Monday, April 28, 2014

The discovery of BRAF mutation in melanoma is shown to be extraordinarily important

by Ellie Pringle

After reading the articles about DNA sequencing and the cancer genome and because for my project topic my partner and I are focusing on how a mutated BRAF gene is a cause of melanoma, I decided I wanted to learn more about how sequencing and the discovery of the relationship between the mutated BRAF gene and melanoma has changed cancer treatments today.  To do this I chose to start by focusing on the initial discovery of the mutated BRAF gene in cancers.

Cytokine Release Syndrome

Freddy Tadros and I are studying the efficacy of Chimeric Antigen Receptors (CARs) in the treatment of Acute Lymphoblastic Leukemia (ALL). To give just a brief overview of the treatment, scientists modify a person's own T-cells to express antibodies that target antigens present on lymphocytes that are involved with the leukemia. These lymphocytes are then destroyed by the body's own immune system (3). This treatment has had great success in clinical trials, with 5 of 5 participants experiencing a complete remission for 12 months, which was the period of time that the individuals had been monitored prior to publishing the paper, so these patients could be experiencing remission for even longer (2). Unfortunately, this promising treatment does have two main drawbacks: the cytokine release syndrome and B-cell aplasia. This blog will focus on the cytokine release syndrome.

Sunday, April 27, 2014

CTC Concentration and Cancer

Joseph and I are looking at the correlation between circulatory tumor cell (CTC) concentration in the circulatory system in individuals with metastatic cancer with cancer progression. Seeing as how the circulatory system is the manner through which nutrients are transported throughout a body, it is a potential manner that cancerous cells may metastasize and reach extremities in the organism that it would not have otherwise localized to. Seeing this correlation between the metastasis of an otherwise “pinpoint” cancer that would have been localized solely to one general region to cancer cell concentration in the bloodstream is a promising part of current cancer research and may lead to possible future advancements in monitoring cancer growth by analyzing CTC presence.

DOK7 identified as potential Epigenetic indicator of Breast Cancer

        Lauren and I were intrigued by the role of epigenetics in cancerous growth and chose to further investigate this correlation in our Cancer Project, so imagine my excitement after an epigenetic cancer study was introduced in my general psychology class!

This studyconducted by Bellvitge Biomedical Research Institute; University of Coimbra Centre for Neurosciences and Cell Biology; Kings College London Department of Twin Research and Genetic Epidemiology; University of Iceland Molecular and Cell Biology Research Laboratory; and University of Barcelona School of Medicine, looked at 15 monozygotic (MZ) twin pairs discordant for breast cancer, with further examination into the different degrees of methylation affecting gene rich segments within the cancerous cells. In other words, despite the genetic equivalence within each twin pair, an extraneous variable, presumably differences in epigenetics, resulted in one twin exhibiting breast cancer while the other was cancer free. By comparing isolated DNA from blood and cell samples obtained from the cancer positive twin with that of the cancer negative twin, this study isolated 403 differentially methylated CpG sites, or Cytosine-Guanine DNA regions, many of which contain specific genes referred to as “novel breast cancer genes,” genes highly correlated with breast cancer incidence.

Friday, April 25, 2014

Fighter Viruses: Fighting acute leukemia via the use of non-replicating rhabdovirus-derived particles (NRRPs)

            Although this topic is unrelated to my cancer project, I came across the article and was too excited about the abstract to not read it. The article, originally published in the Blood Cancer Journal on July 12th, 2013, details a potential anticancer therapy for multiple tumor types, particularly leukemia (Ref. 2). The method in question is the use of non-replicating rhabdovirus-derived particles or NRRPs, as they are called. I will explain in detail how these particles have the potential to destroy cancer cells in the human body, but first, I will give some background information.

Wednesday, April 23, 2014

Special Students-only Lecture!

Gerald and Sally DeNardo Lectureship


James E. Bradner, M.D.
Staff Physician, Division of Hematologic Malignancies, Dana-Farber Cancer Institute
Associate Professor in Medicine, Harvard Medical School
  • The implications and challenges of biotech development
  • His life as a scientist--what motivates him, what excites him?
  • What new frontiers is he exploring?
  • What might be future career opportunities in research?
  • What is on the horizon for new cancer therapies?
  • And more!

