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  • Cancer genomics testing

    What is cancer genomics? Cancer cells are not similar to normal cells. They acquire mutations. These mutations make them different. Most of these mutations give cancer cells power of unlimited growth, resulting in removal of normal functioning cells of the tissues, and subsequently leading to organ failure. Some mutations are repetitive, means they appear in cancer patients very frequently. Some mutations are rare, which means it appears rarely. Regardless, cancer cells have multiple gene mutations. The analysis and study of the cancer gene mutations and relating them to better treatment approaches with improved outcome is known as cancer genomics. How are cancer mutations identified? Cancer mutations are identified by collecting the cancer cells from resected tumors and then sequencing the genome of these cells using a technique called NextGen sequencing. Gene sequencing information from thousands of different cancer patients have generated a wealth of information. We have learned a lot about how mutations can alter the outcomes of cancer treatments. Loose cancer cells circulating in the blood can be collected and the DNA can be sequenced. This process is called liquid biopsy. Liquid biopsies are increasingly becoming a tool to predict the progression of caner or to estimate residual cancer. Cancer cells come loose from the tumor itself and enters into the blood stream. This is how they metastasize and enter into another organ. What can be done with the information generated from cancer genomics testing? Below I will describe a few examples to describe this. 1. Targeted therapy in lung cancer The molecular profiling of lung cancers has uncovered several mutated proteins. They are shown below. • EGFR – mutated in 52% of never-smokers, 15% former smokers, 6% current smokers • KRAS – predominant in smokers or former smokers • ALK – predominant in non-smokers {fusions in 3%-7% of the non-small cell lung cancer (NSCLC)} • HER2 – predominant in non-smokers (mutation present in 2% of the tumors) • BRAF – predominant in smokers or former smokers (mutation present in 1% - 3% of the tumors) • PI3KCA – mutation present in 2% of the tumors • AKT1 – mutation present in 1% of the tumors • MAP2K1 or MEK1 – mutation present in 1% of the non-small cell lung cancer (NSCLC) • MET – amplification of this gene is associated with secondary resistance to EGFR tyrosine kinase inhibitors Lets talk about EGFR mutations. EGFR stands for epidermal growth factor receptor. EGFR mutations such as exon 19 deletion or exon 21 L858R mutation can be treated with medications such as Afatinib Dimaleate, which significantly increases the median overall survival when compared to cisplatin treatment in NSCLC patients. In addition, Atezolizumab, a humanized monoclonal antibody against PD-L1 shows significantly improved overall survival in patients with EGFR mutations. 2. Liquid biopsy results Here we are going to talk about a different scenario. A liquid biopsy result from a breast cancer patient shows several mutations identified from floating cancer cells. Let's suppose the one of the mutations is TP53 R273C. The doctor's office or the lab will report that this mutation is non-actionable, which means, there can nothing be done with this information treatment wise. However, they may be correct on the treatment part, but there is a lot that a patient can learn from this mutation status. A patient can learn how this TP53 mutation alters the survival outcome. Below is a survival curve generated by analyzing 7469 breast cancer patients. The red line shows patient survival with this particular TP53 mutation. The analysis shows that patients with TP53 mutation/s survive less longer compared to patients without mutated TP53. Median Months Overall (95% CI) Altered group (TP53 mutated) 126.47 (111.97 - 144.67) Unaltered group 169.23 (160.33 - 179.10) But then, with the subtype of breast cancers, this outcome may be different. Majority of the breast cancer patients have breast invasive ductal carcinoma. With this particular type of breast cancer, TP53 mutations may result in better overall survival with proper treatment, when compared to the not mutated group. Below is a survival graph for the breast invasive ductal carcinoma patients. Although not statistically significant, the trend shows that the unaltered group survives less longer compared to the TP53 mutated group. Now when the total number of patients in the database will increase, this result will be statistically significant. Hopefully, this little section is going to get the readers interested enough to learn more about cancer genomics and testing. For questions, please email at --------------------------------------------------------------------------------- Author: Anirban Mukherjee, PhD Research Scientist The Dell Pediatric Research Institute The Dell Medical School College of Pharmacy, The University of Texas at Austin

  • Top 10 gene mutations in non small cell lung cancer (NSCLC) that drives the outcome

