Category: Gene

Introduction

The epidemiology of breast cancer and the methods of overcoming the growth of cancer cells are essential research topics in the current age. Considering that cancer cells can sustain division without necessary signals, this ability becomes a significant obstacle in impeding the advancement of various types of cancer. The Human Epidermal Growth Factor Receptor 2, commonly referred to as HER2, has been outlined as a gene, the overamplification of which is linked to the emergence of breast cancer tumors in numerous populations (1). As this gene belongs to the membrane tyrosine kinase group and dimerizes on ligand binding, its activation is significant for upholding cell division and apoptosis, regulating the normal flow of cell development (1). Nevertheless, when HER2 is amplified, the created heterodimers become biased, negatively impacting the HER signal-transduction network and altering the transmission of growth factors (1). The resulting abnormal kinase activity and incorrect signaling lead to the excessive proliferation of breast cancer cells (1). Thus, HER2 amplification can become a significant factor in the progression of breast cancer tumors.

Although usually coordinated, uncontrolled proliferation caused by the mutation exceptionally harms the normal evolution cycle, contributing to the emergence of malignant tumors and carcinogenic growth. Similar instances of gene overexpression are BRCA1 and BRCA2 gene mutations, which alter the process of DNA repairment (2). In addition, TP53, ER, and CHEK2 gene abnormalities have been found to influence proliferative signaling pathways, as well as activate invasion and metastasis and evade immune destruction, which is also two prominent breast cancer hallmarks (3). Nevertheless, considering that the malfunction in the expression of HER2 can lead to uncontrolled division of breast cells, finding prominent methods that interrupt such advances and restore normal cell development are essential tasks. It has been reported that 18- 20% of invasive breast cancers are related to the amplification of the HER2 gene, which results in aggressive HER2 protein overexpression (4). An increasing prevalence of this cancer subtype is a significant issue, with incidence rates increasing to 88 cases per 100000 women (4). Thus, evaluating the factors that might decrease the growth rates of these tumors becomes an essential task.

The prognosis for this disease is overwhelmingly negative, leading to severe complications or cancer re-occurrence. Contemporary studies show that blocking the ability of cancer cells to transfer signals, thus limiting proliferation, can substantially decrease the possibility of tumor evolution and promote the effectiveness of chemotherapy (3). In this regard, current treatment options introduce anti-HER2 antibodies, namely trastuzumab or pertuzumab, combined with chemotherapy (1). Other common possibilities include radiation therapy and the administration of kinase inhibitors (5). The current study presents the contemporary scholarly perspective on sustaining proliferative signaling in HER2 gene amplification breast cancers, highlighting the most recent advances in this area. Given that this cancer subtype’s mortality and prevalence rates remain overwhelmingly high, it is essential to outline the factors contributing to sustaining proliferation in this disorder, examining approaches to countering HER2 influence.

Proliferation as a Common Hallmark of Carcinogenesis

A substantial body of research shows that the sustainability of proliferative signaling is a crucial factor in developing numerous carcinomas, from gastrointestinal to breast cancer formations (6). As such, cancer cells may secrete multiple varieties of molecules that stimulate the surrounding healthy cells to obtain growth factors or generate such factors themselves, causing the activation of proliferative signaling pathways (6). In the former scenario, a constant loop of cell growth promotion occurs, thus establishing a basis for the subsequent development of carcinogenic masses. Different manifestations of breast cancer are associated with this hallmark, suggesting that sustained proliferative signaling to breast cells, initiated by gene mutations, contributes to the emergence of carcinomas.

The overexpression of the HER2 gene, which leads to abnormal cell growth, is a prominent example of a malignant mutation that disrupts the normal cycle of cell growth and division. These instances are referred to as HER2-positive breast cancers, disorders that possess exceptional proliferative tendencies, manifesting in rapid growth and a highly increased chance of re-occurrence (5). Continuous uncontrolled development of these cells gruesomely affects the human body and requires specific treatment aimed at negating the consequences of amplification.

Primary Factors of Sustained Proliferative Signaling in HER2-Positive Breast Cancer Types

ErBb2 Gene Malfunctions

Mutations in the HER2 gene possess several definitive features that can be outlined using relevant testing methods. It is suggested that utilizing cancer-type classifications based on molecular characteristics of the tumor is the most prominent strategy that allows elevating the accuracy of diagnosis, contributing to the most effective therapeutic decision-making (7). In general, the amplification of the ErBb2 gene is connected with HER2-positive cancer, as this gene encodes the HER2 growth factor (1). The amplification of the gene leads to the abnormal activation of proliferation pathways controlled by HER2, resulting in increased cell growth in breast cancer tumors (1). Studies report that breast cancer cells overexpressing ErbB2 are internally resistant to DNA-damaging agents such as cisplatin due to inhibition in their paired transfectants overexpressing ErbB2 (5).

