion of milk proteins, as described for stress exposure (Bisset et al, 1967; “Catecholamine antagonism to oxytocin‐induced milk‐ejection,” 1971; Chiba et al, 2019; Clapp et al, 1985; S. L. Song et al, 1988). Furthermore, in models of chemically induced breast cancer, it was shown that exposure to stress or to adrenergic agonists can accelerate the onset of cancer (Adamekova et al, 2003; Boyd et al, 2010; Parkin & Neale, 1976), whereas propranolol, a nonselective β‐adrenoceptor antagonist, can delay its appearance (Tibensky et al, 2021). The results from epidemiological studies may also be taken as an indicator for such connection between stress/adrenergic stimulation and cancer incidence since a correlation between stress exposure and breast cancer incidence has been reported (Chiriac et al, 2018; Kruk et al, 2019; P. Li et al, 2016; Lillberg et al, 2003).…”

Section: The Adrenergic System In the Breast Tumor Microenvironmentmentioning

confidence: 99%

Contribution of adrenergic mechanisms for the stress‐induced breast cancer carcinogenesis

Silva

Quintas

Gonçalves

et al. 2022

Journal Cellular Physiology

View full text Add to dashboard Cite

Breast cancer is the most common and deadliest type of cancer in women. Stress exposure has been associated with carcinogenesis and the stress released neurotransmitters, noradrenaline and adrenaline, and their cognate receptors, can participate in the carcinogenesis process, either by regulating tumor microenvironment or by promoting systemic changes. This work intends to provide an overview of the research done in this area and try to unravel the role of adrenergic ligands in the context of breast carcinogenesis.In the initiation phase, adrenergic signaling may favor neoplastic transformation of breast epithelial cells whereas, during cancer progression, may favor the metastatic potential of breast cancer cells. Additionally, adrenergic signaling can alter the function and activity of other cells present in the tumor microenvironment towards a protumor phenotype, namely macrophages, fibroblasts, and by altering adipocyte's function. Adrenergic signaling also promotes angiogenesis and lymphangiogenesis and, systemically, may induce the formation of preneoplastic niches, cancerassociated cachexia and alterations in the immune system which contribute for the loss of quality of life of breast cancer patients and their capacity to fight cancer.Most studies points to a major contribution of β 2 -adrenoceptor activated pathways on these effects. The current knowledge of the mechanistic pathways activated by β 2 -adrenoceptors in physiology and pathophysiology, the availability of selective drugs approved for clinical use and a deeper knowledge of the basic cellular and molecular pathways by which adrenergic stimulation may influence cancer initiation and progression, opens the possibility to use new therapeutic alternatives to improve efficacy of breast cancer treatments.

show abstract

“…Thyroid tumor incidences were maxi mal when X-ray treatments were timed at the peak of cell proliferation and remained high throughout an extended period of elevated thyroid cell proliferation. Parkin and Neale [14] evaluated carcinogenesis in salivary glands of rats treated with isoprenaline sul fate. Isoprenaline sulfate pretreatments pro duced a marked (12-fold) stimulation of cell proliferation in the salivary glands but only a 2-to 3-fold increase in mammary gland cell proliferation.…”

Section: Studies In Tissue Cells In Vivomentioning

confidence: 99%

The Cell Cycle and Chemical Carcinogenesis

Grisham¹,

Kaufman²

1983

Pathol Immunopathol Res

View full text Add to dashboard Cite

The effect of isoprenaline on induction of tumours by methyl nitrosourea in the salivary and mammary glands of female wistar rats

Abstract: Summary.-Pretreatment of rats with isoprenaline sulphate (IPR) stimulated DNA synthesis in both salivary and mammary gland tissues.

Cited by 9 publications

References 25 publications

Morphologic changes in rat parotid following isoproterenol administration and fractionated X‐irradiation

Morphologic changes in rat parotid following isoproterenol administration and fractionated X‐irradiation

Contribution of adrenergic mechanisms for the stress‐induced breast cancer carcinogenesis

The Cell Cycle and Chemical Carcinogenesis

Contact Info

Product

Resources

About