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New immune system-boosting cancer drugs have in clinical trials saved the lives of many people with seemingly untreatable melanoma or lung cancer, but the drugs seem useless against colon cancer. One exception-a man with colon cancer whose metastatic tumors vanished for several years after he was treated in 2007-piqued researchers' interest. They suspected his recovery might have to do with the large number of mutations in his tumors. Now, a small clinical trial suggests that even cancer patients with types of tumors that were thought to be impervious to the new drugs could benefit if those malignancies have the right error-riddled DNA signature, a result that could help 3% to 4% of cancer patients.

Students begin by watching the online video clip and completing a worksheet. After that assignment, instructors can decide which of the two activities (or both!) to use in class. In Activity 1, students identify the locations on chromosomes of genes involved in cancer, using a set of 139 "Cancer Gene Cards" and associated posters. In Activity 2, students explore the genetic basis of cancer by examining cards that list genetic mutations found in the DNA of actual cancer patients. Small-group work spurs discussion about the genes that are mutated in different types of cancers and the cellular processes that the affected genes control. The Activity 1 and 2 Overview document provides short summaries of the two activities along with key concepts and learning objectives, background information, references and rubrics, and answers to students' questions. Both cancer discovery activities are appropriate for first-year high school biology (honors or regular), AP and IB Biology. Activity 2 is also appropriate for an undergraduate freshman biology class.

It is easy to miss something that is difficult to see and breast cancer tumour growth may go unnoticed. That is why knowing the early signs of breast cancer is key. For many, the first sign of breast cancer is a lump in the breast. However, breast cancer symptoms can vary widely - from lumps to some less obvious signs such as skin changes. Discovering a symptom of breast cancer does not necessarily mean it is cancer, however, it is absolutely vital to have a discussion with your doctor as soon as possible.

In the February 19, 2014 issue of Science Translational Medicine (Sci Transl Med. 2014 Feb 19;6(224):224ra24), Bettegowda and colleagues in the Sol Goldman Pancreatic Cancer Research center at Johns Hopkins report on an exciting approach to the detection of pancreatic cancer. Bettegowda and colleagues applied cutting edge DNA sequencing to blood samples from a large number of patients with a number of different cancers. They found that many cancers, even some small curable cancers, shed mutant DNA into the blood.

Cold Spring Harbour cancer site, sections include: Hallmarks of Cancer Causes and Prevention Diagnosis and Treatment Pathways to Cancer

In a paper this week in Science, Vogelstein and Cristian Tomasetti, who joined the biostatistics department at Hopkins in 2013, put forth a mathematical formula to explain the genesis of cancer. Here's how it works: Take the number of cells in an organ, identify what percentage of them are long-lived stem cells, and determine how many times the stem cells divide. With every division, there's a risk of a cancer-causing mutation in a daughter cell. Thus, Tomasetti and Vogelstein reasoned, the tissues that host the greatest number of stem cell divisions are those most vulnerable to cancer. When Tomasetti crunched the numbers and compared them with actual cancer statistics, he concluded that this theory explained two-thirds of all cancers.

The worst cancer cells don't sit still. Instead they metastasize-migrate from their original sites and establish new tumors in other parts of the body. Once a cancer spreads, it is harder to eliminate. A study by developmental biologists offers a fresh clue to how cancer cells acquire the ability to invade other tissues-a prerequisite for metastasis. It reveals that invasion requires cells to stop dividing. Therefore, the two processes- invasion and proliferation-are mutually exclusive. The finding could inform cancer therapies, which typically target rapidly proliferating cancer cells.

When a person dies from cancer, the culprit is usually not the original tumor but rather the cancerous cells that spread throughout the body and replicate in distant organs, a process called metastasis. Researchers have long known that metastasizing cancer cells slip their bonds and avoid immune detection by altering the sugars on their surfaces. They've even come up with a would-be drug to prevent such sugar alterations. But that compound interferes with needed sugars on normal cells, too, with lethal results in animals. Now, Dutch researchers report that they've packaged the drug in nanoparticles targeted exclusively to cancer cells, and they've shown that this combination prevents cancer cells from metastasizing in mice.  