Thursday, May 1, 2014
10:30-11:30 a.m., Wiegand Room, Arts & Sciences Building
Reservations are requested. If you have any questions, or would like to make a reservation, please call
Marie Brancati, 408-554-2301, or email,

Monday, April 21, 2014

Delayed Childbearing and Breast Cancer Risks: A Population Level Study of Women in the United States

A Brief Background 

    For decades we have known that the act of bearing children can have a protective affect against the development of breast cancer in women. This was discussed in 1968 by Joseph Fraumeni Jr. who studied cancer mortality rates of catholic nuns in the United States between 1950 and 1954. He concluded that nulliparity (never bearing children) and the associated lack of hormonal changes that come with pregnancy had a significant impact on the development of cancers, especially cancers of reproductive organs such as the breast. This study sparked a huge debate over whether or not to allow nuns to use oral contraceptives–against the views of the catholic church (2). With this in mind we can look deeper into the conclusions drawn by Joseph Fraumeni concerning child birth and breast cancer. I have chosen to focus on whether the age at which a woman has her first child can affect her risk of developing breast cancer. Currently, women who have children before the age of 24 are thought to have a reduced risk of developing breast cancer. The best way to look at this data is to focus on a small subset of people and look at the data we have available, after-all it is these type of trends and patters that give rise to new forms of diagnostics and treatments.

Our First Notch to Understanding NOTCH

Antonio and I started our search on cancer by looking at an issue that people could relate to. Understanding that we are in college, we looked to the affects alcohol has on cancer. What we first found is that alcohol is directly related to a set of cancers called HNSCC or Head and Neck Cancer. These cancers have to do with the oral, nasal, pharynx and larynx areas.

Breast Architecture and Cancer Development

The article entitled MammaryGland Architecture as a Determining Facter in the Susceptability of the HumanBreast to Cancer, by Jose Russo, focuses on a study done with 3 different classes of patients and the type of breast tissue they exhibit. The first group, the control, were women undergoing reduction mammoplasty (RM), the second undergoing a mastectomy due to genetic familial breast cancer (FAM), and the third group were women who underwent a radical mastectomy due to invasive carcinoma (MRM). Russo postulates that the development and design of the breast tissue plays a part in the likelihood of developing cancer. To understand this we must first look at the types of breast tissue that exist.

Sunday, April 20, 2014

The Cure for One Cancer is the Cause of Another

During my internship last summer I came across this 2012 article from the New England Journal of Medicine titled “Progression of RAS-Mutant Leukemia during RAF Inhibitor Treatment.” I found it particularly interesting because it took what I was working on in vitro with mouse cells and put it in a clinical setting with actual patients. I thought this article would be perfect for the blog for this class because its main focus is on the RAS and RAF oncoproteins that we have been talking about.

An Introduction to NOTCH1's Dual Carcinogous Properties

            In Aaron Madden and I’s cancer project, we explore the mutated NOTCH1 gene and how it can act either as a tumor suppressor gene or an oncogene, which we will ultimately use to observe how genes like these with seemingly contradictory functions alter how cancer should be perceived. The gene was initially noted as acting as an oncogene, however, recent research has been suggesting that it can also function as a tumor suppressor gene.  In our project, we will focus on the NOTCH1 gene’s effects in T-Cell acute lymphoblastic leukemia and head and neck squamous cell carcinoma.  NOTCH1's involvement in cancer was first observed in T-Cell acute lymphoblastic leukemia as an oncogene, but recent research has suggested that it can also acting as a tumor suppressor gene in some types of cancer. In this blog post, I will evaluate a study that suggests that the mutated NOTCH1 has tumor suppressor properties in head and neck squamous cell carcinoma and will briefly explain the potential of NOTCH1 to act both as a tumor suppressor gene and as an oncogene.

BRCA Mutations and Male Breast Cancer

Various websites, like MedicineNet, report that 99% of all breast cancers are found in females.  I then thought about the other 1% of males that acquire breast cancer.  I wanted to learn more about the causation of male breast cancer and possible trends among possible gene mutations.  I narrowed my search down to mutations among both the BRCA 1 and BRCA 2 genes.  Although this is not the subject of mine and Ellie Pringle's cancer project, I thought it would be interesting enough to explore deeper.  

Sunscreen & Skin Cancer: The Basics

Jacey Nishigushi and I are researching the inhibition of p53 mutations by sunscreens and the efficacy of p53 mutations as indicators of melanoma. In order to understand our eventual analysis, several key concepts must be discussed prior to exposure to our final project. We are planning to use our blog posts for this purpose, to consider the basics and build a solid foundation from which we can build off of.

Saturday, April 19, 2014

Blogging about blogging (Part 3)

Step 3: Limit yourself

By now, you’ve found a paper or two that interests you and you’re slowly beginning the process of understanding it. Don’t be a hero! Take it little by little. The key is to begin with something very manageable.
   I mentioned that a small dataset—a small table, a graph, a figure that presents some data you want to explore—is the best place to start. You might even want to try and take it section by section, coming to terms with each as a way to understand the entirety of the paper.