Receptor Tyrosine Kinases impacting HER2 overexpression

Concerning the HER2-enriched classification, the overexpression of this gene is also frequently related to genetic aberrations. Although both classes demonstrate mutations on chromosome 17q12, the molecular structure of the HER2-enriched subgroup is distinguishable from the Luminal B subtype, especially in the high expression of Receptor Tyrosine Kinases (RTKs) (5). For instance, FGFR4 and FGFR2 levels are often significantly expressed in HER2+ cancer cells, proposing that the emergence of aberrant FGFR signaling promotes the development of HER2-positive cancer masses (5). The molecular process behind this mutation includes an altered homo- or heterodimerization process, which leads to the autophosphorylation of tyrosine residues within the cytoplasmic domain of the receptors, causing aberrations in primary signaling pathways. The created ligands bind to FGFRs in an autocrine or paracrine manner using heparan sulfate proteoglycans. Although the specific mechanisms behind the onset of uncontrolled proliferative signaling are still unknown, abnormal alterations in FGFR signals are deemed to be prominent research areas.

TP53 mutations in HER2+ conditions

As highlighted by studies on HER2 aberrations, it is possible that TP53 mutations, the amplification of the PI3K pathway, and aberrant FGFR signals might be the factors contributing to maintaining the proliferative signaling of breast cancer cells. The majority of investigations involving HER2-positive patients report that CpG dinucleotides mutate at a rate ten times higher than other nucleotides, leading to a higher load of CpG transitions in cancers (1). It is possible that such genetic aberrations, when combined with the amplification of the HER2 gene, increase the sustained proliferation of cancer cells and disrupt the appropriate functioning patterns for normal cells, which results in a poor prognosis for the individuals.

After that, the PI3K pathway is also intimately linked to the amplification of the HER2 gene in HER2-positive tumors. Recent findings claim that PI3K might be affected by HER2 mutations, strengthening the signals and producing growth factors later used by cancerous masses for subsequent development (1). This pathway contains p110α and p85α subunits; p110α is inhibited by p85α and catalyzes the phosphorylation of the lipid phosphatidylinositol 4,5-bisphosphate to phosphatidylinositol 3,4,5-trisphosphate (PIP3) (5). When PIP3 accumulates at the plasma membrane, downstream signaling is activated by the PIP3-binding protein phosphoinositide-dependent kinase 1 (PDK1) and by the mammalian target of rapamycin complex 2 (mTORC2) (5). Therefore, it is possible that the abnormal activation of these pathways leads to the carcinomas’ proliferation strength, driving this hallmark.

The role of the FGFR system in HER2+ breast cancers

The most prominent recent advance refers to the role of aberrant FGFR signals in the occurrence of HER2-positive cancers. The FGFR system consists of four RTKs, namely FGFR1, FGFR2, FGFR3, and FGFR4, which regulate proliferative signaling and control normal cell growth in breast regions, thus affecting various transduction pathways (5). Alterations in this signaling cascade were found in 32.1% of breast cancer cases, and several studies report that these aberrations can coexist with HER2 mutations, increasing the expression levels of FGFR2 and FGFR4 (5). Furthermore, several investigations report that FGFR4 promotes the progress from the Luminal B subtype to the HER2-enriched one, and suppressing the amplification of this gene is correlated with higher treatment effectiveness and lower cancer recurrence (4). In this regard, targeting both FGFR signaling pathways and HER2 overexpression creates the most productive approach to mitigating the consequences of sustained proliferative signaling.

However, the distinction between FGFR RTKs appears to be a crucial detail in the current research endeavors. Scholars claim that overexpression of FGFR levels can differ based on the FGFR subtype in question, resulting in diverse outcomes in tumor progression (5,8). For instance, elevated levels of FGFR1 were found to increase the individuals’ resistance to anti-HER2 therapy, diminishing the possibility of productive recovery (8). Nonetheless, contradictions in the existent findings require additional investigations, as HER2-enriched cancer types are less responsive to this type of treatment.

In comparison with FGFR1, FGFR2 is more strongly linked to HER2+ positive treatment outcomes. Given that FGFR2 activation results in HER2 transactivation and elevated resistance to HER2-targeted therapies, inhibition of the FGFR2 gene allows for impeding the tumor progression (9). However, it is possible to mitigate this influence by FGFR2 inhibition, which hinders abnormal activation of the HER2 gene and induces apoptosis in cells that are especially resistant to relevant therapies (9). In this regard, supplementing the standard treatment with FGFR2 inhibition strategies appears to establish good response rates.

Considering the involvement of FGFR3 in this cancer subtype, the majority of statistical evidence reports a low possibility of FGFR3 amplification in breast cancer. Although this RTK might influence the individuals’ resistance to tamoxifen, decreasing therapy efficiency, only 1.1% of relevant cohorts demonstrate the prevalence of FGFR3 overexpression (8). Therefore, FGFR2 is currently considered to be a more prominent approach in contrast with FGFR3.

