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Lung Cancer

Johnson DH, Blot WJ, Carbone DP, et al. Cancer of the lung: non-small cell lung cancer and small cell lung cancer. In: Abeloff MD, Armitage JO, Niederhuber JE, et al, eds. Abeloff’s Clinical Oncology . 4th ed. Philadelphia, PA: Elsevier Churchill Livingstone; 2008:chap 76.

National Comprehensive Cancer Network. NCCN Clinical Practice Guidelines in Oncology: Non-small cell lung cancer. Version 4.2014. Available at: Accessed August 31, 2014.

National Comprehensive Cancer Network. NCCN Clinical Practice Guidelines in Oncology: Small cell lung cancer. Version 1.2015. Available at: Accessed August 31, 2014.

National Cancer Institute: PDQ Non-Small Cell Lung Cancer Treatment. Bethesda, MD: National Cancer Institute. Date last modified 08/30/2013. Available at: Accessed August 31, 2014.

National Cancer Institute: PDQ Small Cell Lung Cancer Treatment. Bethesda, MD: National Cancer Institute. Date last modified 08/06/2014. Available at: Accessed August 31, 2014.

Nature’s Chemo for Lung Cancer

When it comes to cancer, it doesn’t get much scarier than lung cancer.

But now an herb has shown to not only stop the growth of cancerous cells but to also prevent any more from forming.1

The research comes out of Colorado, where researchers tested this herb on mice. Scientists injected 90 mice with a chemical that causes lung cancer. Two weeks later, they divided the mice up and fed them various amounts of the herb.

After four and a half months scientists checked the mice for inflammation, cancer cell growth, and death. The mice that consumed the herb fared significantly better. How significant? An amazing 93 percent fewer large lung tumors.

But that’s not all the herb did.

At 27 weeks, the cancer growth percentage remained but the mice that ate the herb also had fewer new blood vessels in their lung tumors and lower levels of cancer-promoting chemicals. The herb actually stopped lung cancer! And with no side effects. You don’t get those types of results with chemo and drugs.

What is this cancer-preventing herb?

Milk thistle.

Milk thistle has been used for over 2,000 years.2 You may have heard about it in connection with liver disease. It contains a flavonoid in its seeds called silymarin. Silymarin is the active compound that helps flush the liver of toxins. And now we’re finding that it may help prevent lung cancer.

Colorado researchers continued studying the effects of milk thistle on lung cancer cells in mice and published another study in Molecular Carcinogenesis.3 Yet again, the herb stopped the spread of lung cancer.

They found that milk thistle stops inflammation that speeds up cancer growth. And it does this by breaking a link in the chain of signals that leads to inflammatory enzymes that promote tissue damage. So by interrupting the cell signals it halts cancer growth.

Researchers are continuing to study milk thistle as a chemopreventive treatment.

But for now the studies show promising results. The herb is safe. So you have nothing to lose. Add some natural milk thistle into your daily supplement regimen to help ward off the deadliest cancers. It may just save your life.

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Treatment for Non-Small-Cell Lung Cancer

Non-Small-Cell Lung Cancer: Advances in Treatment

Reviewed by Jennifer Robinson, MD

A decade ago, chemotherapy was the only drug doctors could prescribe to someone with non-small-cell lung cancer (NSCLC). Not only does today’s chemotherapy work better than past versions, but there are also two new kinds of medications to treat this disease.

One group of drugs changes the way certain cancer cells grow or change in your body. This is called targeted therapy. Others boost your immune system to better fight cancer. This is called immunotherapy.

Non-Small-Cell Lung Cancer: Treatment by Stage

Read the Non-Small-Cell Lung Cancer: Treatment by Stage article > >


The word chemotherapy may make you think of unpleasant side effects like nausea and vomiting. Although some patients today have those symptoms, today’s drugs cause less of them than in years past.

‘Patients are tolerating chemotherapy better, partly because we have better supportive medication and better anti-nausea medication,’ says Kenneth Ng, MD, chief of medical oncology at Memorial Sloan Kettering Cancer Center Rockville Centre in New York.

Sometimes chemo does cause fatigue, depression, nerve problems, memory problems, or hair loss. That’s because of the way that the drugs work.

‘Chemotherapy actually kills the cancer cells, but it doesn’t only kill cancer cells, it kills normal cells, as well,’ says Shakun Malik, MD, at the National Cancer Institute’s Cancer Therapy Evaluation Program.

But there is chemo for NSCLC that doesn’t cause hair loss, and memory problems can be milder for some people. This applies to both the new drugs and updated versions of the old drugs. ‘It’s better compared to before,’ Ng says.

