Advanced stage of breast cancer hoist alkaline phosphatase activity: risk factor for females in India

Singh, Anand; Pandey, Abha; Tewari, Mallika; Rajnish, Kumar; Sharma, Anju; Singh, Kritika; Pandey, Harsh; Shukla, H. S.

doi:10.1007/s13205-012-0113-1

Cited by 22 publications

(19 citation statements)

References 12 publications

(12 reference statements)

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“…Malignant lesions were seen in older age group (40-49 yrs) i.e 52.5% ( 16 found the levels of serum ALP were significantly higher in patients of carcinoma breast as compared to controls and that there was progressive increase in serum ALP activities with advance in stage of disease and metastasis.…”

Section: Vdiscussionmentioning

confidence: 90%

“A study of Serum levels of LDH and ALP in carcinoma breast: An Observational study”

Shrivastava¹,

Meena²,

Nandwani³

et al. 2016

IOSR

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Section: Vdiscussionmentioning

confidence: 90%

“A study of Serum levels of LDH and ALP in carcinoma breast: An Observational study”

Shrivastava¹,

Meena²,

Nandwani³

et al. 2016

IOSR

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“…ALPI has been closely linked to various malignancies and reported to be widely circulating in breast cancer patients (Singh et al 2013). ALPI activity has been reported to increase following the administration of a PPARa agonist (Stunes et al 2011).…”

Section: Discussionmentioning

confidence: 99%

MK886 inhibits the pioglitazone-induced anti-invasion of MDA-MB-231 cells is associated with PPARα/γ, FGF4 and 5LOX

2016

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The goal of this study was to determine the effects of PGZ and MK886 on the mRNA expression of PPARa and other associated genes in MDA-MB-231 cells, and the biological mechanisms induced by both drugs were also assessed. The levels of PPARa mRNA expression in PGZ-treated and MK886-treated MDA-MB-231 cells were determined using real-time PCR; the growth inhibitory effects of PGZ and MK886 were determined using the trypan blue exclusion assay; the induction of apoptosis by PGZ and MK886 was determined using DNA fragmentation assay and real-time PCR; and the invasion of PGZ-treated and MK886-treated MDA-MB-231 cells was determined using the wound healing and transwell migration assays. In addition, we correlated the expression of PPARa mRNA with other genes, including PPARc, FGF4 and 5LOX, in drug-treated MDA-MB-231 cells. Our results demonstrated that the treatment of MDA-MB-231 cells with PGZ increased the expression of PPARa/c mRNA and that this expression could be inhibited by treatment with MK886. Both drugs reduced the viability of MDA-MB-231 cells independently of PPARa/c mRNA expression but did not induce apoptosis. The wound caused by invasion was not healed by PGZ-treated MDA-MB-231 cells, but it was healed by MK886-treated cancer cells, indicating that the reduction of invasion in PGZ-treated MDA-MB-231 cells was eliminated by treatment with MK886, and this finding was validated by the transwell migration assay. This phenomenon might also be associated with the expression of PPARa/c, FGF4 and 5LOX mRNA in the treated cancer cells. This study provides useful information regarding the mRNA expression levels of PPARa and other related genes in MDA-MB-231 cells. These genes could be attractive targets for reducing the invasion of breast cancer.

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“…Mineralizing cell lines (MDA-MB-231 and SKBR3) displayed higher levels of ALP activity that was further increased by the addition of mineralization-promoting media [ 117 ]. Additionally, elevated levels of ALP in the serum of breast cancer patients were detected when compared to controls [ 118 ], in patients with bone metastases in comparison to patients without bone metastases [ 119 , 120 ], and also in advanced stages of breast cancer as compared to early stages and/or healthy controls [ 121 , 122 ]. These data suggest that in certain circumstances, a subpopulation of epithelial breast cancer cells may switch to osteoblast-like cells.…”

Section: Cellular and Molecular Mechanisms For Calcification In Thmentioning

confidence: 99%

Molecular Aspects of Thyroid Calcification

Ferreira

Gimba

Vinagre

et al. 2020

IJMS

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In thyroid cancer, calcification is mainly present in classical papillary thyroid carcinoma (PTC) and in medullary thyroid carcinoma (MTC), despite being described in benign lesions and in other subtypes of thyroid carcinomas. Thyroid calcifications are classified according to their diameter and location. At ultrasonography, microcalcifications appear as hyperechoic spots ≤ 1 mm in diameter and can be named as stromal calcification, bone formation, or psammoma bodies (PBs), whereas calcifications > 1 mm are macrocalcifications. The mechanism of their formation is still poorly understood. Microcalcifications are generally accepted as a reliable indicator of malignancy as they mostly represent PBs. In order to progress in terms of the understanding of the mechanisms behind calcification occurring in thyroid tumors in general, and in PTC in particular, we decided to use histopathology as the basis of the possible cellular and molecular mechanisms of calcification formation in thyroid cancer. We explored the involvement of molecules such as runt-related transcription factor-2 (Runx-2), osteonectin/secreted protein acidic and rich in cysteine (SPARC), alkaline phosphatase (ALP), bone sialoprotein (BSP), and osteopontin (OPN) in the formation of calcification. The present review offers a novel insight into the mechanisms underlying the development of calcification in thyroid cancer.

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Advanced stage of breast cancer hoist alkaline phosphatase activity: risk factor for females in India

Cited by 22 publications

References 12 publications

“A study of Serum levels of LDH and ALP in carcinoma breast: An Observational study”

“A study of Serum levels of LDH and ALP in carcinoma breast: An Observational study”

MK886 inhibits the pioglitazone-induced anti-invasion of MDA-MB-231 cells is associated with PPARα/γ, FGF4 and 5LOX

Molecular Aspects of Thyroid Calcification

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