Finally, FGFR4 may be a potentially significant factor in the progression of HER2-enriched tumors through proliferative signaling. Both Luminal and HER2-positive breast cancer subtypes demonstrate a prevalence of FGFR4 overexpression, which possibly promotes tumor development and can be associated with endocrine resistance, decreasing the efficiency of HER2-targeted therapy (8). Therefore, FGFR4 inhibitors’ impact on the management of diverse breast cancer types is an exceptionally prominent strategy, which allows targeting particular biomarkers related to FGFR4 overexpression.

The prominence of FGFR family research

Although the highlighted strategies of accounting for the overexpression of FGFR family RTKs FGFR1, FGFR3, and FGFR4 present positive results, a key detail should also be addressed. As such, it is proposed to include the co-expression of other RTKs related to the erbB family, as well as alterations in signaling pathways affected by FGFR and HER2 genetic aberrations. The previous connection to PI3K pathways appears to be a prominent solution, which, however, necessitates extensive empirical exploration. Multiple studies mention that outlining singular responses might be insufficient to achieve necessary outcomes, especially in the cases of HER2 amplification, which are linked to exceptional tumor invasiveness and speed of growth (1). Considering that therapies combining the inhibition of FGFR RTKs and HER2-targeting demonstrate remarkable productivity, accounting for additional correlating issues might be highly efficient.

In light of the discovered tendencies, the connection between FGFR amplification in HER2-positive cancer types is a considerable advancement in breast cancer research. Although the specific mechanisms behind the FGFR family’s influence on the patterns of tumor emergence are still unknown, their impact on the sustainability of proliferative signaling is a tremendous achievement that could be utilized to manage the development of cancer growths (5). For instance, while the FGFR1 locus might be responsible for aberrations in cell copy numbers, FGFR2 is less connected with this phenomenon and is attributed to increased therapy resistance (8). Altogether, each of the discussed RTKs possesses a unique potential to alter the development of HER2-positive tumor types depending on the carcinoma’s attributes, which is an essential accomplishment in diversifying the available treatment options to achieve higher efficacy.

Open Questions Regarding Sustained Proliferative Signaling in Breast Cancer

Even though the results attained are a significant advancement for this clinical area, there are several considerations regarding the sustainability of proliferative signaling in HER2-positive breast cancer types. As such, TP53 mutations and the impact of HER2 gene amplification on the PI3K signaling pathway remain underexplored, and it is still unclear whether healthy manifestations of TP53 might protect individuals from developing particular tumor classes (10). After that, the PI3K pathway, although reported to be significantly affected by the genetic mutations occurring in the HER2 gene, is still to be evaluated based on its connection to HER2-targeted therapy resistance (1). Furthermore, it is vital to ascertain how HER2 inhibitors impact PI3K signaling and whether such downstream inhibition is less toxic for the patients.

After that, the involvement of the FGFR family RTKs in the progression of HER2 positive tumors can be considered an exceptionally undiscovered area of investigation, which necessitates further inquiry. Given that the FGFR inhibition approach is relatively novel, additional studies are required to establish its efficacy for individuals who demonstrate both resistance to HER2-targeted therapy and receptivity towards it. For instance, almost all FGFR RTKs’ levels have been observed as increased in HER2+ breast cancer types, but their impact on the prognosis and the development of the tumor is especially diverse (4). It is unknown whether the amplification of FGFR1 is correlated with FGFR inhibition sensitivity, meaning that FGFR1 might be an inappropriate drug target in specific cases.

Concerning the FGFR2 overexpression, although the preclinical data is favorable, the importance of copy number aberrations and their influence on therapy resistance is still not distinguished. Concerning the FGFR3 phenomenon, it is essential to compare its overexpression manifestations to other family RTKs, clarifying whether it positively induces the resistance to tamoxifen (8). Finally, FGFR4 is considered to be a potential therapeutic target, but the mechanisms behind FGFR for fusions and their frequency are still to be established, and its significance for HER-enriched cancer types requires additional supporting findings.

I believe that the highlighted questions are especially relevant for contemporary research on breast cancer types demonstrating the amplification of the HER2 gene, primarily due to their connection to maintaining proliferative signaling in the human body. The outlined genes and their mutations significantly affect the production of valuable proteins and cell growth factors, as well as play an imperative role in signaling pathways essential for cell cycling. Considering the preliminary data that suggests positive tendencies in the implementation of combinative approaches targeting both HER2 aberrations and TP53, PI3K, and FGFR family markers, it is vital to answer the proposed prompts and establish the most efficient treatment strategies.