Friday, April 18, 2014

Thyroidectomies from Patients with a History of Therapeutic Radiation During Childhood and Adolescence Yield Unique Mutational Profiles

           Since the 1950’s it has been observed that radiation in childhood is a risk factor for thyroid carcinoma, however, radiation may also be related to benign nodular hyperplasias. There are two scenarios of exposure to radiation that have been studied in relation to thyroid cancer; nuclear fallout, such as the nuclear accident in Chernobyl,  and therapeutic radiation. Most research has been base on the radiation exposure due to nuclear fall out, however exposure due to therapeutic radiation of the head and neck, is more common. Because of the observation that radiation was creating a great risk for cancer, the therapeutic radiation treatments are now only used in response to morbidity and mortality cases. Unfortunately,  due to the long lag time between exposure and thyroid disease onset, the children from the 1950s and 60s are only recently being treated for thyroid disease.
In recent studies, rat thyrocytes subjected to radiation were found to have clonal DNA damage.  In a new study conductedby Adel Assaad, Laura Voeghtly and Jennifer L. Hunt, differences in genetic alterations were observed between the radiation-induced and sporadic papillary carcinoma and follicular derived carcinomas. The most commonly studied mutations in papillary carcinomas have been the ras gene mutations and, RET/PTC translocations, and BRAF mutations. However, after studying the Chernobyl patients with papillary carcinoma, it was observed that the  radiation-induced tumors had higher mutational rates for ras gene mutations and the RET/PTC translocations, while the BRAF mutations were uncommon. In another study, BRAF mutation frequencies were also found to be low in tumors of patients with history of therapeutic radiation in childhood. This lead to the idea that BRAF mutations are generally uncommon in radiation induced tumors. Investigators, however, took into account the findings that the translocations alone were likely insufficient to induce carcinomas and that there are likely other genetic and molecular events leading to the malignant transformation. Tumor suppressor gene mutations are likely the missing link, however tumor suppressor gene genotype has not been well studied in radiation-induced tumors of either of the two exposure scenarios.  
PCR was also performed  for 18 different genetic  loci, identified from the comparative study of the rats, using thyroids from patients with a history of radiation (30 cases: 3 chronic lymphocytic thyroiditis, 11 benign hyperplastic nodules, 7 follicular adenomas, 2 follicular carcinomas, 7 papillary thyroid carcinomas), patients who had recent therapeutic external beam radiation for laryngeal carcinoma (12 cases), and patients who had no radiation and underwent thyroidectomy with laryngectomy for laryngeal carcinoma (15 cases). The reasons for the use of therapeutic radiation treatment are listed in Table 3. After a semiquantative capillary electrophoresis analysis was performed, the frequency of allelic losses from each group was calculated. The frequency of allelic loss from non-radiated patients was 2.3%, while the frequency of allelic loss of patients radiated as children was 39%.  The frequency of allelic loss was also high in patients with benign nodular diseases who were subjected to radiation as a child.

                  It was clear that the growing thyroid of children is at greater risk than that of adults for carcinomas due to radiation exposure. Even if the transformation is not malignant, radiation could cause other problems with the thyroid such as hyperthyroidism, thyroiditis, autoimmune thyroiditis, and hyperplastic changes. The development of these problems is caused by the propagation of the mutation abnormalities as the thyroid matures.

Thursday, April 17, 2014

Chernobyl Acident and Thyroid Cancer


Analisa and I are looking in the effects of radiation and thyroid cancer. An interesting incident occurred in Chernobyl which led to high numbers of thyroid cancer, which is detailed in this article.
   In 1986 a nuclear power plant in Chernobyl exploded causing the surrounding areas of Belarus, Russia and Ukraine to receive high doses of radiation.  The major radioactive material that contaminated the area, which affected more than 5 million people, was iodine-131 and caesium-137.  One of the major health problems reported were high incidents of Thyroid cancer in children and young adolescent.  This is significant because the thyroid gland is the major organ responsible for the metabolism of iodine, here inherently is the problem.  The iodine released from the plant contaminated the surrounding areas soil therefore contaminating the grass the cows ate.  The cows produced iodine enriched milk which was consumed by many children and young adults near the power plant and surrounding areas.  On average the amount of radiation one was exposed to was about 0.03 Gy (gray, the SI unit for ionization radiation), and the threshold for many organs in the body is 45 Gy.  But, by directly consuming the iodine milk on more than one occasion the thyroids received enough radiation to induce cancer.

Wednesday, April 16, 2014

Therapeutic Implications of Inhibiting Cdk4

  Recently, while I was perusing through the Wall Street Journal I stumbled across an article on a phase I study of a potential monotherapy for metastatic breast cancer patients. According to the AACR, Lilly Pharmaceutical's has developed a drug (LY2835219) with the aide of South Texas Accelerated Research Therapeutics that resulted in preventing tumor growth in 33 of 47 patients. The drug inhibits Cdk4. These articles fail to offer any information on the significance of targeting Cdk4 and not other Cdk's. Crucially, the data presented may be unreliable due to the small sample size.