    Mutations are common in cancer genome Cancer genome is heterogenous. There are many mutations. Over time, the cancer genome mutates more and more. Some of these mutations can alter protein functions. For example, TP53 is a known oncogene and is mutated in many different cancer types. The figure below shows the different mutation hotspots in TP53 in NSCLC. A majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). TP53 is a tumor suppressor TP53 gene is located in the short arm of chromosome 17. To fulfill its proper biological function four TP53 polypeptides, synthesized from the gene, must form a tetramer which functions as a transcription factor. This transcription factor regulates expression of many genes including genes involved in cell cycle arrest, apoptosis, DNA repair, autophagy, and metabolism regulation. To learn more about TP53 tumor suppressor protein, click here. While a large proportion of cancer genomics research is focused on somatic variants, TP53 can also be mutated in the germline leading to cancer-prone Li-Fraumeni syndrome. TP53 is the most frequent mutation observed in cancer. Is TP53 mutation treatable in NSCLC? No. Not yet. The mutations seen in TP53 protein are "loss of function" mutations. As TP53 protein acts as a tumor suppressor, loss of function causes tumors to form. In the future, it may be possible to correct the single nucleotide mutations through therapeutic genome editing technologies such as CRISPER/Cas9. Are there other NSCLC mutations that are treatable? Yes. If a mutation causes a gain of function that contributes towards the tumor formation, then it can be treated with a drug to inhibit the improper function of the mutated protein, such as the KRAS and the EGFR mutations. How can you determine the mutations in the NSCLC genome? It can be done via NextGen DNA sequencing. Molecular profiling of the lung cancer genome is necessary in order to ensure the best treatment approach. Is there something that can be done to avoid TP53 mutation? Cancer is a biological accident. Mutations happen when the protein (called a DNA polymerase) puts in the wrong DNA base during DNA replication process by accident. Some of these mutations may change a protein function, which may lead to cancer. Cancer is the loss of cell cycle regulation resulting in unlimited cell division. These cancer cells keep dividing and replace the normal cells in the our organs. As a result, the organs fail to function properly and the patient dies. But cancer is a not a death sentence anymore. Cancer treatment has improved cancer survival a lot in the past 25 years. It is only going to get better. Eventually cancer is going to become a chronic disease, which may not be curable but patients may be able to live a long good quality life. ---------------------------------------------------------------------------------- Author: Anirban Mukherjee, PhD June 2, 2021 Founder | Cancer Therapies 4 U LLC

  • Breast Cancer Adjuvant Therapy - Adriamycin + Cyclophosphamide

    USED WHEN? Used as a combination add-on (adjuvant) chemotherapy to treat breast cancer patients with auxiliary lymph node involvement after surgical removal of the primary cancer. DOSAGE ●Adriamycin (doxorubicin) is administered at 40 to 75 mg/m2 when administered in combination chemotherapy. ●Cyclophosphamide capsules are 25 mg or 50 mg. It can also be administered via infusion. Hydration is very important to reduce the risk of urinary tract toxicity. A total of 4 cycles of AC is administered every 21 days. Overdosing may happen. Takes 3-4 weeks to recover. MECHANISM OF ACTION ●Adriamycin inhibits cell proliferation and in duces DNA strand breaks in cells. ●Cyclophosphamide is a prodrug, which is processed in the liver. The products induce covalent crosslinks in cellular DNA, which inhibits replication and induces cell death. Both of these drugs are cytotoxic drugs. SIDE EFFECTS ● Adriamycin related severe side effects: cardiomyopathy, cardiac arrhythmias, secondary cancers, leakage of blood vessels, tissue necrosis, severe low blood cell count, tumor lysis syndrome, radiation sensitization etc. ● Cyclophosphamide related severe side-effects: hyper-sensitivity, low blood counts, urinary tract and renal, cardiac and pulmonary toxicity, secondary cancers, infertility etc. CLINICAL STUDIES There are many clinical studies published and several meta-analyses have been performed. The following clinical study is presented in a simplified fashion. Clinical study 1 ♦ In a phase 3 clinical trial with 1016 patients who had surgically removed stage I to III invasive breast cancer, patients were treated with either doxorubicin + cyclophosphamide or with docetaxel+ cyclophosphamide. The results are as follows: ● Doxorubicin + cyclophosphamide : 5-year disease-free survival rate = 80% 5-year overall survival rate = 87% ● Docetaxel + cyclophosphamide: 5-year disease-free survival = 86% 5-year overall survival rate = 90% For more information: We can help you with more simplified data so that you can make informed decisions about your treatment options. Visit for more information. OTHER COMBINATIONS AC-T = Adriamycin + cyclophosphamide + taxol BREAST CANCER OUTCOME 5-year overall survival is 90% in the USA. 15% of all cancer cases is breast cancer but 7% of all cancer related mortality is due to breast cancer. There are 39 FDA-approved drugs to treat breast cancer in the USA. Sources: NCI and NIH. #breastcancer #chemotherapy #cancer #AC #cancertreatments #doxorubicin #adriamycin #cyclophosphamide ------------------------------------------------------------------------------- Author: Anirban Mukherjee, PhD The author is a scientist at the University of Texas at Austin and researches novel chemotherapeutic targets and chemotherapeutic DNA damage processing .