Conclusion

To conclude, over-amplification of HER2 protein mutations in connection to sustained proliferative signaling in breast cancer was discussed in detail in this paper, presenting the most recent scientific advancements in this area. TP53 aberrations, PI3K pathway amplification, and aberrant FGFR signaling appear to be the most prominent advances in the current age, which allow distinguishing prognostic factors in Luminal B and HER2 enriched cancer types. Modifying the functioning patterns of these systems might potentially resolve several significant issues in cancer treatment, specifically the sustainability of proliferative signaling, tumor re-occurrence, and HER2 targeted therapy resistance.

References

Hart V, Gautrey H, Kirby J, Tyson-Capper A. HER2 splice variants in breast cancer: investigating their impact on diagnosis and treatment outcomes. Oncotarget. 2020 Nov 17;11(46):4338–4357.

Amina B, Lynda AK, Sonia S, Adel B, Jelloul BH, Miloud M, et al. Fibroblast growth factor receptor 1 protein (FGFR1) as potential prognostic and predictive marker in patients with luminal B breast cancers overexpressing human epidermal receptor 2 protein (HER2). Indian J Pathol Microbiol. 2021;64(2):254–257.

Cartaxo AL, Estrada MF, Domenici G, Roque R, Silva F, Gualda EJ, et al. A novel culture method that sustains ERα signaling in human breast cancer tissue microstructures. J Exp Clin Cancer Res. 2020;39(1).

Chew NJ, Lim Kam Sian TCC, Nguyen EV, Shin S-Y, Yang J, Hui MN, et al. Evaluation of FGFR targeting in breast cancer through interrogation of patient-derived models. Breast Cancer Res. 2021;23(1).

Santolla MF, Maggiolini M. The FGF/FGFR system in breast cancer: Oncogenic features and therapeutic perspectives. Cancers. 2020;12(10).

Lengyel CG, Habeeb B, Khan SZ, El Bairi K, Altuna SC, Hussain S, et al. Role of Her-2 in gastrointestinal tumours beyond gastric cancer: A tool for precision medicine. Gastrointest Disord. 2021;3(1):1–22.

Costantini M, Amoreo CA, Torregrossa L, Alì G, Munari E, Jeronimo C, et al. Assessment of HER2 protein overexpression and gene amplification in renal collecting duct carcinoma: Therapeutic implication. Cancers. 2020;12(11).

Erber R, Rübner M, Davenport S, Hauke S, Beckmann MW, Hartmann A, et al. Impact of fibroblast growth factor receptor 1 (FGFR1) amplification on the prognosis of breast cancer patients. Breast Cancer Res Treat. 2020;184(2):311–24.

Fernández-Nogueira P, Mancino M, Fuster G, López-Plana A, Jauregui P, Almendro V, et al. Tumor-associated fibroblasts promote HER2-targeted therapy resistance through FGFR2 activation. Clin Cancer Res. 2020;26(6):1432–1448.

Baruah R, Sumana BS. Immunohistochemical expression of Ki67 and p53 in primary breast carcinoma and combined Ki67-p53 status phenotypes in hormone receptor positive breast carcinoma. J Clin Diagn Res. 2020;14(3):21–28.

Introduction

Traditionally epidemiologists use descriptive, analytic, and experimental research methods to investigate public health issues. Once the descriptive epidemiology of a disease is known, specific analytic or experimental methods are utilized to study the issue further. As research continues and new questions are asked, it is not uncommon for new methods to be introduced. Often, these cutting-edge methods let researchers investigate public health issues in new ways. For example, consider meta-analysis, a relatively new method in biostatistics. To apply this method, no new data are collected. Instead, results from previous studies are combined and analyzed in new, complex ways. In recent years, meta-analysis has gained popularity among epidemiologists. Nevertheless, this approach has limitations and is not appropriate for all epidemiological research (Williams, 2005). Another method used in epidemiology research is gene-environment interactions. It is applied for the investigation of many complex diseases which are influenced by both genetic and environmental factors.

Article Summary and Method Description

Gene-environment interplay was used by Bookman et al. (2011) to develop an integrative model to deal with common complex diseases. The researchers state that complex diseases and disorders, such as cancer, diabetes, cardiovascular disease, or psychiatric disorders, are the major concern of society since they have a high prevalence (Bookman et al., 2011). Thousands of genetic variants were screened to reveal the associations with the diseases. However, genetics is not the only factor conditioning these diseases. The role of various environments in the modification of novel genes should also be considered. Thus, gene-environment interaction should be discovered. It will give a better understanding of complex diseases etiology and contribute to the prevention strategies. The environments in their broad sense include “airborne chemical and biological agents, dietary intake, physical activity, addictive substances, and psychosocial stress” (Bookman et al., 2011, p.220).

Anno (2016) mentions that gene-environment interactions have an impact on the development of complex diseases. The results of these interactions can be applied in different spheres. The investigation of gene-environment interactions includes the understanding of skin color variations as adaptation, the application of information theoretic methods for their analysis, the practice of regional epidemiological study, etc. (Anno, 2016). On the whole, gene-environment interaction is the method that allows modeling the reaction of different genotypes to environmental changes based on the previous investigations of their interactions. It makes possible the prediction of influences that a certain environment has on the development of common complex diseases.

