Senior Molecular And Cell Biologist : Interview Task

Significance: understanding the mechanism of drug resistance in cancer leads to developing more potent drugs.

Some of traditional drugs may be effective in patients whose cancers have a specific molecular target, and not for other patients. To solve this problem of patient-specificity, pharmaceutical research have seen the expansion of individually tailored cancer treatment, which is an application of targeted therapy, and this is where biopharmaceuticals are. As an increasing part of the population is diagnosed with cancer and as these patients live longer, increasing care will be given to patients who have received these drugs. Moreover, in the case of cancer therapy, those drugs and especially with mABs are a promise of less side effects : recombinant DNA technology makes it possible to genetically engineer an antibody to reduce the risk of host immune response.

A team from the Brazilian university says the experimental drug binds with tumor cells and causes the loss of key molecules.

Compound 3a was selected by the National Cancer Institute (NCI) USA for anticancer screening with the NCI code D-785902/1. Compound 3c was found in the already tested cancer candidates in the NCI data base under NCI code NSC: 650353[42]. Both candidates were screened on human tumour cell lines at 10-5 M at the 60-Cell-Line Screenings of the Developmental Therapeutics Program (DTP) of the National Cancer Institute (NCI, Bethesda, Maryland, USA) under the drug discovery program of the NCI. The 60-cell-line-screening of the NCI includes 60 different tumour cell lines, the nine various organs and tumour types derived (leukaemia, non-small-cell lung cancer, colon cancer, CNS cancer, melanoma,

that can play a role in tumor development." These 300 altered genes could or could not change

The next goal was to find a molecule that could bind into a growth-factor receptor that was more common in cancer cells. This was done in 2001 and it had great success immediately; “Then just this year researchers at Sloan-Kettering showed that the drug could dramatically boost the effectiveness of standard colorectal-cancer chemotherapy, shrinking tumors in more than a fifth of otherwise hopeless cases.”[7] These discoveries paved the way for Gleevec to be made by rational drug design.

Over the past few decades, researchers have made significant advancements to the treatment and detection of cancers and similar diseases. However, these treatments have certain limitations due to cancer’s ever changing entity. If even an undetectable sliver of a tumor is left, it can mutate, multiply and wreak havoc once more. Cancer patients in remission usually face this unfortunate scenario. What’s worse is that the previous treatment is consistently compromised by the cancer’s new mutations. We are constantly chasing after cancer, it has been evading us at every turn and opportunity until now.

Cancer is very complex and different throughout every person. Throughout the years there has been advancements in science and technology toward a more personalized approach, trying to understand the causes and treatments best for each patient’s cancer. Through the launch of Precision Medicine Initiative researchers, doctors, pharmaceutical companies, government agencies and more will come together in the efforts of introducing personalized medicine.

We identified the affected components of most influential components in both type of perturbations. We combined all the four environmental conditions to construct the network of the most influential components with downstream targets. On these networks we mapped druggable proteins and cancer associated genes. Under inactivating perturbations, we obtained the network of PI3K, EGFR, PP2A, GRK and CaM (Figure 7A). Under activating perturbations, we obtained the network of influential components i.e. EGFR, IL1_TNFR, ERK, SHP2, RKIP, Ras, Gbg_i, Fak, Integrins, and PP2A (Figure 7B).

MolecularMatch offers a public-facing web site for people looking for oncology treatments, searchable by diagnosis, specific gene mutation, comorbidities etc.

Cancer treatment is extremely costly, frequently physically taxing and never guaranteed to work. However, as drug companies such as ours strive to improve conditions with regard to the latter two characteristics, we must face a worsening set of conditions with respect to the first characteristic. The focus of our discussion is on using newly focused ways of fighting cancer cells without attacking their healthy host cells, particularly with an emphasis on the genetic characteristics of breast cancer treatment. We proceed with the thesis that there is great opportunity for the improvement of treatment outcomes and financial growth potential for our drug company with the development of a breast-cancer cell-specific drug therapy, but this opportunity will come with a high price tag to the patient, insurance company and healthcare system.

Genetic instability and the accumulation of several molecular alterations are the cause of cancers through the development of a proliferative cell mass. However, it is restricted to the current prognostic and diagnostic classifications since there is no reflection of the entire tumor clinical heterogeneity. Therefore, they are not sufficient in making predictions for the adequate treatment of patients. The chances of survival for the patients suffering from cancer normally depends on the timely detection of the disease and in this perspective, the highly specific and sensitive methods of curing the disease take play. Notably, oncology can be revolutionaliuze3d through the development of the bio affinity particle and in the

Development of drugs with high potency and inhibitory activity against specific activating mutation, while showing significantly less activity against wild type mutations, made testing specific sensitizing mutation necessary. (1) (EGFR) T790M mutation a successful example of a biomarker for non-small cell lung cancer (NSCLC) treatment with Osimertinib that gained a wide acceptance in clinical practice in Europe and US (), One question that needs to be asked, however, is whether testing for similar mutations in different cancer will be of clinical value. an unknown subpopulation of patients with CRC will have an activating EGFR mutation, such as L858R, which is thought to activate the receptor constitutively, regardless of ligand status promoting cellular proliferation and growth. in patients with colorectal cancer, Targeting activated EGFR, hypothetically, will lead to growth inhibition of cancer cell dependent on the oncogenic drive of sensitising EGFR mutation.

I am very interested in cancer research in general but more specifically I am interested in figuring out why some cases of cancer are much more aggressive than others. I’m mainly interested in cancer because there are a lot of cases of aggressive of cancer that run through my genes for example, my great grandma is dying from breast cancer, my grandma was diagnosed with stage three cancer a few years ago, my mom was diagnosed with uterine cancer and fortunately it was caught very early and has had surgery to remove the cancerous cells, and I had a cancer scare when I was 17. I’ve lost family members due to aggressive cases of cancer and I have family members that have had cancer but their cases weren’t nearly as aggressive as other friends and

For all my life, due to rapid increase in the number of cancer patients and my fear of it, I was thinking about a new way to find a drug that can treat it without major side effects. That's why I planned to study pharmacy to be aware of cancer biology and latest approaches for it's treatment. Then I decided to continue my studies and to get my masters in the field of Molecular Biology so I can perform researches and try to find a new treatment for this disease.