Survival in inflammatory breast cancer 6k,ford edge 2007 white,first aid kit emmylou polarprize - PDF Books

Despite advances in multimodality treatment, inflammatory breast cancer (IBC) remains the most aggressive and lethal form of breast cancer.
Since its early descriptions by Lee and Tannenbaum in 1924, inflammatory breast cancer (IBC) has been recognized as the most aggressive and lethal form of primary breast cancer. The pathologic hallmark of IBC on biopsy is invasion of the dermal lymphatic vessels by tumor emboli that impede the flow of lymph fluid, causing the clinical presentation to mimic classic inflammation.
Biologic FeaturesThree biologic features make IBC a unique form of locally advanced breast cancer (LABC).
These three traits seen in IBC are believed to confer an extremely high potential for metastasis. Perhaps the most concerning epidemiologic issue is the stark contrast in survival between the races.
More recently, Lo and colleagues uncovered important differences in the molecular and histologic characteristics of IBC between Egyptian and US patients, indicating that the North African patients tended to have many more emboli and higher expression of the RhoC oncogene.[12] These features suggest a more aggressive form of the disease, which presents in a qualitatively identical manner throughout the populations studied so far.
In summary, IBC presents with a unique clinical syndrome brought about by well defined histologic features that are rare in other subtypes of breast cancer. In recent years, the primary endeavor of IBC research has been the elucidation of the molecular and genetic alterations (so-called genetic determinants) that underlie its aggressive phenotype and differentiate it from non-IBC. Molecular analysis technology—including comparative genomic hybridization, gene-expression profiling, cDNA and tissue microarrays, and differential display technology—has been harnessed to compare the genetic distinctions among different forms of breast cancer in order to define a signature profile of IBC. Initial research on the molecular biology of IBC was done by evaluating biologic markers known or thought to have prognostic significance in non-IBC such as the status of hormone receptors, epidermal growth factor receptor (EGFR), and the p53 tumor-suppressor gene. The use of primary human IBC cell lines and functional in vivo xenograft cancer models have revealed characteristics innate to IBC thought to confer a strong metastatic potential and aggressive phenotype. With distinct clinical, pathologic, biologic, and molecular features, IBC presents unique challenges and opportunities to breast oncologists and breast cancer researchers.



A mass is present in approximately one-third to one-half of cases on clinical or radiologic examination, and mammography is nearly always abnormal, with the most common findings being skin and trabecular thickening as well as axillary lymphadenopathy. In fact, it is this embolic invasion, and not an inflammatory infiltrate, that leads to the erythema, edema, and induration seen in this syndrome and resulted in the misnomer “inflammatory” breast cancer. First, the tumor is rapidly progressive; in fact, the rate of progression is so rapid as to be easily misdiagnosed as acute infection.
According to staging guidelines published by the American Joint Committee on Cancer, IBC is considered a T4d tumor. As we will summarize below, the puzzle that is IBC has begun to be assembled from the perspective of its molecular determinants. This has been accomplished through a body of work that was spearheaded by the development of two IBC cell lines, SUM149 and SUM190, derived from primary human IBC tumors.[13] With these cell lines, functional in vivo xenograft cancer models have been created. The ultimate goal of this research is to utilize an integrated profiling approach to gene-expression differences and thereby accurately identify markers of disease, improve diagnostic tools and predictors of response to treatment, and even suggest targeted IBC-specific therapies that afford improved survival. While these molecular markers may serve as general prognostic tools, they are not specific to IBC and therefore cannot be employed for diagnostic purposes.
Classic descriptive markers in IBC (eg, estrogen and progesterone receptor status) often guide optimal therapy and aid in development of new diagnostic and prognostic technologies.
This symptom is often used to differentiate primary IBC from recurrent or untreated LABC with inflammatory signs. African-American race has been shown to be an independent predictor of elevated risk for breast cancer mortality, advanced stage at diagnosis, and tumor aggressiveness.[7-11] This last quality is evidenced by a higher histologic grade in tumor specimens and higher rates of locoregional recurrence despite equivalent response rates to local and systemic therapy. It is important to note that these tumors in North Africa are not neglected stage III indolent tumors.
These are implanted into the mammary fat pads of immunocompromised mice.[4,14] The SUM149 xenografts form primary tumors that often metastasize to the lungs through lymph and blood vessels.


Recent IBC research has examined two genes, RhoC GTPase and WISP3, which are concordantly altered in the majority of IBC tumors but not in non-IBC specimens. These data suggest a biologic difference between IBC tumors in blacks and whites, and perhaps with further study, these differences can be elucidated and utilized for improved prognostic and therapeutic outcomes. The latter may show tumor invasion into dermal lymphatics but they seldom show the profusion of dermal lymphatic emboli that characterizes the main tumor burden in IBC (see Figures 1 and 2). RhoC serves as a transforming oncogene by regulation of genes involved in the cell cycle, secretion of angiogenic factors, and activity of insulin-like growth factor (IGF). And finally, the aggressive nature and angiogenicity are intrinsic to the tumor and are present from its inception rather than as late events during progression.
WISP3 functions as a tumor-suppressor gene by modulation of IGF activity and resultant inhibition of cell proliferation, growth, and angiogenesis.
This was elegantly demonstrated after immunocompromised mice were transplanted with a human IBC xenograft called MARY-X. Continued research with molecular analysis technology is imperative in order to harness differential gene expression and fully discover a signature profile of IBC.
The ultimate goal is to reveal the specific molecular determinants that underlie its aggressive phenotype so that we may accurately identify markers of disease, improve diagnostic tools and predictors of response to treatment, and even suggest targeted IBC-specific therapies that afford improved survival.



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