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На сьогодні бухгалтерська звітність є одним з найбільш динамічних елементів методу обліку. Перш за все, це пов’язано з відповідністю його предметa вимогам різних користувачів, які бажають дізнатися, що економічні умови в реальності швидко змінюються. Тому, застосовуючи методи економічного аналізу на основі даних бухгалтерського обліку, можна розрахувати діапазон цифр, що дають можливість оцінити як фінансовий стан, так і економічний потенціал підприємства в майбутньому і минулому. Тому для обчислення таких цифр у справах бухгалтерського обліку повинна бути інформація про надзвичайні наслідки, що впливають на виробничі процеси, вартість продукції і фінансові результати підприємства. Ця умова дозволить оцінити їхній вплив на фінансові показники та економічний потенціал підприємства. Сформульовано напрями розширення фінансової звітності за змістом і формою. Фінансова звітність удосконалюється з метою відображення інформації про надзвичайні наслідки за рахунок розширення факторів у наявних главах (як частина інших витрат) і формування нової глави V «Зовнішні та внутрішні ризики впливу на навколишнє середовище», що містить інформацію про відокремлення надзвичайних наслідків від витрати на діяльність. Фрагменти приміток до річної фінансової звітності розроблено, що дає можливість оцінити вплив надзвичайних наслідків на необоротні та оборотні активи і виробничий процес. Побудова конкретної інформації для внутрішнього використання про надзвичайні наслідки здійснюється на основі обґрунтованих напрямів формування внутрішньої звітності та розроблення шляхів і механізмів формування їхніх факторів. Це дозволило підвищити якість інформаційного простору управління діловою діяльністю в надзвичайних умовах. Використання пропозицій на практиці сприяло підвищенню якості інформаційного простору при ухваленні рішень користувачами і розробленні комплексу заходів щодо запобігання надзвичайним наслідкам та їх ліквідації . У свою чергу, аналітичні заходи, розраховані на основі їхніх фактів, ураховуватимуть низку факторів, що дозволяють повністю оцінити фінансовий стан та економічний потенціал., На сегодня бухгалтерская отчетность является одним из наиболее динамичных элементов бухгалтерского учета. Прежде всего, это связано с соответствием его предмета требованиям различных пользователей, желающих узнать, что экономические условия в реальности быстро меняются.Поэтому, применяя методы экономического анализа на основе данных бухгалтерского учета, можно рассчитать диапазон цифр, которые дают возможность оценить как финансовое состояние, так и экономический потенциал предприятия в будущем и прошлом. Построение конкретной информации для внутреннего использования о чрезвычайных последствия осуществляется на основе обоснованных направлений формирования внутренней отчетности и разработки путей и механизмов формирования их факторов. Использование предложений на практике способствовало повышению качества информационного пространства при принятии решений пользователями и разработке комплекса мероприятий по предотвращению и ликвидации чрезвычайных последствий., Nowadays accounting statements is one of the most dynamic accounting method elements. First and foremost it is related to the correspondence of its subject-matter to the demands of different users willing to know economic conditions in reality changing rapidly. Thus, applying methods of economic analysis on the basis of accounting data it is possible to calculate a range of figures giving an opportunity to estimate both financial condition and economic potential of the enterprise in the future and the past. That is why to calculate such figures in the copes of accounting there should be information about emergency consequences cases affecting the production processes, product cost and further the enterprise’s financial results. This condition will allow estimate their influence on the financial figures and economic potential of the enterprise. The directions of financial statement’s expanding in content and form are articulated. Financial statement is improved in order to reflect information about emergency consequences through expanding factors in already existing chapters (as a part of other costs) and formation of the new chapter V «External and internal risks environmental impact» containing information about separation of emergency consequences from activity costs. Fragments of notes to the annual financial statement are developed giving an opportunity to estimate the impact of emergency consequences on noncurrent and current assets and the production process. Building specific information for internal use about emergency consequences is performed on the basis of justified directions of internal reporting formation and development of ways and mechanisms of their factors formation. It allowed to increase quality of information space of business activity management in emergency conditions. The use of suggestions in practice contributed to increasing the information space quality in users’ decision-making and developing a complex of measures to prevent and address the emergency consequences. In its turn analytical measures calculated on the basis of their facts will take into account a number of factors allowing to fully estimate the financial condition and economic potential.

ErbB3 harbors weak kinase activity, but strongly activates downstream phosphatidylinositol 3-kinase/Akt signaling through heterodimerization with and activation by other ErbB receptor tyrosine kinases. We report here that ErbB3 loss in the luminal mammary epithelium of mice impaired Akt and MAPK signaling and reduced luminal cell proliferation and survival. ERBB3 mRNA expression levels were highest in luminal mammary populations and lowest in basal cell/stem cell populations. ErbB3 loss in mammary epithelial cells shifted gene expression patterns toward a mammary basal cell/stem cell signature. ErbB3 depletion-induced gene expression changes were rescued upon activation of Akt and MAPK signaling. Interestingly, proliferation and expansion of the mammary basal epithelium (BE) occurred upon ErbB3 targeting in the luminal epithelium, but not upon its targeting in the BE. Multiple cytokines, including interleukin 6, were induced upon ErbB3 depletion in luminal epithelium cells, which increased growth of BE cells. Taken together, these results suggest that ErbB3 regulates the balance of differentiated breast epithelial cell types by regulating their growth and survival through autocrine- and paracrine-signaling mechanisms.