You’re likely to get more than one type of chemo drug to start with. That’s the new standard of care, and it packs a powerful punch. ‘Combining two to three different chemotherapy drugs works better than giving one chemotherapy drug,’ Ng says.

Targeted Therapy

A decade ago, doctors began to treat some NSCLC with these types of drugs. They target cells that have certain types of genetic information and kill these cancer cells without harming healthy ones around them.

Doctors will take a sample of your tumor through a biopsy or surgery. Then they’ll see if the cancer cells will respond to one of these drugs. About 15% to 20% of people with NSCLC can get targeted therapy. If you’ve never smoked, the odds are even better that it’ll work for you.

Targeted therapy in non-small cell lung cancer

Educational aims
  • To explain the clinically relevant molecular pathways in lung cancer.

  • To understand the basic principles of tests useful for targeted therapies.

  • To present a basis for current treatment approaches.


The ErbB family of receptors includes the four members: ErbB-1 (EGFR), ErbB-2 (HER-2) which is relevant especially in breast cancer treatment, ErbB-3 and ErbB-4. The extracellular component is responsible for ligand binding; whereas the intracellular component consists of the tyrosine kinase, which is responsible for signal transduction.

After a ligand ( e.g. epidermal growth factor, transforming growth factor-α) binds to the extracellular receptor, a dimerisation results in the activation of the receptor. The signal is passed along various downstream pathways. The most relevant seem to be the RAS/RAF/MEK/MAPK pathway, the PI3K/AKT pathway and the STAT3/STAT5 pathway [ 8]. These pathways lead to changes in gene transcription and alterations in the cell cycle, resulting in increased cell proliferation and angiogenesis, inhibition of apoptosis and changes in their capacity for migration, adhesion and invasion. As one would expect, changes in these parameters and properties have an impact on the behaviour of the cancer.

There are various mutations that have been discovered in the EGFR gene. Some of these mutations lead to an increased activity of the tyrosine kinase and subsequent sensitivity to targeted therapy whereas others increase cell resistance to treatment with tyrosine kinase inhibitors (TKIs).

VEGF receptor

After ligand binding, proliferation and migration of endothelial cells are activated, leading to increased blood supply of tumour cells and contributing to cancer cell survival [ 9].


]This oncogene is created by an inversion on chromosome 2p. In this mutation the N-terminal end of EML4 fuses with the intracellular domain of ALK. Breaking points in EML4 vary, whereas they seem to be constant in ALK, several fusion variants have been discovered. The fusion leads to a constitutive activation of a chimeric tyrosine kinase leading to increased cell proliferation [ 10, 11].

PCR and DNA sequencing

Mutations within a gene may lead to a change in the functioning of the resulting protein. An identified gene is amplified (multiplied) by PCR before it can be sequenced. With DNA sequencing specific variants (mutations) of genes may be identified. Depending on the gene and the mutation these may lead to reduced or even increased function.

Sequencing nucleotide by nucleotide has been made possible by new technologies. With increased capacities and capabilities, sequencing has become available outside research settings.

With gene sequencing, various changes in the DNA sequence can be identified; these include insertions, deletions or point mutations. The changes in sequence lead to changes in transcription to amino acids, thereby changing the form of a protein.

The advantage of gene sequencing is that specific mutations can be identified. Currently, many EGFR mutations have been identified. Many of those have shown to be associated with good responses to EGFR inhibiting drugs ( e.g. deletion in exon 19 or point mutation in exon 21 L858R), some however have shown to be associated with resistance ( e.g. exon 20 T790M).

Kirsten rat sarcoma viral oncogene homologue (KRAS); activating KRAS mutation have demonstrated to be associated with resistance to EGFR inhibitors. KRAS and EGFR mutations are considered to be mutually exclusive in lung cancer patients [ 12]. In practice, however, both tests are usually performed for control.


FISH is a technique that allows the visualisation of specific chromosome nucleic acid sequences (genes) within a cellular preparation. Specifically, FISH involves the precise annealing of a single-stranded, fluorophore-labelled DNA probe to complementary target sequences. After preparation, the DNA of the tissue on slides is denatured to single-strands and hybridised with DNA probes. Following hybridisation, the unbound probe is removed by a series of washes. The flurophore-labelled probes, now bound to the cellular DNA, can be visualised in fluorescence microscopy.

To detect EML4-ALK fusion genes, fluorescence in situ hybridisation can be used. When hybridised with the appropriate labelled FISH probes, the 2p23 ALK region in its native state will be seen as two immediately adjacent or fused (overlapping) orange/green (yellow) signals. However, if a chromosome rearrangement at the 2p23 ALK breakpoint region has occurred (inversion), one red and one green signal separated by at least two signal diameters will be seen.