Advantages of the Method

The advantage of the method of gene-environment interaction is that it allows assessing both environmental and genetic influences with certain accuracy. Since the method gives the possibility to model the etiology of disorders conditioned by both environmental and genetic influences, it also helps to identify ” individuals most susceptible to risk exposures or most amenable to preventive and therapeutic interventions” (Manuck & McCafferym, 2014, p.41). The method has a broad implementation in the research of various diseases. For example, Nickels et al. (2013) provide the evidence of gene-environment interactions between breast cancer susceptibility and environmental risk factors. In this case, it was the best method since there were many common genetic susceptibility loci for breast cancer but their connection with environmental or lifestyle risk factors was not traced. Another example of successful implementation of gene-environment interactions is the study of obesity origins (Bouret, Levin, & Ozanne, 2015). The authors concentrate on the interactions of genetic and environmental variables which influence the predisposition of people to obesity which is often accompanied with diabetes. The knowledge of those interactions can help in the development of prevention strategies.

Conclusions

It is considered that both genetic and non-genetic factors influence the development of common complex diseases. The genetic factors cannot be easily changed while non-genetic or environmental can be altered. The method of gene-environment interactions allows tracing the dependence of both factors. Consequently, the information on the interactions can be used to provide the work on prevention of complex diseases through the chance of environment. It can result in the increase of the preventive strategies efficiency and the improvement of general health of population.

References

Anno, S. (Ed.). (2016). Gene-environment interaction analysis: Methods in bioinformatics and computational biology. Boca Raton, FL: CRC Press.

Bookman, E. B., McAllister, K., Gillanders, E., Wanke, K., Balshaw, D., Rutter, J., … Birnbaum, L. S. (2011). Gene-environment interplay in common complex diseases: Forging an integrative model – Recommendations from an NIH workshop. Genetic Epidemiology, 35(4), 217-225.

Bouret, S., Levin, B.E., & Ozanne, S.E. (2015). Gene-environment interactions controlling energy and glucose homeostasis and the developmental origins of obesity. Psychological Reviews, 95(1), 47-82. Web.

Manuk, S.B., & McCaffery, J.M. (2014). Gene-environment interaction. Annual Review of Psychology, 65, 41-70.

Nickels, S., Truong, T., Hein, R., Stevens, K., Buck, K., Behrens, S., … Chang-Claude, J. (2013). Evidence of gene-environment interactions between common breast cancer susceptibility loci and established environmental risk factors. PLOS Genetics, 9(3), 1-14. Web.

Gene therapy is a promising vector in modern medicine that has been actively researched for a few decades. This field of scientific knowledge has the potential to cure many acquired and inherited diseases. Although studying gene therapy has faced many challenges over the years, scientists worldwide put much effort into uncovering its full potential, which is why this medical treatment is rapidly developing.

The interest in gene therapy can be explained by its intended purpose: achieving a significant clinical benefit with a single treatment. The first steps in studying this field were taken almost fifty years ago when an American researcher Theodore Friedmann evaluated the potential and challenges related to the usage of gene therapy (as cited in Dunbar et al., 2018, p. 2). It can be highly effective in curing neurodegenerative and immune disorders, hemophilia, different forms of cancer, and other illnesses. However, this form of medicine also has many disadvantages, which is why it is not approved in many countries. The first trials of gene therapy “exposed serious therapy-related toxicities, including inflammatory responses to the vectors and malignancies caused by vector-mediated insertional activation of protooncogenes” (Dunbar et al., 2018, p. 1). In order to deal with the associated issues, additional research is conducted in cell biology, immunology, and virology (Dunbar et al., 2018). Scientists continue to explore gene therapy and seek new ways to make it as efficient and safe as possible.

However, the therapy under discussion is associated with a significant problem related to informed consent. The disadvantages of gene therapy may affect the patient and their entire bloodline due to possible germline mutations (Dunbar et al., 2018). Genotoxicity is a serious issue, and many patients may fear it and reject therapy even though it can liquidate their most severe diseases. Therefore, informed consent will remain a crucial problem until the methods to stabilize the germline and prevent negative consequences of gene therapy appear.

There is also a problem of implanted genes being passed on to the next generations. Nowadays, heritable germline editing is a realistic possibility due to the technological advancements in this area, yet many people do not find it an advantage (Dunbar et al., 2018). An international group of scientists and other professionals published a report in 2017 revealing a possible pathway to correct germline mutations (as cited in Dunbar et al., 2018). It would mean that the negative consequences of implanting genes could be reversed. However, the federal governments of different countries have put many restrictions on gene therapy as there is currently no guaranteed method to prevent implanted genes from being passed on to the next generations.