To identify molecular alterations involved in the initiation and progression of breast carcinomas, we analyzed the global gene expression profiles of normal mammary epithelial cells and in situ, invasive, and metastatic breast carcinomas using serial analysis of gene expression (SAGE). We identified sets of genes expressed only or most abundantly in a specific stage of breast tumorigenesis or in a certain subtype of tumors through the pair-wise comparison and by hierarchical clustering analysis of these eight SAGE libraries (two/stage). On the basis of these comparisons, we made the following observations: Normal mammary epithelial cells showed the most distinct and least variable gene expression profiles. Many of the genes highly expressed in normal mammary epithelium and lost in carcinomas encoded secreted proteins, cytokines, and chemokines, implicating abnormal paracrine and autocrine signaling in the initiation of breast tumorigenesis. Very few genes were universally up-regulated in all tumors regardless of their stage and histological grade, indicating a high degree of diversity at the molecular level that likely reflects the clinical heterogeneity characteristic of breast carcinomas. Tumors of different histology type and stage had very distinct gene expression patterns. No genes seemed to be specific for metastatic or for in situ carcinomas. We found that the most dramatic and consistent phenotypic change occurred at the normal-to-in situ carcinoma transition. This observation, combined with the fact that many of the genes involved encode secreted, cell-nonautonomous factors, implies that the normal epithelium-to-in situ carcinoma transition may be the most promising target for cancer prevention and treatment.

In recent years, significant effort has been made to identify genes that influence breast cancer risk. Because the high-penetrance breast cancer susceptibility genes BRCA1 and 2 play a role only in a small fraction of breast cancer cases, understanding the genetic risk of the majority of breast cancers will require the identification and analysis of several lower penetrance genes. The estrogen-signaling pathway plays a crucial role in the pathophysiology of breast cancer; therefore, polymorphism in genes involved in this pathway is likely to influence breast cancer risk. Our detailed analysis of gene expression profiles of estrogen- and 4-OH-tamoxifen-treated ZR75-1 breast cancer cells identified members of the sulfotransferase 1A (SULT1A) phenol sulfotransferase family as downstream targets of tamoxifen. On the basis of the induction of SULT1A by 4-OH-tamoxifen and the known inherited variability in SULT1A enzymatic activity, we hypothesized that polymorphism in sulfotransferase genes might influence the risk of breast cancer. Using an RFLP that distinguishes an arginine to histidine change in exon 7 of the SULT1A1 gene, we characterized SULT1A1 genotypes in relation to breast cancer risk. An analysis of 444 breast cancer patients and 227 controls revealed no effect of SULT1A1 genotype on the risk of breast cancer (P = 0.69); however, it did appear to influence the age of onset among early-onset affected patients (P = 0.04). Moreover, individuals with the higher activity SULT1A1*1 allele were more likely to have other tumors in addition to breast cancer (P = 0.004; odds ratio, 3.02; 95% confidence interval, 1.32, 8.09). The large number of environmental mutagens and carcinogens activated by sulfotransferases and the high frequency of the SULT1A1*1 allele in human populations warrants additional studies to address the role of SULT genes in human cancer.

Aberrant crypt foci with dysplasia are thought to be the first detectable lesions of colorectal neoplasia. Because cell cycle disruption appears crucial for tumorigenesis, we analyzed the immunohistochemical expression patterns of the prototype cyclin-dependent kinase inhibitor p21 WAF1/CIP1 and the proliferation marker Ki67 in the early stages of colorectal tumorigenesis. In colorectal epithelium, p21 WAF1/CIP1 expression was undetectable in the lower third of the crypts, where Ki67 was expressed, but then sharply increased as cells passed out of the proliferating zone and migrated toward the humen. Hyperplastic polyps retained this normal compartmentalized pattern. In contrast, markedly decreased p21 WAF1/CIP1 immunostaining was observed in dysplastic aberrant crypt foci as well as in small adenomas. Moreover, the compartmentalization of Ki67 and p21 WAF1/CIP1 was lost, as Ki67 expression extended into the small p21-expressing zone at the top of the crypts. These data suggest that the dysregulated expression of cell-cycle-controlling genes and the consequent release from normal cell cycle controls may represent an essential early step in colorectal neoplasia.

The p27Kip1 gene codes for a cyclin-dependent kinase inhibitor implicated in G1 arrest by transforming growth factor beta, cell-cell contact, agents that elevate cyclic AMP, and the growth-inhibitory drug rapamycin. p27 binds to and inhibits complexes formed by cyclin E-cdk2, cyclin A-cdk2, and cyclin D-cdk4. The involvement of p27 in the negative regulation of cell proliferation suggests that it may also function as a tumor suppressor gene. Using a combination of somatic cell hybrid panels and fluorescence in situ hybridization p27Kip1 has been mapped to the short arm of chromosome 12 at the 12p12-12p13.1 boundary, reported to harbor deletions and rearrangements in leukemia and mesotheliomas. In order to assess potential p27Kip1 gene alterations, we have screened a total of 147 human primary solid tumors and found no detectable cancer-specific mutations. These results argue that the often observed loss of antimitogenic transforming growth factor beta responsiveness in human cancer cells is not due to structural defects in p27Kip1.