  In order to validate these claims, I investigated the science behind the drug and discovered a study entitled "A Synthetic Lethal Interaction between K-RAS Oncogenes and Cdk4 unveils a Therapeutic Strategy for Non-small Cell Lung Carcinoma." This study was especially, enlightening in revealing what the article failed to articulate about the therapeutic potential of Cdk4 and how it augment cancer cell growth. In this study researchers implemented the synthetic lethal interaction hypothesis proposing,"disruptions of one gene will sensitize cells to disruption of another pathway while sparing cell that retain either one of the two functions"(Sherr 3693). Subsequently, researchers ablated Cdk2,Cdk4, and Cdk6 in mice by controlling gene expression. Only the inhibition of Cdk4 prompted a senescence response from lung cells with an activated K-RAS oncogene. Ultimately, the result of only inhibiting Cdk4 was the prevention of tumor growth. Moreover, the study compared these results to the selective inhibitor drug PD0332991 that targets both Cdk4,6 to conclude that the targeting of Cdk4 is a more potent method to induce cell senescence.

Figure C and D below demonstrates the effects of PD0332991 compared to vehicle. Figure C is an immunohistochemical analysis of Cdk4 specific phosphorylated Rb in a lung section from a K-Ras activated wild type mouse after 30 days of treatment with vehicle (left) or 150mg/kg of PD0332991 (right). Figure D is a Western blot analysis of individual tumors from the lung of a K-Ras activated wild type after 30 days of treatment with vehicle (T1-T3) or 150 mg/kg of PD0332991 (T1-T6) with antibodies specific for pRb phosphorylated residues Ser 807 and Ser 811.

It may be concluded that tumors exposed to PD0332991 did decrease the inhibition of pRb in the Cdk4 specific Ser 807 and Ser 811 residues. However, the tumors exposed to PD0332991 did not express SA-beta galactosidase or an increase in tumor suppressors such as p53 or ARF. SA beta galactosidase is commonly used to determine if senescence is occurring. Since SA beta galactosidase is not expressed it appears that no senescence is occurring. In comparison the inhibition of Cdk4 resulted in the expression of SA-beta galactosidase. Furthermore, Cdk4 is a known inhibitor of pRb. This study would suggest a synthetic lethal interaction occurs with the loss of Cdk4 for K-RAS because inhibition of Cdk4 is the best means to induce cell senescence. 

   The science behind Lilly's new drug appears promising as inhibition of Cdk4 is central to deterring cell growth. Still, many questions regarding how to implement the inhibition of Cdk4 remain unanswered. 


Puyol,Marta, Alberto Martin Pierre Dubus, Francisca mulero, Pilar Pizcueta, Gulfaraz Khan, Carmen Guerra, David Santamaria, and Mariano Barbacid. "A Synthetic Lethal Interaction between K-Ras Oncogenes and Cdk4 Unveils a Therapeutic Strategy for Non-small Cell Lung Carcinoma."Cell. 18. (2010): 63-73 

"New Drug Demonstrates Early Promise in Metastatic Breast Cancer". AACR.April 6, 2014.  

Sherr, Charles J. "The Pexcoller Lecture: Cancer Cell Cycles Revisted". AACR.60.(2000):3689-
3695.Web 16 Apr. 2014. 

"Two Drugs Show Promise in Slowing Breast Cancer". Rockoff Jonathan D. and Ron Winslow. Wall Street Journal. April 6, 2014.

Sunday, April 13, 2014

DNMT3a Mutation in Acute Myeloid Leukemia: Introduction

Shreshtha and I are researching how a mutation in DNA-methyltransferase DNMT3a contributes to the development of Acute Myeloid Leukemia (AML). Though the existence of cancerous stem cells is still a very controversial topic, recent studies of acute myeloid leukemia provide evidence that neoplastic cells differentiate into different lineages of cell types.

Nature’s article, “Cancer: Persistence of leukaemic ancestors”, summarizes Slush’s findings that a DNMT3a gene mutation was not only common across AML patients, but carried at low rates in T cells, and other immune cells at the time of diagnosis. Since AML is characterized by cancerous myeloid cells and this DNMT3a mutation was found in non-myeloid cells of patients, it suggests that the mutation begins in the precursor cell that gives rise to blood cells of both lineages. Previously, it was believed that the gene NMP1 was the cause of AML, since it initiates the cancer in mice, but both mutations NMP1 and DNMT3a are present in these founder clone populations.

The chart below shows the routes of 3 intermediate stages of acute myeloid leukemia: undetected pre-leukemia, myeloid-cell dysplasia, and chronic myeloid leukemia. Each stage begins with hematopoietic stem cells, and only progresses to AML after the addition of secondary mutations. In the most common form, they are differentiated by DNMT3a mutation, but the cancer can also progress from a patient already having myeloid cell dysplasia, or mutation in BCR-ABL1.

