Anatomy and Cell Biology 4461B Lecture Notes - Gadolinium, Ct Scan, Aconitase

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tanhippopotamus305

13 Jun 2012

School

Western University

Department

Anatomy and Cell Biology

Course

Anatomy and Cell Biology 4461B

Professor

Geordie Shepherd

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Document Summary

Jl lecture 2: the role of imaging in prostate cancer. Interaction with host blood cells: clonal expansion, growth, diversification and angiogenesis, migration through the basement membrane. 5: formation of tumor embolus, arrest in capillaries and adhesion to basement membrane, extravasation, metastatic deposit and growth in secondary organ. Metastasis is extremely inefficient; less than 0. 01 of cell that originated from the primary tumor actually metastasize. Models of prostate cancer: other than man, dog is the only animal known to have spontaneous high grade pin and prostate cancer and have similar disease characteristics including age of onset, metastasis and androgen independence. Animal models: xenografts - can be subcutaneous or orthotopic (in the prostate). For ex. haploinsufficiency of pten is an early event in prostate tumorigenesis, resulting in the development of high-grade pin. If you in- ject tumor cells in the chick embryo, can see a dramatic increase in blood vessel growth.

Related Questions

Circulating Tumor Cells (CTCs) are linked with metastasis andtheir presence can be used to indicate the onset of metastaticcancer. Likewise, the Cancer Stem Cell (CSC) hypothesis suggeststhat tumorigenic stem cells are the source of cancer. However,microscopy experiments and cytometry have suggested that themorphology of CTCs and CSCs are quite different. Essentially, wehave not been able to find Circulating Cancer Stem Cells (asidesMyeloma since they are circulating anyways).

My question is how similar are these cells? If they aredifferent, is relapse caused by the CSCs from the primary tumor orCTCs in metasises that have become CSC-like?

Abstract 1

Breast cancer-associated metastasis is significantly increased ina
model of autoimmune arthritis

Lopamudra Das Roy,1,2 Latha B Pathangey,1 Teresa L Tinder,1,2 JorgeL Schettini,1,2 Helen E Gruber,3 and Pinku Mukherjee1,2

Breast Cancer Res. 2009; 11(4): R56.

Introduction

Sites of chronic inflammation are often associated with theestablishment and growth of various malignancies including breastcancer. A common inflammatory condition in humans is autoimmunearthritis (AA) that causes inflammation and deformity of thejoints. Other systemic effects associated with arthritis includeincreased cellular infiltration and inflammation of the lungs.Several studies have reported statistically significant risk ratiosbetween AA and breast cancer. Despite this knowledge, available fora decade, it has never been questioned if the site of chronicinflammation linked to AA creates a milieu that attracts tumorcells to home and grow in the inflamed bones and lungs which arefrequent sites of breast cancer metastasis.

Methods

To determine if chronic inflammation induced by autoimmunearthritis contributes to increased breast cancer-associatedmetastasis, we generated mammary gland tumors in SKG mice that weregenetically prone to develop AA. Two breast cancer cell lines, onehighly metastatic (4T1) and the other non-metastatic (TUBO) wereused to generate the tumors in the mammary fat pad. Lung and bonemetastasis and the associated inflammatory milieu were evaluated inthe arthritic versus the non-arthritic mice.

Results

We report a three-fold increase in lung metastasis and asignificant increase in the incidence of bone metastasis in thepro-arthritic and arthritic mice compared to non-arthritic controlmice. We also report that the metastatic breast cancer cellsaugment the severity of arthritis resulting in a vicious cycle thatincreases both bone destruction and metastasis. Enhancedneutrophilic and granulocytic infiltration in lungs and bone of thepro-arthritic and arthritic mice and subsequent increase incirculating levels of proinflammatory cytokines, such as macrophagecolony stimulating factor (M-CSF), interleukin-17 (IL-17),interleukin-6 (IL-6), vascular endothelial growth factor (VEGF),and tumor necrosis factor-alpha (TNF-alpha) may contribute to theincreased metastasis. Treatment with anti-IL17 + celecoxib, ananti-inflammatory drug completely abrogated the development ofmetastasis and significantly reduced the primary tumorburden.

Conclusions

The data clearly has important clinical implications for patientsdiagnosed with metastatic breast cancer, especially with regards tothe prognosis and treatment options.

Abstract 1 Evaluation: Trace the use of the scientific method thatwas used in this study- include a statement of the hypothesis andan analysis of their experimental design. You do not need to knowwhat the specific molecules called âcytokinesâ are â just realizethat when they are made in a tissue they increase the level ofinflammation.

peartrout167

Mr. Brown is 60 years old. Hewas diagnosed with prostate cancer five years ago. Over the pastfew days, Mr. Brown has been feeling increasingly tired and hasalso been suffering from a headache that did not respond toover-the-counter medications. He scheduled an appointment with hisphysician.

His physician performed aphysical examination and recommended a battery of laboratory testsand imaging procedures.

His blood pressure is 165/100 mmHg. MRI revealsmetastasis(spread of tumor cells) of prostate cancer toosseous(bone) tissue. Abdominal CT shows obstruction of intestinedue to nodular enlargement of adrenal glands.

Question: Based on the data provided, whatlaboratory tests were performed and what samples were taken fromthe patient? Select one of the laboratory tests ordered for Mr.Brown and discuss why Mr. Brown

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Anatomy and Cell Biology 4461B Lecture Notes - Gadolinium, Ct Scan, Aconitase

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