I think gene therapy is ethical since it aims to cure severe illnesses. Having cancer or a neurodegenerative disorder is worse than having an edited genome. Furthermore, heritable germline editing can decrease future generations’ chances of inheriting a chronic disease from people who have undergone gene therapy. Still, I do not think that people will “design” their babies in the future, as it is not the initial purpose of gene therapy. It is a medical instrument intended to cure diseases and help people who suffer from them. While that is true, I do not see an ethical issue in gene therapy, but using it for “designing” babies seems unethical at all points.

Reference

Dunbar, C. E., High, K. A., Joung, J. K., Kohn, D. B., Ozawa, K., & Sadelain, M. (2018). Gene therapy comes of age. Science, 359(6372), 1-11. Web.

On June 2006 President Bill Clinton praised the completion of the Human Genome project as a great step towards developing a healthy human kind. However, he did not infer to the beginning of an era of high sales in the industry. In less than a decade dealers in genetic tests and dietary supplements have flooded the web hawking nutritional genetics. They claim that they are able to look at a person’s genetic information and decipher what the individual should eat to promote good health. This has led to a worrying trend whereby commercialization of gene detection technology has taken place even before the scientists have gained a good understanding on how specific genes affect health or disease (Hercher, 2007).

Sciona for example, a small British firm has a product called Cleff which can be obtained through their site. The client is to fill a questionnaire with some personal details such as weight, age, smoking status and provide a DNA sample from saliva. In return the client is provided with an analysis report of his or her gene structure as well as how the person should eat and exercise. There has also been an increasing demand of gene tests whereby one unidentified dealer made sales of over 35,000 within three years starting in 2003. Investors have also identified this field as a potential market for future profits (Hercher, 2007).

Governments and consumer groups have opposed this trend. For instance, Sciona withdrew its products from the UK and shifted to the US when the Human Genetics commission threatened to investigate its dealings. The US Government Accountability Office (G.A.O) also carried out an investigation in to the operation of these companies due to an increasing concern of direct marketing of gene tests. They sent profiles of fictitious consumers to the testing companies and received assessment reports as well as dietary recommendations. G.A.O. found out that these companies misled consumers because some of the assessment reports provided could not be determined from questionnaires and genetic results only (Hercher, 2007).

Some of the information provided to customers was so ambiguous and medically unproven. Hence, they did not offer any meaningful information. For instance, some companies provided only general information on how the customer should exercise and eat, such as those obtained in health magazines. These included advising smokers to stop smoking, non-smokers not to start smoking and those eating junk food to change their eating habits. Some of the reports sent to customers were tactics of marketing dietary supplements. A case in point is a company that recommended a particular nutritional formula to different customers with different personal profile at an annual cost of $ 1,200. It later tuned out that the formula consisted of multivitamins available at local drugstores and supermarkets at a lower cost of $35 per year (Hercher, 2007).

The initiatives taken by the Human Genetics commission in UK that led to withdrawal of Sciona from the market was a great step. However, just threatening was not enough. The institution should have done investigations in to the operations of such companies to find out the impact of their products to consumers because such products might find their way back to the UK market. Secondly, the initiatives taken by the G.A.O were remarkable because they were able to find out how gene test companies swindled customers of their money. However, the government needs to come up with policies that will ensure that the FDA covers all organizations that deal in nutrigenetics. In addition, strict rules should be implemented to ensure that genetic testing is not marketed directly to customers (Hercher, 2007).

Reference

Hercher L. (2007). Diet Advice from DNA?. Scientific American Magazine, 297, 84-89

Strategies to be adopted by Gene One

Intensive Embrace of Technology

In the current technological environment which becomes more and more dynamic, the success of firms depends to a greater degree on the extent to which they embrace the technology. Firms which use new technological developments have been found to report high outputs and quality of the products and services which satisfy the needs of the customers.

Gene One seems to be under the leadership of ambitious and talented leaders who have the company’s welfare at heart. This is a right leadership environment, thus the right strategies are required to enhance the achievement of the company’s objective of being market leaders.

The changes in lifestyles and consumer needs and preferences call for technological improvement in the production processes. By using high and intensive technology, Gene One could enhance the quality of its products. This strategy is suitable for Gene One considering the nature of the industry they are in and the nature of their products.

The Biotech industry requires players to improve their survival through adoption of high technology. This involves embracing the right technology so that changes and advancement in technology do not render production processes outdated. Many firms are known to fail because of implementing the wrong technology which does not stand the test of time (Robbins et al., 2011).

This strategy will be greatly enhanced through the research in the technological field. The company should invest in researching on the various technological techniques in the Biotech industry.

A strong technological department is thus recommended in this case. The company should be willing to finance the technology department to contribute to the success of this strategy. This will involve a research on what the market players are adopting and the degree of the profit achieved. The technology adopted should increase the production of high quality products (Yukl, 2009).

This strategy will help Gene One in achieving high customer satisfaction which will lead to customer loyalty. It will thus enhance the expansion of the firm’s customer base and, consequently, boost its market share. Customer loyalty will also lead to repeated purchases, thus increasing the firm’s profitability.