With specific dyes, antibodies to proteins can be labelled and can then be visualised under the microscope.

Immunohistochemistry refers to the process of detecting proteins by binding labelled antibodies to these. Visualising an antibody-antigen interaction can be accomplished in a number of ways. In the most common instance, an antibody is conjugated to an enzyme, such as peroxidase, that can catalyse a colour-producing reaction.

IHC methods have been successfully used to evaluate the expression (over-expression) of the EGFR, which is of clinical relevance for EGFR antibody therapy.

EGFR inhibition

With the identification of receptors and pathways playing important roles in cancer, drugs have been developed to influence them. In the case of the EGFR, drugs have been developed to inhibit the transfer of the activating signal to intracellular pathways. These include agents which can block the receptor from outside the cell (antibodies) or drugs acting intracellularly (tyrosine kinase inhibitors (TKIs)).

VEGF inhibition

Antibodies specific for the VEGF Receptor can inhibit the downstream signalling leading to inhibition of angio- and vasculogenesis. The principle is analogous to the antibodies in EGFR inhibition. In addition, numerous small molecule tyrosine kinase inhibitors, including sunitib, sorafenib, vandetanib and others, have been explored.

EML4-ALK inhibition

The EML4-ALK fusion oncogene is responsible for cell proliferation. With the help of a targeted agent against the ALK intracellular tyrosine kinase, the function of the tyrosine kinase can be inhibited, thus blocking further downstream signalling. This is analogous to the functioning of the TKIs in the aforementioned EGFR example.


Although the principles of treatment seem very clear and effective, the clinical activity is limited by the development of resistance to these agents. For EGFR tyrosine kinase inhibitors (erlotinib, gefitinib) secondary mutations or bypass activation of alternate pathways, which may lead to a downstream signalling, lead to resistance. These mechanisms have been specifically described and represent a significant proportion of resistance development [ 13, 14]. With other targeted treatments, similar mechanisms have been described, e.g. for crizotinib and the EML4-ALK fusion oncogene [ 10].


Patients whose tumours harbour an activating EGFR mutation ( e.g. deletion in exon 19 or point mutation in exon 21 (L858R)) derive significant benefit from the treatment with small molecule TKIs. The first trial to demonstrate, that the first-line use of a TKI is superior to chemotherapy in these patients was a subgroup analysis of the IPASS study which enrolled >1,200 Asian patients and compared carboplatin/paclitaxel with gefitinib in patients with adenocarcinoma who were light or never smokers [ 15]. Since this report, several prospective randomised phase-III studies in patients with EGFR mutations confirmed these findings, demonstrating a progression free survival of about 1 year and survival rates of up to 28 months [ 1618]. Based on these results, EGFR TKIs ( e.g. erlotinib, gefitinib) today represent the preferred initial systemic treatment option for patients with an activating EGFR mutation.

EGFR antibodies

Cetuximab is an inhibitory anti-EGFR antibody which interacts with domain III of the soluble extracellular region of EGFR, sterically preventing the receptor from adopting the extended conformation required for dimerisation and ultimately intracellular pathway activation. In the phase-III FLEX trial, cetuximab improved response rate and overall survival when added to cisplatin/vinorelbine in patients with advanced NSCLC expressing EGFR by immunohistochemistry. Response rates were statistically significantly improved from 29 to 36%; however, the median survival was only improved from 10.1 to 11.3 months [ 19]. As the survival benefit was relatively small, approval was denied by health authorities. Reports have shown that a high IHC-EGFR score ( i.e. >200) can be used to identify about a third of patients in whom the addition of cetuximab to chemotherapy was associated with an increased benefit [ 19].

Anti-angiogenic treatment

Bevacizumab is a recombinant humanised monoclonal antibody that binds to and neutralises the biological activity of human VEGF [ 20]. This agent was the first targeted treatment showing a survival advantage in lung cancer [ 21]. Interestingly, the two randomised phase-III trials with bevacizumab did not show the same results. Although both trials demonstrated improved response rates and progression free survival with the addition of bevacizumab to a combination chemotherapy regimen with carboplatin/paclitaxel and cisplatin/gemcitabine, respectively, prolongation of overall survival (OS) has only been demonstrated for the carboplatin/paclitaxel/bevacizumab combination (OS: 12.3 versus 10.3 months; HR 0.80; p = 0.013) [ 21, 22]. The recently presented AVAPEARL study [ 23], which was investigating the role of maintenance pemetrexed and bevacizumab after an induction cisplatin/pemetrexed/bevacizumab phase, confirmed the activity of bevacizumab, also in combination with newer chemotherapy agents and demonstrated very promising preliminary survival times. As a result of these trials, bevacizumab combined with a platinum-based chemotherapy is a treatment option in patients with performance status 0-1 and non-squamous cell histology.

