Spectroscopic Raman Analysis of Tumor Micro- and Macroenvironments in Human Breast and Rat Mammary Cancer

Author(s):  
Sixian You ◽  
Haohua Tu ◽  
Youbo Zhao ◽  
Yuan Liu ◽  
Eric J. Chaney ◽  
...  
2016 ◽  
Vol 2016 ◽  
pp. 1-12 ◽  
Author(s):  
Maria Isabel Carvalho ◽  
Ricardo Silva-Carvalho ◽  
Isabel Pires ◽  
Justina Prada ◽  
Rodolfo Bianchini ◽  
...  

Infiltrating cells of the immune system are widely accepted to be generic constituents of tumor microenvironment. It has been well established that the development of mammary cancer, both in humans and in dogs, is associated with alterations in numbers and functions of immune cells at the sites of tumor progression. These tumor infiltrating immune cells seem to exhibit exclusive phenotypic and functional characteristics and mammary cancer cells can take advantage of signaling molecules released by them. Cancer related inflammation has an important role in mammary carcinogenesis, contributing to the acquisition of core hallmark capabilities that allow cancer cells to survive, proliferate, and disseminate. Indeed, recent studies in human breast cancer and in canine mammary tumors have identified a growing list of signaling molecules released by inflammatory cells that serve as effectors of their tumor-promoting actions. These include the COX-2, the tumor EGF, the angiogenic VEGF, other proangiogenic factors, and a large variety of chemokines and cytokines that amplify the inflammatory state. This review describes the intertwined signaling pathways shared by T-lymphocytic/macrophage infiltrates and important tissue biomarkers in both human and dog mammary carcinogenesis.


1977 ◽  
Vol 63 (2) ◽  
pp. 155-162 ◽  
Author(s):  
Eugenia S. De Lustig ◽  
Nuria Cortada De De La Peña ◽  
Abel Canonico

The interferon production ability by leukocytes in vitro from 37 patients with mammary cancer was studied. The leukocytes were derived from patients between 27 and 80 years of age, 6 months and up to 28 years after removal of the primary tumor. The interferon titer of 34/37 human breast cancer leukocytes was 2–8 times lower than that of 35 normal donor leukocytes and 3 non-neoplastic diseases. No correlation between interferon titers, the patient's age, and the histologic tumor features was observed; however, interferon production was observed to return to normal in those patients who had a long remission period or whose tumors were locally confined. Interferon response of patients under different therapy was modified: radiotherapy affected interferon production more severely than chemotherapy. A tendency for association between the skin DNCB test and interferon response was found. An inverse correlation was observed between interferon titers and the PHA-induced transformation index.


2007 ◽  
Vol 28 (1) ◽  
pp. 39-51 ◽  
Author(s):  
Alexander N. Shoushtari ◽  
Aleksandra M. Michalowska ◽  
Jeffrey E. Green

2020 ◽  
Author(s):  
Sadaf Ambreen ◽  
Li Guanhan ◽  
Binbin Zhao ◽  
Gang Bao ◽  
Yiwen Song ◽  
...  

AbstractCanine mammary cancer is poorly characterized at the genomic level. Dog really can be an appropriate experimental model for human cancers from the genomic and evolutionary perspective or not? Here, we perform a cross-species cancer genomics analysis, independent evolution of cancer from normal tissues, which provide us an excellent opportunity to address an evolutionary perspective of cancer. As, evolutionary theories are critical for understanding tumorigenesis at the level of species as well as at the level of cells and tissues, for the development of effective therapies. Analysis of canine mammary cancer reveals a diversity of histological types as compare to human breast cancer. Our systematic analysis of 24 canine mammary tumors with whole-genome sequences, reveals 185 protein-coding cancer genes carried exonic mutations. Cross-species comparative analysis of 1080 human breast cancers identifies higher median mutation frequency in human breast cancer and canine mammary cancer shows lower across exonic regions (2.67 and 0.187 average no. of mutations per tumor per megabase (Mb), respectively). A comparison of somatic mutations in the PIK3CA gene, reveals common recurrence of the conserved mutations, in both species. However, the Ka/Ks ratio in the human PIK3CA gene 2.37 is higher and 1.43 in dogs is lower. To address the mutation accumulation and antagonistic pleiotropy theory, we investigated Ka/Ks value 237 aging-related genes from human and canine, the aging-related genes do not show selection in canine mammary cancer. It demonstrates new aspects of cancer genes that are evolving in different species instantaneously. These findings may suggest, the same organs in different mammals impose different selective pressures on the same set of genes in cancer. In both species, some genes may experience strong selective pressures, but do not converge genetically or the conserved genes do not show the same selection pressure in both species. However, human breast cancer shows transcriptomic similarity with canine mammary carcinoma but the other subtypes are quite different. We found canine mammary tumor can be used as a model for inter and intra-tumor heterogeneity. These findings provided insight into mammary cancer across species and possessed potential clinical significance. Collectively, these studies suggest a convergence of some genetic changes in mammary cancer between species but also distinctly different paths to tumorigenesis.