In Hanahan and Weinberg’s article, “Hallmarks of Cancer: The Next Generation”, they explain how cancer stem cells take over the process of self-renewal for their growth, and hypothesize that the creation of cancer stem cells is related to the process of the EMT program, where epithelial carcinoma cells are converted to mesenchymal for dissemination. Similarly in AML, high levels of competitive self-renewal of DNMT3a mutant cells are what prevents normal self-renewal of the normal hematopoietic stem cell. Hanahan and Weinberg are focusing on cancer stem cells in tumors, and leukemia does not form tumors, but Slush’s research of hematopoetic stem cells in AML still supports the basic ideas behind the resistance of cancer stem cells.

This data is important because since AML is an aggressive, rapidly progressing disease, early detection and treatment are critical. If ancestors of precancerous cells in acute leukemia can be identified at an earlier stage in the cancer, by detecting a DNTM3a mutation, the precancerous cells can be treated before progressing into a secondary mutation. Additionally, cells with this mutation can be targeted and tracked specifically in therapies, to more effectively avoid remission from leftover traces of the disease.

The main questions this article raises are whether a mutation of DNTM3a by itself will lead to acute myeloid leaukemia, and whether it is the DNTM3a mutation that is initially responsible for starting the cancer’s growth. As we continue our research, we will delve further into the reasons behind hematopoietic stem cell differentiation.


Hanahan, Douglas, and Robert A. Weinberg. "Hallmarks of Cancer: The Next Generation."
      Cell 144.5 (2011): 646-74. PDF file.

Potter, Nicola E., and Mel Greaves. "Cancer: Persistence of leukaemic ancestors."
      Nature 12 Feb. 2014: 300-01. Web. 13 Apr. 2014. 

Introduction to the Stem Cell Origin of Acute Myeloid Leukemia (AML)

I. Purpose: In our cancer project, we will be focusing on the role of DNMT3A gene mutation in the progression of Acute Myeloid Leukemia. As these studies have been published recently in the past few months, we will be analyzing how this new data fits in with previous studies on the prevalence of cancer stem cells leading to development of AML cancer. Further research into the differentiation of pre-leukemic stem cells would improve treatment methods by targeting the root causes of AML.

II. Introduction: 

Adult Acute Myeloid Leukemia (AML) is a cancer of the blood and bone marrow and it is the most common type of acute leukemia in adults. Normally, the bone marrow makes immature, blood stem cells that become mature blood stem cells later over time. A blood stem cell, that is essentially a multipotent stem cell derived from a hemotopoietic stem cell (see discussion below), can become a myeloid stem cell or a lymphoid stem cell. The myeloid stem cell can give rise to one of three types of mature blood cells: red blood cells, white blood cells that fight infection and disease, and platelets that form blood clots to stop bleeding. The lymphoid stem cell becomes a white blood cell. In AML, myeloid stem cells usually become immature blood cells called myeloblasts (myeloid blasts). These myeloid blasts are abnormal and do not become healthy, normal white blood cells. If too many of these stem cells become abnormal red and white blood cells or platelets, then they are called leukemia cells or blasts. These leukemia cells can then spread to other parts of the body, including the central nervous system, skin and gums. 

Wednesday, April 9, 2014

Blogging about blogging (Part 2)

Step 2: Finding the data

In our last post, we (hypothetically) found a news feature that interested us, likely because it’s related to our cancer project, but it can be on almost anything related to cancer. A news article on a web site is a good place to start, but if you simply summarize a news story that is already a summary of a research article, then you risk being derivative (remember, paraphrasing or summarizing is a relatively low order of critical thinking). You can dissect the reporters work, finding inconsistencies and flaws in the argument or reporting—this is very good. But it raises the question: are the flaws due to the inadequacies in the science or in the reporting? Perhaps the reporter got the facts wrong. In order to really see whether the data support the claims, we must look at the primary research article.

Monday, April 7, 2014

Blogging about blogging (Part 1)

This is the first in a series of posts intended to help you identify something to write about in a blog entry, narrow down the scope of the topic, and ask the right questions so that your readers come away having learned something. While it’s a blog post about creating blog post, I want it to be a little more—an attempt to help you think critically about your topic at hand.

