Indicate whether each of the following descriptions applies to an oncogene, a proto-oncogene, or a tumor suppressor gene. Some descriptions may apply to more than one of these gene types

oncogene

proto-oncogene

tumor suppressor gene

oncogene and proto-oncogene

oncogene and tumor suppressor gene

proto-oncogene and tumor suppressor gene

oncogene, proto-oncogene, and tumor suppressor gene

- gene(s) whose presence can cause cancer.

- type of gene(s) found in normal cells.

- gene(s) that could code for a normal growth factor.

- type of gene(s) found only in cancer cells.

- type of gene(s) found in cancer cells.

- type of gene(s) found in normal cells and cancer cells.

- gene(s) whose absence can cause cancer.

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28 Sep 2023

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paraphrase the review in your own words?

The tumor suppressor PTEN (phosphatase and tensin homolog deleted from chromosome 10), is a lipid phosphatase that converts phosphatidylinositol-3, 4, 5- triphosphate (PIP3) into phosphatidylinositol (4, 5)- diphosphate (PIP2). PTEN is well-known as the most highly mutated tumor suppressor gene in the p53-post era [66, 67]. Recently, three papers by Nadav Bar and Rivka Dikstein, Linhua Liu and colleagues, and Laura Poliseno and colleagues, have demonstrated that PTEN was a bona fide target of miR-22 in a small cohort of cancer cell lines that are driven from breast cancer, cervical cancer, prostate cancer, and bronchial epithelial cancer. These studies contradict a uniform role of miR-22, indicating that under certain circumstances, miR-22 may function as an oncogene because of its antagonistic effects on tumor suppressive PTEN signaling [26, 68, 69] (Fig. 3). Using various miRNA target prediction programs and/or RNAhybrid program for evaluating the minimum free energy hybridization, these three groups all found that miR-22-PTEN was a high scoring miRNA-target pair. Enforced or reduced expression of miR-22 in human HEK293T, cervical cancer HeLa and breast cancer MCF-7 cell lines (Nadav Bar and Rivka Dikstein), anti-benzo[a]pyrene-7, 8-diol-9, 10-epoxide (anti-BPDE)-induced transformed human bronchial epithelial cancer cell line 16HBE-T (Linhua Liu and colleagues) and prostate cancer cell line DU145 (Laura Poliseno and colleagues), revealed that miR-22 negatively regulated PTEN protein expression. Intriguingly, an inverse correlation between miR-22 and PTEN mRNA expression has been presented by Poliseno et al., while Liu et al. found that there was no change of PTEN mRNA expression regardless of miR- 22 levels. A similarly inverse association of miR-22 and J. Xiong PTEN protein levels was observed in 16HBE-T and its parental normal cell line16HBE (Linhua Liu and colleagues), and in several prostate cancer cell lines, prostate cell lines and a prostate tumor tissue microarray (Laura Poliseno and colleagues). Furthermore, the mature levels of miR-22 were significantly increased in these tumor cells versus their normal counterparts. In line with this result, a direct correlation between miR-22 expression and phosphorylated AKT or between the expression of miR- 22 and that of DICER was also identified by Laura Poliseno and colleagues. These three groups all showed that an intact binding site at the 3âUTR of PTEN mRNA was required for miR-22 targeting. Functional analyses showed that miR-22 could induce apoptosis, inhibited colony formation and suppressed motility of bronchial epithelial cancer cells (Linhua Liu and colleagues), and intrinsically promote prostate cancer cell growth and tumorigenesis in tumor-bearing nude mice (Laura Poliseno and colleagues). Subsequently, the influence of miR-22 on the downstream signaling of PTEN was tested. Bar et al. showed that miR-22 could stimulate AKT activity, and in turn, AKT significantly upregulated miR-22 expression, suggesting a regulatory loop comprising miR-22, PTEN and AKT. Analogously, Poliseno et al. showed that miR-22-mediated oncogenic activity was dependent on decreased PTEN expression and increased phosphorylated AKT [26, 68, 69]. Surprisingly, the conclusion presented by these three papers is challenged by a more recent study that argues against the downregulation of PTEN by miR-22 [70]. The cytotoxicity of paclitaxel, a featured anti-tumor activity, can induce apoptosis, and inhibit proliferation and survival of p53 wild-type colon cancer cells, rather than chemoresistant p53-mutated colon cancer cells. Chemoresistance assay showed that overexpression of miR-22 prevented the chemoresistance to paclitaxel and induced apoptosis, and inhibited proliferation and survival of p53-mutated colon cancer cells. Finally, Li et al. pinpointed that tumor-suppressive miR-22 decreased AKT activity and MTDH expression, and subsequently increased Bax and active caspase-3 expression through upregulation of PTEN expression. These studies emphasize the complex of miR-22 function in tumor pathways, and provide another good example identical to miR-17-92 cluster that functions as either tumor suppressors or oncogenes due to cell types and expression profiles of miRNA-target pairs [71]. Paradoxically, contrary to the conventional view that different target repertoire of one miRNA contributes to its distinct functional role, miR-22 leads to the opposite effects on the regulation of the same target gene PTEN and the acquisition of tumor cell phenotypes. Further investigations will be required to elucidate this cellular context-dependent role of miR-22 as a key negative or positive regulator of PTEN, and as a tumor suppressor or an oncogene.

skydeer878

Which of the following provides the earliest indication of genetic problems in a fetus?
-Amionocentesis

-Chorionic Villus sampling

-Maternal and paternal karyotyping

-All of the above

Select the factors that would not indicate that a disease had a genetic, rather than an environmental, cause.

	a.	The disease spreads from person to person.
	b.	The disease has a specific age of onset.
	c.	There is a high level of the disease's concordance among monozygotic twins.
	d.	The disease does not spread to people sharing similar environmental situations.

Can someone help me match these, I keep getting two wrong

Match each term below with the appropriate description. Each term may be used only once.

- .	Oncogene
-	Transformation
-	Locus heterogeneity
-	Monozygotic twins
-	Growth factor

a.	With retinitis pigmentosa (an inherited retinal degeneration) there are multiple genes that, when mutated, can cause the retinitis pigmentosa phenotype
b.	A malignant cell results from the conversion of a normal cell
c.	abl tyrosine kinase, for example
d.	A gene-encoded extracellular hormone
e.	The high concordance suggests a genetic basis for disease

ivorylion763

Match the type of phenotypic change between the type of Gene and chain you're most likely to cause it. Each type of Gene and change may be used more than once or may not be used at all.

phenotypic changes
1. A protein normally localized in the nucleus is not localized in the cytoplasm
2. A protein acquires a DNA binding domain
3. Tandem copies of a gene are found in the genome.
4. A copy of a bacterial Gene is now found integrated on a human chromosome.
5. A protein becomes much more unstable
6. A protein normally expressed only in the liver is now expressed in blood cells.

A. mutation within a gene
B. Gene duplication
C. mutation in a regulatory region
D. Exon shuffling
E. horizontal Gene transfer

could I get some help with this problem I'm not too sure about my answers thank you