EML4-ALK gene rearrangement

The most common rearrangement of the ALK gene arises from an inversion in the short arm of chromosome 2 that creates a fusion between the 5′ portion of the EML4 gene and the 3′ portion of ALK. The incidence of the ALK fusion gene, which possesses potent oncogenic activity, is estimated to be 4% in NSCLC. Patients with ALK gene rearrangements have been reported to exhibit marked sensitivity to crizotinib, a small molecule inhibitor of ALK [ 24]. A recent retrospective review focusing on the impact of ALK rearrangement on OS in patients treated with crizotinib suggested improved survival compared with that of crizotinib-naïve controls [ 11]. An update of the pivotal phase-I trial with this agent reported on 119 mostly heavily pretreated patients. The median progression-free survival and the one- and two-year survival were 10 months, 70% and 55%, respectively, which by far exceeds anything previously observed [ 25]. Results from randomised crizotinib trials in pretreated or chemotherapy naïve are eagerly awaited.

Other mutations

In a recently published article the results of mutation testing in >1,000 patients with adenocarcimoma of the lung in North America were presented. The incidence of rarer mutations is 2% for BRAF and <2% for AKT1, HER2, MEK, NRAS and PIK3CA [ 26]. In addition, gene amplification of MET was also detected in <2%. The majority of these genetic alterations are considered to be oncogenic drivers and clinical investigations with corresponding experimental drugs are warranted and ongoing. KRAS mutations are present in approximately one out of five adenocarcinomas and drugs targeting several downstream signalling pathways of RAS such as PIK3ACA, ERK, MEK and mTOR or their combinations are currently being explored. While recent research has primarily focused on genetic subtypes of adenocarcinomas, potential targets for squamous cell carcinoma such as focal fibroblast growth factor receptor 1 (FGFR1) amplification (22%), DDR2 mutations (4%) and other mutations have been identified and results of early trials are eagerly awaited [ 27, 28].

View Abstract

Lung Cancer – Non-Small Cell – Statist...

ON THIS PAGE: You will find information about how many people are diagnosed with this type of cancer each year and some general survival information. Remember, survival rates depend on several factors. To see other pages, use the menu on the side of your screen.

NSCLC is the most common type of lung cancer. Statistics for lung cancer include both small cell and non-small cell lung cancer. This year, an estimated 221,200 adults (115,610 men and 105,590 women) in the United States will be diagnosed with lung cancer. Lung cancer is the second most common cancer and the leading cause of cancer death for men and women. It is estimated that 158,040 (86,380 men and 71,660 women) deaths from this disease will occur this year.

The one-year survival rate is the percentage of people who survive at least one year after the cancer is found. For all people with lung cancer, the one-year survival rate is 44%. The five-year survival rate is 17%. Survival rates depend on several factors, the subtype of lung cancer and the stage of disease.

Of the 15% of lung cancers detected at an early stage (stages I to III), the five-year survival rate is 54%. If the cancer has spread to a distant part of the body (stage IV), which is its latest stage, the five-year survival rate is 4%.

Lung cancer makes up 13% of all cancer diagnoses and 27% of all cancer deaths. For men, death rates have declined consistently for the past two decades, recently at a rate of about 2.9% each year. The death rates for women with lung cancer have declined 1.9% per year. For unclear reasons, black men have the highest incidence and the lowest survival rates of lung cancer.

These statistics should not be taken as a death sentence. It is important to remember that statistics do not apply to an individual person. No doctor can tell a person how long he or she will live with lung cancer. Some patients with advanced lung cancer can live many years after diagnosis. Sometimes, patients who are told that their lung cancer is curable do not live as long as those who are told that their lung cancer cannot be cured. The important thing to remember is that lung cancer is treatable at any stage, and these treatments have been proven to help people with lung cancer live longer with better quality of life.

Furthermore, these estimates are based on data from thousands of people with this type of cancer in the United States each year so the actual risk for a particular individual may be different. Because cancer survival statistics are often measured in multi-year intervals, they may not represent advances made in the treatment or diagnosis of this cancer. Learn more about understanding statistics.

Statistics adapted from the American Cancer Society’s publication, Cancer Facts & Figures 2015.

The next section in this guide is Medical Illustrations and it offers drawings of body parts often affected by this disease. Or, use the menu on the left side of your screen to choose another section to continue reading this guide.

Prognosis for Extensive-Stage Small Cell Lung Canc...