Thursday, April 3, 2014

Freddy's Inaugural Post

Hey everybody,
My name is Freddy Tadros and I am a junior Biology major and Chemistry minor. I am beyond excited to have the opportunity to take a class in undergrad solely dedicated to cancer. I hope that this class will give me better perspective on my aspiration to become an oncologist because I find all aspects of cancer fascinating: the cellular mechanisms, physiology, biochemistry, genetics, and epidemiology, all of it.
For my first post I thought I would write about a strange incidence of cancer that I recently heard about on the radio that I found fascinating. Unfortunately, "Taz,"one of my favorite cartoon characters, and his people, are threatened by an odd cancer epidemic that has caused the tasmanian devil to become an endangered species. The decline in the devil population has been seen for decades but only in the last ten years have scientists begun to understand the cause. In 2006, a paper published in Nature showed that the chromosomes from these cancer cells found were all genetically identical, meaning that they all have a one unique ancestor and therefore must have originated outside of each ill individual (Pearse 2006). This form of cancer that is endangering the Australian devil population is known as devil facial tumor disease (DFTD) and is thereby actually infectious. Due to high inbreeding among this island species, if a viable tumor cell from an infected individual were to physically invade another individual it can survive and proliferate (similar to a parasite/host relationship) in the same manner because of this lack of genetic diversity. DFTD is one of only two observed clonally transmissible cancers observed among mammals, however, it just so happens that cases of cancer infection have occurred in humans when organ transplants come into play (Murchison 2009).
Although the tasmanian devil is one of the coolest animals, due to its certain je ne sais quoi, this case is fascinating regardless of the afflicted species. I hope to learn as much as I can about cancer this quarter and leave this class with a couple more fascinating medical or scientific cases that I can think about.

KP's First Post

My name is KP Bugtong and I am a senior bioengineering major. I chose to take this class because I am very interested in cancer as I did breast cancer research last summer. It was fascinating to learn about the molecular and cellular basis behind a certain type of breast cancer (HER2+) because this type of cancer evolved to become resistant to treatment. Also, there have also been instances of cancer within my family. With this class I hope to gain more knowledge of various types of cancers as well as an overview of different types of cancer treatments.

I'm attaching a picture showing the family of receptors, the HER family.

HER2 breast cancer is a particularly nasty form of cancer because it carries a higher risk of metastasis and a lower survival rate.  

Wednesday, April 2, 2014

Annika's First Post


My name is Annika van Leynseele, and I am a sophomore Biology major. Eventually, I hope to work in the infectious disease field; cancer is interesting to me because it is, similarly, a human pathology. My family has had some instances of cancer: my maternal grandma battled breast cancer in her 40's, and my paternal grandpa battled prostate cancer in his 70's. It is amazing to me that both of them were able to overcome their cancer and continue to live full lives. Therefore, I am excited to learn about both practiced and new ways of preventing and treating cancer.

Below is a list of estimated new cancer cases and deaths in the US in 2014.

Cancer is so widespread, both in the US and worldwide. Many diseases that are researched discussed in the media are present only in other countries. I think cancer is so fascinating, and of such importance, to so many Americans because it hits much closer to home. 

Tuesday, April 1, 2014

Carlos's First Post

Hey everyone,

My name is Carlos Rivera and I am currently a sophomore Biology major. The reason why I am interested in this class is because I lost a close relative of mine to pancreatic cancer. What interests me most about cancer is the fact that there is so much we don't know about it despite the years of research that have gone into it. By taking this class, I hope to get a better understanding as to what causes this irregularity as well as the differences between the different types of cancers and how they affect the body with respect to their location.

Though the causes for pancreatic cancer is largely still a mystery, John Hopkins University has given a general overview as to the possible causes for the development of pancreatic cancer. Below is an image from showing the number of recorded incidences of pancreatic cancer in the world in 2008.

Abraham's first post

Hello everyone,

My name is Abraham Munoz and I am a senior bioengineering major. I am interested in this class because I have had a family member and personal friend battle with pancreatic and breast cancer and I really want to learn more about these diseases. Pancreatic cancer is one of the most deadly cancers and has one of the highest mortality rates for its patients. Most battles with pancreatic cancer are short lived, and I hope to learn more about why and how pancreatic cancer is so malignant. Breast cancer on the other hand is not always as malignant, but is very prominent in the US population. Every year more and more cases of breast cancer arise, which has lead to the development of better therapies for this disease and I am looking forward to learning about these treatments.

I attached a graph below that illustrates the rise of incidence of breast cancer dependent on age from 2008-2010 in the UK. This shows how significant breast cancer is becoming to our world's populations.

Steve's First Post

Hi everyone,
My name is Steve Davies and I am Junior Biology major. I am taking this course because my grandpa was recently diagnosed with stage 4 metastatic prostate cancer. This diagnosis has generated a lot of talk and speculation within my family, much of which I believe to be false information. I hope to gain an adequate understanding of cancer so that I can effectively evaluate how cancer develops and spreads, as well as the most effective treatment options available. The chart I found shows that prostate cancer is the most prevalent cancer is in the U.S., indicating that we must focus on researching various methods that control the spread of this cancer to other organs of the body.