It is every company’s objective to improve its production and returns through which financial stability is achieved. The firm’s profitability will, therefore, depend on the extent to which the customers prefer to buy its products over those of the other companies. In order for the firm to achieve its objectives within the 36-month maximum deadline, it is to ensure that customer satisfaction is attained through their products (Robbins et al., 2010).

Technological superiority also helps in enhancing positive company image. A firm which employs constructive technology will attain positive public image. At this stage when Gene One is planning to be the market leader, its reputation will play a major role in achieving this objective.

This strategy could be implemented through the use of high technology means of production and using equipments and facilities which are technologically superior. It can be also implemented through refurbishing the technological department to ensure competent personnel are in charge of the company’s operations (Yukl, 2009).

This strategy will lead to the desired gains since it will improve the quality of the firm’s products and services. The adoption of intensive technological methods also leads to high outputs.

This is in line with the firm’s desire to increase its market share and customer base. This strategy supports the firms desire to be innovative for the success in the process of change and development depends on the extent to which a firm adopts the right technology. Technology has been known to enhance innovation, thus this strategy will lead to the firm being innovative (Robbins et al., 2011).

High Quality Human Resource

The success or failure of any company depends on the quality of the workforce it employs. A company with high quality human resource is always successful due to high quality output. For Gene One to achieve its objectives, it is proposed to adopt this strategy. The company should employ personnel of highly qualified workers with vast skills and experience in the Biotech industry. This will lead to high quality output and more customer satisfaction.

The quality of service offered to customers depends largely on the quality and experience of a company’s staff. By employing high quality human resource, Gene One will also improve its public image and reputation. This will have a great impact on the market segment it currently serves and the potential market share (Robbins et al., 2011).

This strategy will involve proper recruitment, selection, training and development of employees. It, therefore, means that the company should make its human resource department improve. This strategy could be implemented through support to this department. This will enhance effective and efficient recruitment practices. The company could use drives, talks in educational institutions and online recruitment means.

This will help in pooling a wide variety of applicants from which the company can choose the desired talents to be included in its workforce. Proper selection should also be applied by the company which will lead to choosing the right employees. The selection criteria should be multidimensional, and the selected candidates should have a wide variety of talents which will contribute to the firm’s success (Yukl, 2009).

Gene One should train its staff in a manner that enhances competitiveness in the market. Proper training is known to instill into workers the right company’s culture, thus enabling consistency in achieving the aims and objectives by every staff member. This also ensures that the firm has the employees with the right skills available in the market, which contribute to its reputation through their quality work.

The company should also organize workshops and talks for its human resources to enable exchange of ideas and employee development. This should be done irrespective of employees’ departments to improve interdepartmental harmony and work relations (Yukl, 2009).

This strategy of employing high quality human resources will lead to the desired outcomes since it will aim at improving the quality of output. The quality of output, as stated above, greatly depends on the quality of staff employed. High quality human resources also lead to high customer satisfaction. This could result in the desired outcomes since it increases customer loyalty leading to repeated purchases and, therefore, enhancing the profitability of the firm. This strategy also meets Gene One’s desire to be innovative since high quality personnel bring about new fresh ideas. The staff will also determine the creativity, thus meeting the firm’s desire to be innovative.

Conclusion

The above two strategies will allow Gene One to become more innovative and thus help in achieving its objectives which include market leadership. High quality of human resource and intensive embrace of the right technology will enable the company to implement the desired changes within its operations and products, thus achieving growth and development. This will also strategically position the firm in the industry enhancing its competitiveness.

References

Robbins, S.P, Judge, T. A. & Campbell, T. T. (2010). Organizational Behavior. 14th edn., New Jersey: Financial Times Prentice Hall.

Yukl, G. (2009). Leadership in Organizations. 7th ed., New Jersey: Prentice Hall.

Introduction

Since its establishment in 1996, Gene One is a biotechnology company experiencing great success in every move it makes in the market and the larger society (Gene One, n.d). Success at the company has been achieved through combination of many factors such as presence of sophisticated technology, good management and teamwork and an adequate and able market team.

Further, there is increasing external factors resulting to healthy growth of the company such as the change of leadership at Food and Drug Administration and a growing interest at the Wall Street in biotechnology (Gene One, n.d). As a result there is an overall investor confidence in the industry thus future prospects for Gene One are bright. However, this is not to say external market conditions are friendly.

There is high competition in the market place from the related biotechnology companies and therefore, just like any other company, Gene One has to stay abreast in the market place by adopting effective strategic management strategies. For instance, the company hopes to realize an increase in its annual growth targets by about 40% and IPO has been identified as the best source of capital to drive this target (Gene One, n.d).