Author(s):  
John L. Swedo ◽  
John H. L. Watson ◽  
R. W. Talley

The literature is limited in its reporting of viral agents being found in solid tumor masses of human mammary cancer origin. In this continuing study of solid tumor masses, from intradermally located metastatic nodules of human breast cancer, particles have been seen which strongly resemble viruses. Their ultrastructural morphology is varied, leading to a large variety of particle types which present problems of interpretation. The present communication constitutes a survey of the variety of these particles which may represent viruses, the cytological conditions under which they are found and their relationship to the neoplastic cells.The first general group of particles are characterized by a single dense outer membrane and a dense inner core separated from the outer membrane by an electron lucent area (Fig. 1).


2005 ◽  
Vol 72 (S1) ◽  
pp. 51-57 ◽  
Author(s):  
John P Wiebe

Among the species investigated, the rate of spontaneous cancers of mammary glands is highest in humans and dogs (Hamilton, 1974; Owen, 1979). In addition, spontaneous mammary tumours are known to occur in strains of mice (Webster & Muller, 1994), rats (Russo et al. 1990; Sukumar, 1995) and cats (Hamilton, 1974; Kessler & von Bombard, 1997). Although both oestrogen and progesterone are known to be involved in normal mammary development as well as in the proliferative changes that occur during the oestrous or menstrual cycle, pregnancy and lactation (Going et al. 1988), only the role of oestradiol has been extensively investigated. The role of progesterone in mammary cancer is not understood and, although progesterone metabolism is known to occur in mammary tissue, the potential autocrine/paracrine role of the in situ metabolites has only recently begun to be explored in human breast tissues and cell lines (Wiebe et al. 2000).


2003 ◽  
pp. 153-159 ◽  
Author(s):  
E J S√°nchez-Barcel√≥ ◽  
S Cos ◽  
R Fern√°ndez ◽  
M D Mediavilla

Melatonin is an indolic hormone produced mainly by the pineal gland. The former hypothesis of its possible role in mammary cancer development was based on the evidence that melatonin down-regulates some of the pituitary and gonadal hormones that control mammary gland development and which are also responsible for the growth of hormone-dependent mammary tumors. Furthermore, melatonin could act directly on tumoral cells, as a naturally occurring antiestrogen, thereby influencing their proliferative rate. The first reports revealed a low plasmatic melatonin concentration in women with estrogen receptor (ER)-positive breast tumors. However, later studies on the possible role of melatonin on human breast cancer have been scarce and mostly of an epidemiological type. These studies described a low incidence of breast tumors in blind women as well as an inverse relationship between breast cancer incidence and the degree of visual impairment. Since light inhibits melatonin secretion, the relative increase in the melatonin circulating levels in women with a decreased light input could be interpreted as proof of the protective role of melatonin on mammary carcinogenesis. From in vivo studies on animal models of chemically induced mammary tumorigenesis, the general conclusion is that experimental manipulations activating the pineal gland or the administration of melatonin lengthens the latency and reduces the incidence and growth rate of mammary tumors, while pinealectomy usually has the opposite effects. Melatonin also reduces the incidence of spontaneous mammary tumors in different kinds of transgenic mice (c-neu and N-ras) and mice from strains with a high tumoral incidence. In vitro experiments, carried out with the ER-positive MCF-7 human breast cancer cells, demonstrated that melatonin, at a physiological concentration (1 nM) and in the presence of serum or estradiol: (a) inhibits, in a reversible way, cell proliferation, (b) increases the expression of p53 and p21WAF1 proteins and modulates the length of the cell cycle, and (c) reduces the metastasic capacity of these cells and counteracts the stimulatory effect of estradiol on cell invasiveness; this effect is mediated, at least in part, by a melatonin-induced increase in the expression of the cell surface adhesion proteins E-cadherin and beta(1)-integrin. The direct oncostatic effects of melatonin depends on its interaction with the tumor cell estrogen-responsive pathway. In this sense it has been demonstrated that melatonin down-regulates the expression of ERalpha and inhibits the binding of the estradiol-ER complex to the estrogen response element (ERE) in the DNA. The characteristics of melatonin's oncostatic actions, comprising different aspects of tumor biology as well as the physiological doses at which the effect is accomplished, give special value to these findings and encourage clinical studies on the possible therapeutic value of melatonin on breast cancer.


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