Jacey's First Post

Hi everyone, my name is Jacey Nishiguchi and I'm a sophomore bio major here at SCU. I am taking this class because I still have no idea what I want to do after college, and one of the fields that I want to learn more about is cancer research. I guess you could say I'm basically starting from scratch because I really don't know much about cancer. I'm hoping to learn more about how the disease works and the types of treatments there are for people who have this disease. I'm also interested in learning about research methods and how people develop treatments, as well as what differentiates each type of cancer. To get a brief overview of cancer in the U.S., I looked at the American Cancer Society's website, and something I found interesting and hope to learn more about is the varying numbers of survivors for the different types of cancers.
Overall I'm hoping to develop a better understanding of the impact of cancer on the U.S., and how researchers are working to find treatments and learn more about the disease.

Ashley's First Post

I am a senior finishing a biology and public health double major with a minor in sociology.  I chose to take this course because cancer has played a large role in my life, affecting many of my family members, and thus has been a growing interest of mine for some time.  Given my own experience and from reading my fellow bloggers posts, cancer is a disease that has, in one way or another, touched most people's lives.  The fact that it is so prevalent, displays such great diversity, and is largely incurable adds to its intrigue.

Below is a table of the estimated number of leading new cancer cases and deaths in the U.S. in 2014. 

I am specifically interested in the genetic versus lifestyle components of cancer.  In the epidemiology class I took lat quarter I learned a little about mammograms and the BRCA 1 and BRCA 2 gene mutations with relation to breast cancer screening and would like to learn more about that.  The controversy over the use of potentially carcinogenic artificial sweeteners such as aspartame is another topic with which I am interested.

Matthew Perez's First Post

Hi my name is Matthew Perez! I am a sophomore biology major public health minor. I am interested in this course because of the multiple family members diagnosed with cancer. I am very interested in the way in which clinical trials are advancing the diagnosis and mainly the treatment of cancer. We see childhood cancer becoming more and more prevalent. It will be interesting to see what new technologies come about to help mitigate this. 

This graph helps us to see the different types of cancer and the survival rates in children.

This article more deeply explains childhood cancer survival rates. 

Aaron's First Post

Hi there everyone! My name is Aaron and I am a sophomore biology major. To be sincerely honest, I cannot say I know a whole lot about cancer. However, throughout this past year, my family and I have had to make many changes in our lives due to this disease. I understand that many others have probably experienced this as well, and I also understand that this may sound a tad bit cliche, but it is because of this personal experience that I want to learn more about cancer and how it can be prevented and contained. Although this is not the biggest issue in the topic of caner, I am very interested in either disproving or understanding the stereotypes and myths of how to prevent or cure cancer. For example, I would like to know if and how substances such as red wine and chocolate are meant to prevent cancer. A vast majority of people have heard of these common stereotypes and myths, but very few actually understand why they have come to be. I believe that being able to understand these beliefs could be very beneficial to myself and society as a whole.

Charles's First Post

Hi everyone, my name is Charles Walker and I am a senior biology major. I am taking this class because I have always been interested in cancer in general and because I feel that my future career (though I don’t know what that will be) will require me to know something about different types of cancer.

Over the years, cancer survival rates have drastically increased. For instance, the 5 year relative survival rate for all cancers diagnosed from 2002-2008 has increased to 68%, 19% higher than it was between 1975 and 1977 ( This table from the American Cancer Society's Cancer Facts & Figures 2013 shows how much the 5-year survival rates for cancer have generally increased while highlighting the lower survival rates of some cancers.

Because the 5-survival rates for so many cancers have significantly increased since 1975, I am interested in learning how new medicines combined with greater understandings of the mechanisms of different cancers were able to facilitate these increases. I am also interested in what the future holds for cancer prognosis and treatment with the incorporation of new technologies, such as whole-genome sequencing.

Anisha's First Post

Hi everyone! My name is Anisha and I am a sophomore majoring in biology. As with many of us, people close to me have been diagnosed with cancer, including relatives and a close friend. I'm especially interested in going more in-depth on the various methods of treatment/management and how they work. Cancer is an interesting topic to study due to how broad and widespread the disease is, as well as the mystery of how much is still unknown. I think it’s important area for research since it is growing increasingly common across the world, and I am looking forward to learning more through this class!

The chart above, published by the California Healthcare Foundation, shows that overall in California, both the incidence and mortality of cancer increase with age.

Caitlin's First Post

Hello, my name is Caitlin Kennedy. I am a Sophomore Biology student here at Santa Clara University. Although cancer has not had much of a direct effect on my family, my best friend from childhood's father battled cancer throughout my youth and recently lost his battle a month ago. Smoking cigarettes causes 90% of the cases of lung cancer and this man was always surrounded by a cloud of smoke. While smoking is the largest Cause of Lung Cancer, there are a few other contributors.

Below is a graph showing the risk in men of developing lung cancer based off how many cigarettes they smoke per day.
Figure 1.1: Relative of risk of lung cancer according to duration and intensity of smoking, men
You can access more information about this chart at this website.