Moreover, the company needs more money for new developments, advertisement, and marketing in order to remain successful in the market place. Key strength of the company can be seen to lie in leadership and organizational capabilities that majority of company’s senior managers exercise.

Strategic Leadership Management

Gene One selling aspects is its possession of new, sophisticated, and efficient technology that is manifested through excellent innovations and market-leading products (Gene One, n.d). Investment in technology thus constitutes the positive decision the company can take given that competition from other companies is increasing.

Given that Gene One has a sound and effective leadership and organizational capabilities, adoption of sophisticated technology is likely to be realized with ease. However, how can enhancement of technology and innovation in the company be realized? First, by looking at the market environment, it is clear that more companies in the biotechnology industry are investing heavily in research and design.

Through investment in research and designs the companies hopes to realize innovation of appropriate and excellent technologies that are market-winners (Gene One, n.d). For Gene One to have the best research innovations which in turn can be transformed and developed into market winning products, there is need for the company to invest in talent development especially of young talented scientists.

Investing in R&D and developing a pool of talents scientists require effective leadership and management. From the conversation and discussion, Gene One top management has indicated that there still exists disagreements and lack of proper communication connection among top managers (Gene One, n.d).

In other words, established leadership culture cannot ride the entire organization in a uniform agreement in major decisions without disagreements (Yukl, 2010). IPO issue has revealed this lack of leadership aspect in the company, which needs to be developed if the company hopes to realize its goals of growth and expansion.

In order to be competitive organizations need to attract, retain, and develop top leadership talent in line with the needs and prospects of IPO and growth of the company (Gene One, n.d). In one conversation, John tells Don that, some of the current members in the senior leadership team lack ability to lead an IPO transformation process due to their lack of experience (Gene One, n.d).

Development is regarded to be important because leaders who are perceived to be effective need continued learning opportunities (Mintzberg, Lampel, Quinn, & Ghoshal, 2003). In the case of Gene One, leadership development is important as the company aims to stay ahead of the competition and ensure business challenges are transformed into opportunities (Gene One, n.d).

Therefore, how can Gene One create an effective leadership strategy that has potential to help the company realize its goals? First, an effective leadership strategy requires a systematic lens of understanding leadership requirements and merge together elements of learning about the whole system of the company.

Given that IPO and the need to grow the company beyond its current position (Gene One, n.d) requires cooperation among leaders, an effective leadership strategy needs to build on collective work where the understanding is that collective work requires setting direction, creating alignment, facing adaptive challenges to unexpected situations and more importantly maintaining employee commitment and energy (London, 2002).

Leadership management at Gene One is necessary especially after numerous disagreements arose over the IPO issue and some resignation were witnessed (Gene One, n.d). If for instance there was an effective leadership strategy in place, then it is likely that the experienced setbacks could have been avoided.

Effective leaders have to be sensitive to the needs and input of others (Robbins, & Judge, 2011). In the case of Gene One, leadership development strategy should build on the need for sustainable leadership capacities that are evident in the company. In this way, the leaders in the company will be in a position to serve themselves as well as the needs of the company.

In this way, minor conflicts being realized at the company will be minimized. It should be noted further that effective leadership strategies have to reflect the needs for interpersonal and cognitive competencies of the leaders and managers to manage people and their relationships.

At the present, these aspects seems to be absent at Gene One as reflected in the acceleration of conflict over IPO and direct accusation and confrontation of managers (Gene One, n.d).

Through this, it can be deduced that there will be much more organization harmony since organization’s implicit and explicit aspects and mutual influence will be possible as the process of finding common ground among diverse views will be possible (Fulmer and Goldsmith, 2001). Moreover, an effective leadership development strategy needs to build on principles of education and continuous training.

Conclusion

In summary, it can be said that for effective leadership strategy at Gene One, there should be interdependency of leadership strategy with other systematic factors in the organization such as rewards, performance feedback, reviews and production systems (Ryan, 2007).

More importantly, leadership development strategies should be based on thorough understanding of the specific needs of situation and this may involve degree of interdependence among individuals and work groups in the organization.

References

Fulmer, R. M and Goldsmith, M. (2001). The leadership investment: how the world’s best organizations gain strategic advantage through leadership development. NY: AMACOM Division American Management Association.

Gene One. (N.d). Company overview. (Attached notes).

London, M. (2002). Leadership development: paths to self-insight and professional growth. NY: Routledge..

Mintzberg, H., Lampel, J., Quinn, J. B., & Ghoshal, S. (2003). The strategy process: Concepts, contexts, cases. Fourth edition. Upper Saddle River, NJ: Prentice Hall.

Robbins, S. P., & Judge, T. A. (2011). Organizational behavior. 14th edition. Upper Saddle River, NJ: Pearson Education.

Ryan, R. (2007). Leadership Development: A Guide for HR and Training Professionals. NY: Routledge.

Yukl, G. (2010). Leadership in organizations. Seventh edition. Upper Saddle River, NJ: Pearson Education.