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Malignantly transformed cells

Many growth factors that become soluble after having been processed arc not shed and remain anchored to the membrane. Therefore, the distinction between membrane-anchored and diffusible growth factors is somewhat ambiguous. In malignant transformed cells, diffusible factors may be retained in the membrane of the same cell where they are S3tithesized and processed. This can stimulate the cell in an autocrine fashion with deleterious effects. [Pg.7]

Fig. 4. Four routes of cellular secretion of gastrin. Several other regulatory systems, wherein the same peptide acts as hormone, neurotransmitter, and growth factor, are also released as they occur in these four cell types. Autocrine and paracrine secretion are assumed to play decisive roles for the growth of malignantly transformed cells. Fig. 4. Four routes of cellular secretion of gastrin. Several other regulatory systems, wherein the same peptide acts as hormone, neurotransmitter, and growth factor, are also released as they occur in these four cell types. Autocrine and paracrine secretion are assumed to play decisive roles for the growth of malignantly transformed cells.
Comment. For gains of viability or virulence, the unicellular eukaryotes frequently use fused gene product proteins (enzymes). For gains of viability, malignantly transformed cells of higher multinucleated hosts frequently use fused gene product proteins (tyrosine kinase oncoproteins). [Pg.165]

Aneuploidy is consequential to mitotic errors malignantly transformed cells frequently commit mitotic errors. In fetal life, the developing human brain suffers of chromosomal segregational defects during mitoses of glial cells and neurons. Aneuploid brain cells are eliminated by apoptosis. Areas not cleared by apoptosis, remain confined to sites of chromosomal mosaicism. The presence of functionally active aneuploid neurons negatively affect neuron-to-neuron and neuron-to-gUal interactions [1291]. [Pg.301]

Comment. The ancestral arginine methyltransferases serving the survival and life cycles of their unicellular hosts, and their descendants, but now constitutively expressed, promote and sustain the malignantly transformed cells in their multicellular hosts, in the state of their incessant mitoses, locomotion and invasiveness. [Pg.329]

In their host, tumor cells and lymphocytes (immune T cell NK cells) encounter each other, and both subjects of observation emit exosomes. The exosomes are engulfed by various host cells. Even in the case of an incipient and localized tumor, the entire host is made aware that a malignantly transformed cell colony is on board. It is under extensive investigation what biological effects exosomes may convey. With considerable oversimplification, it appears that exosomes of tumor cell-derivation are more immunosuppressive than immunostimulatory. Whereas exosomes derived from reactive DCs and immune T cells convey immunostimulatory effects. Tumor cells communicate to re-assert their presence by releasing microvesicles in the host s blood and lymph circulation [1960-1964]. [Pg.433]

The HeLa cells originally were transformed by the HPV-encoded oncoproteins (that neutralize p53 and Rb cellular mmor suppressor genes). Distinction between self and non-self probably did not exist when ancient chimeric cells were formed, and engulfed bacteria were accepted as self (proteobacteria for the mitochondrion cyanobacteria for the chloroplast). Malignantly transformed cells appear to be impervious, as to the distinction between self and non-self, when it comes to... [Pg.480]


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See also in sourсe #XX -- [ Pg.14 , Pg.15 , Pg.17 , Pg.214 , Pg.313 ]




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Adhesiveness of Transformed and Malignant Cells

Cell transformation

Cells malignant

Cells malignant transformation

Cells malignant transformation

Malignancy

Malignant

Malignant transformation

Transformed cells

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