I also have been very interested in the HPV shots. When I received the set of three shots, the vaccine was still experimental; I have been curious to what it does/prevents ever since. I would really like to work on this topic specifically during my cancer project. A link explaining the purpose of this series of shots given to children is here.

Brendan's First Post.

Hello this is my first post.  My name is Brendan Burke and I am a junior Biology major.  I am very interested in this cancer biology class because of the impact cancer has had on the people surrounding my life.  Embedded in my blog below is a figure that shows death rates for lung cancer among different age groups.  Death rates for cancer are highest among middle aged and older populations.  This is the first leading cause of cancer death in the United States.
I found this graph from the National Cancer Institute website.

My first post

Hi Everyone,
My name is Abbie Read and I am a junior biology major and biotech and chemistry minor. I am interested in taking this cancer biology class because last summer I interned in Dr. McMahon's lab at UCSF studying a type of lung cancer called non-small cell adenocarcinoma using in vitro and in vivo studies. Starting this summer and carrying through my senior year I will be interning in Dr. Sweet-Cordero's lab at Stanford where the focus is on pediatric oncology but my main project will be looking at chemotherapy resistance in lung cancer. I hope this class will give me a better understanding of cancer as a whole since so far what I have learnt is very focused in on one specific area. A broader look at cancer will help me make connections in my research. I also plan on going to graduate school where I will most likely continue my research in the cancer field. Here is a picture I took last summer of a Hematoxylin and Eosin stain of the airways of a mouse that had lung cancer.

Ramez's First Post

Hello everyone, my name is Ramez and I am a sophomore Biology major. I am interested in studying Cancer Biology due to its impact on people close to me and in order to easily separate reputable scholarly sources from misleading ones. Especially as cancer continues to grow, in both prevalence and popular culture.

For example, a study from The Lancet Oncology predicts that incidences of cancer will increase by 75% within two decades. However, it is obviously difficult to attempt to evaluate and foresee the fluctuating patterns of cancer.

Nicole's First Post

Hi my name is Nicole Mattson and I am a Sophomore Biology major.  I am interested in cancer biology because I have had family members suffer from cancer and I want to make a difference to prevent others from having to go through the same situation.  I would like to better understand the longevity and life cycle of cancer.  More specifically, why some cancers last longer than others and why it is difficult to predict when cancer will cause life threatening problems.   Below is a picture of a long that has been infected with cancer and one that has not been infected.  You can see the differences in the structure of the lungs. I got this picture from this website.

Ellie's Post

This is my first post on here.  I am a Junior Public Health Science major.  I'm interested in cancer biology because of the personal impact that cancer has had on me and my family.  I am interested in pursuing cancer research and cancer prevention methods. Embedded is a picture that shows the number of cases of various types of cancer that are attributable to smoking cigarettes.  This graph shows the detrimental affects of smoking and how not smoking is a powerful preventative method.
I found this graph from an article taken from the American Cancer Society's website.

Shiona's First Post

Hello Everyone! My name is Shiona (pronounced Sheena) and I am a sophomore Biology major with a biomedical emphasis. I am interested in the class because many of my family members have been diagnosed with cancer and I would like to know more about what they have been going through and why it is happening. I am particularly interested in lung cancer because it usually has a direct correlation to smoking and has had the greatest impact on my family. I find it so strange that a simple cylinder can cause so much damage. It is truly fascinating how we have all this technology today, yet we seem to be at least one step behind cancer. I am interested to see the new technology that is out there to help us with cancer detection early on.

Joseph's First Post

Hello, my name is Joseph Wojcik and I am currently a Junior majoring in Chemistry and minoring in Mathematics. I am excited to learn about cancer due to the gravity it holds. Many people have felt this weight in some way. I, myself, have felt this several times for both friend and family alike. For some, cancer can be more closely synonymized with death rather than illness. However, the disease itself generally does not evoke such imagery through appearance. Compared to many other diseases, cancer looks relatively benign. While some of the most feared diseases such as the plague are characterized by oozing sores and quick death, cancer can show little to no outward signs and can take years to overwhelm the patient. A cancer patient can look and feel healthy even when the cancer has metastasized to many areas of the body. However, the word cancer carries a degree of weight due to the seeming incurability of the disease. Cancer is enormously hardy and can sometimes withstand or escape current treatment techniques. Even in some of the cases in which it seems to have been completely eliminated, the cancer can still return due to small surviving patches that were missed during treatment. Furthermore, specific types of cancer can require specific therapy in order to be treated most effectively. However, it can be difficult to identify the type of cancer if it has metastasized throughout the body. Nevertheless, new ways of treating and diagnosing cancer are constantly being researched in order better aide patients. Some of the ones I am most interested in involve the utilization of the cancer cell's own biology against it, such as the use of circulating tumor cells in identifying the cancer as well as detecting its progress or relapse.