Dr. Carolyn Henry, a veterinary oncologist at the University of Missouri veterinary school, says that, unlike lab mice, dogs get cancer naturally, just like humans. So their cancers are more likely to behave like human cancer when treated. "It's the same disease, it really doesn't matter what the species is," Henry says. "It's the same disease if it occurs naturally. And so, answers in one species should translate to answers in other species in many cases."

In our view, and that of organizations such as the American Society of Clinical Oncology, the World Cancer Research Fund International, and the American Cancer Society, obesity-related cancers will arguably be the most urgent issue in the cancer field in the next decade.

In this interrupted case study students analyze the complexities surrounding identification and confirmation of cancer clusters. The case challenges students to consider the evidence from two different perspectives; a local family physician representing the community, and a cluster investigation officer who has worked on several cancer cluster investigations. This case was inspired by the discussion about a possible cancer cluster in Clyde, Ohio, where around 20 cases of childhood cancer since 2001 fueled public concern, leading to an investigation by the Ohio department of health in 2006. This case was designed for introductory courses in biology and environmental sciences, taken by both science majors and non-science majors. In addition to introductory college classes, this case could also be used in advanced high school biology classes.

The American Joint Committee on Cancer (AJCC) and the International Union for Cancer Control (UICC) maintain the TNM classification system as a tool for doctors to stage different types of cancer based on certain standards. It's reviewed every 6 to 8 years to include advances in our understanding of cancer.

This flipped case study begins with a video in which a student reveals a family member's diagnosis with breast cancer and then considers the whirlwind of questions that arise in such a situation. Students are asked to relate to the main character and identify what questions they would have and what resources they could consult to seek information.  This sets the context for students to use websites and videos to investigate the nature of cancer, its causes, and progression. Students then learn about the major methods of cancer treatment (surgery, radiation therapy, and chemotherapy), how they work, and the limitations and side effects of each. The case concludes by addressing the claim of one of the characters that there is a conspiracy to hide a cure for cancer. The case would be implemented near the middle of a high school, non-majors, or introductory biology course after discussion of basic cell biology and the cell cycle.

In this case, developed for an introductory genetics class, students meet a woman whose family has a history of colon cancer. Students create a pedigree based on information from the case and discuss what it means to be genetically predisposed to cancer. Using bioinformatics tools from the NCBI database, students identify and examine the mutation in the woman's APC gene that results in genetic predisposition to colon cancer. Finally, they investigate the biological function of the APC protein to understand why this mutation contributes to the development of cancer and determine whether APC is a proto-oncogene, tumor suppressor gene, or genome stability gene.

Fact sheet: Metastatic cancer is cancer that has spread from the place where it first started to another place in the body. A tumor formed by metastatic cancer cells is called a metastatic tumor or a metastasis.

This biomarker, called the KRAS-variant, is linked to more cancers than any other known inherited genetic mutation. It is present in 1 out of every 4 people with cancer, and in more than half of people who develop multiple cancers. KRAS-variant carriers tend to get highly aggressive and recurrent breast, ovarian, head and neck, lung and pancreatic cancers.

In 1977, a University of Oxford statistician named Richard Peto pointed out a simple yet puzzling biological fact: We humans should have a lot more cancer than mice, but we don't. Dr. Peto's argument was beguilingly simple. Every time a cell divides, there's a small chance it will gain a mutation that speeds its growth. Cells that accumulate several of these mutations may become cancerous. The bigger an animal is, the more cells it has, and the longer an animal lives, the more times its cells divide. We humans undergo about 10,000 times as many cell divisions as mice - and thus should be far more likely to get cancer.

For researchers, understanding how cancer cells function differently from normal cells lays the foundation for developing treatments designed to rid the body of cancer cells without damaging normal cells.

A stride to understand the cancer and move towards its prevention, this time experts from around the world involved in searching the genome of cancer have analyzed the mutational signatures, the processes of mutation in the DNA of cells (which are always in the origin of cancer) and they follow a fixed pattern.

Penn Medicine Cancer resources for patients and healthcare professionals