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  • Cancer treatment options | Cancer treatment results

    google-site-verification: googlee486e52497104abb.html things you MUST KNOW BEFORE CANCER TREATMENT Helping cancer patients make educated data-driven decisions for best treatment outcomes We provide cancer patients with cancer-specific clinical data, which includes treatment-specific disease-free survival and overall survival data, cancer mutation based response to treatment and survival, liquid biopsy data analysis, cancer genome sequencing data analysis, simplified yet comprehensive information about all the FDA-approved cancer treatment drugs, mutation analysis, alternative treatments, clinical trials and pipeline drugs, cancer follow up care, and much more. Cancer Therapies 4 U is your one stop shop for all cancer treatment-specific information. We use bioinformatic analysis of large scale patient databases to find the answers your are most curious about and serves you the best. We summarize the results in forms of reports, which is available to you for purchase through our website. Your healthcare provider is going to answer your basic questions. For additional personalized information research, we can help. Email us at for more information. $25 ​ Cancer Treatments and Outcomes - all you need to know to make informed decisons ​ Reports on individual cancer types $200 ​ Your cancer specific NextGen sequencing results analyzed and actionable answers provided $500 ​ Meet with our cancer experts to ask cancer treatment and outcome related questions - from chemotherapy to immunotherapy to alternative therapy to side effects What we do for cancer patients Develop disease-free, progression-free and overall predictive survival charts based on their specific diagnosis and treatments Provide guidance with residual cancer detection and cancer mutation analysis Prepare case studies Information on latest treatments offered in the biggest cancer hospitals in the USA Identify the best cancer hospitals and labs in your area Analyze genomic mutations identified through liquid biopsies and correlate mutations with disease-free, progression-free and overall survival Search clinical trials and pipeline drugs for patient specific cancer management Research alternative cancer treatment options What we do for clinicians Bioinformatic analysis for precision oncology Variant analysis Prepare case studies Clinical trials data summary Journal club contact us Give us a call. Know the latest in cancer treatments. Email: Phone: +1 512-366-0888 | Monday - Friday 8:00 am - 6:00 pm CST Name Email Subject Leave us a message... Submit

  • Cancer therapies simplified for patient education |

    Myths about cancer treatments Choose evidence based therapeutic approaches CAN HIGH DOSES OF VITAMIN C REPLACE CHEMOTHERAPY, RADIOTHERAPY, IMMUNOTHERAPY AND TARGETED THERAPY? No. There is no clinical evidence to support this theory. Chemotherapy/radiation therapy cannot be replaced with high doses of any vitamin. Vitamins do not treat cancer. "HERBAL MEDICINE WORKS BETTER WITHOUT THE SIDE EFFECTS." No. There is no such evidence that proves clinical benefit with herbal remedies over chemotherapy, immunotherapy, targeted therapy and other forms of therapy. "THE GOVERNMENT AND THE PHARMA COMPANIES HAVE THE CURE FOR CANCER ALREADY!" No. No one has the cure for cancer, yet. But cancer treatment is getting better everyday. Breakthrough treatments are being discovered faster than ever before. Cancer is not a death sentence anymore. "CHEMOTHERAPY IS POISON AND IT KILLS THE PATIENT FASTER" C hemotherapy does not kill you faster. It is true that chemotherapeutic drugs are toxic to the cells but all the FDA approved chemotherapeutic drugs show survival benefit over no treatment. "CANNABIS OIL CAN CURE CANCER" No. Recent meta analysis of patients suggests that cannabis and cannabinoids does not help in cancer regression. In fact, use of cannabis products reduces the clinical benefit of immunotherapy in some instances. Cannabis may lower the side effects of cancer and cancer treatments. "SURGERY AND BIOPSY CAN CAUSE THE CANCER TO SPREAD FASTER" No. Cancer cells undergo a physiological changes before they start spreading, which is called "transformation". Surgery or biopsy has nothing to do with it. ARE THERE DOCTORS IN MEXICO AND GERMANY WHO CURE ADVANCED CANCERS WITH SECRET IMMUNOTHERAPY? Best cancer treatments are provided in the USA. The US FDA properly evaluates the efficacy of a drug and approves it. Cancer patients need to make informed decisions before choosing to get treatments that are not FDA-approved. There are many scammers who use the vulnerability of cancer patients and sell them treatments. "CHEMOTHERAPY AND RADIATION THERAPY CAN CAUSE CANCER" Chemotherapy and radiation therapy sometimes can cause secondary cancer . But the risk outweighs the benefit. Without the treatment, the lifespan of the cancer patient will be much shorter.

  • Cancer therapies simplified for patient education |

    The Full Story About It is about knowing that you did your best to fight the beast that cancer is. It is about having access to all the information you need to make critical decisions with confidence. Mission Our mission is to help all cancer patients understand their treatment options and outcomes and educate them with information from large scale data analysis so that they can make informed decisions together with their doctors. Vision Every cancer patient should have access to data, so that they have the freedom to make informed decisions, to choose what is best for them.

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