The Abramson Cancer Center of the University of Pennsylvania
Last Modified: May 8, 2013


My Mom was diagnosed with small cell lung cancer in January. They found some spots around her aorta, in her lymph nodes, and in the spine. She is just completing her 4th cycle of chemotherapy. The doctor said now we stop treatment and watch and wait. My question is, what are the chances of recurrence? We were told that there is a 50% mortality rate in 9 months, and 90% mortality in 2 years. Statistically speaking, does that mean it will take a turn for the worse in the next few months, and most likely she will die in the next 1-2 years?


Barbara Campling, MD, Medical Oncologist, responds:

From what you say, it sounds like your mother has ‘extensive-stage’ small cell lung cancer, which means that the cancer had spread outside of the chest at the time of diagnosis. Chemotherapy is generally quite effective at treating this in the short term. The goals of treatment for extensive-stage small cell lung cancer are to shrink the tumor, relieve symptoms, and improve survival, all of which chemotherapy can do. Unfortunately, once the cancer has spread outside of the chest, the cancer cannot be eradicated. She is now completing her planned chemotherapy, and you are now wondering what the future holds for her, and how long she has to live.

Because the cancer had already spread outside of the chest at diagnosis, it is almost inevitable that it will start to grow again in the future, regardless of how well she responded to chemotherapy. How long will it be before this happens? That depends, to a certain extent, on how well she has responded to the initial chemotherapy treatment. If she has had a ‘complete response’ to chemotherapy, meaning that the tumor can no longer be detected on any of her imaging scans, then it is likely to remain dormant for longer than if the response was more limited.

You have been told that the expected mortality is 50% at 9 months. This means that in a large group of patients with extensive-stage small cell lung cancer, half of the patients will be still be alive 9 months after diagnosis, whereas the other half will have died. However, these statistics do not tell us whether your mother will be alive 9 months after diagnosis. A Canadian study that included patients with small cell lung cancer (WJ Mackillop and CF Quirt. Measuring the accuracy of prognostic judgements in oncology. Journal of Clinical Epidemiology. 1997;50:21-29.) demonstrated that doctors are very good at predicting which patients would or would not be cured, but we are not very accurate when it comes to predicting how long individual incurable patients would survive. I often hear patients make statements like ‘my doctor gave me 10 months to live,’ and I try to avoid making these predictions myself.

If your mother has had a very good response to chemotherapy treatment, it could be many months before the cancer starts to cause problems again. Once she has recovered from the side effects of the chemotherapy, she could get back to feeling well for a period of time. When the cancer does recur, it may respond again to chemotherapy, and this could relieve her symptoms and improve her survival. Unfortunately, this type of cancer nearly always becomes resistant to further chemotherapy. Even when this occurs, there is usually something that can be done to alleviate symptoms and relieve pain.

Lung Cancer: Facts on Symptoms and Treatments

Lung Cancer

Lung cancer is a group of diseases characterized by abnormal growths (cancers) that started in the lungs.

Lung cancer is the leading cause of cancer deaths in women and men both in the United States and throughout the world. Lung cancer has surpassed breast cancer as the leading cause of cancer deaths in women for the past 25 years. In the United States, there are more deaths due to lung cancer than the number of deaths from colon and rectal, breast, and prostate cancer combined.

If lung cancer is found at an early stage, at least half of such patients will be alive and free of recurrent cancer five years later. Once lung cancer has metastasized, that is, spread to other distant organs, the five-year overall survival is less than 5%.

Cancer occurs when normal cells undergo a transformation that causes them to grow abnormally and multiply without control and potentially spread to other parts of the body. The cells form a mass or tumor that differs from the surrounding tissues from which it arises. Cancers are also called malignant tumors. Such tumors are dangerous because they take oxygen, nutrients, and space from healthy cells and because they invade and destroy or reduce the ability of normal tissues to function.

Most lung tumors are malignant. This means that they invade and destroy the healthy tissues around them and can spread throughout the body. The lung is a bad place for a cancer to arise because it contains a very rich network of both blood vessels and lymphatic channels through which cancer cells can spread.

  • The tumors can spread to nearby lymph nodes or through the bloodstream to other organs. This process of spread is called metastasis.
  • When lung cancer metastasizes, the tumor in the lung is called the primary tumor, and the tumors in other parts of the body are called secondary or metastatic tumors.

Some tumors in the lung are metastatic from cancers elsewhere in the body. The lungs are a common site for metastasis. If this is the case, the cancer is not considered to be lung cancer. For example, if prostate cancer spreads via the bloodstream to the lungs, it is metastatic prostate cancer (a secondary cancer) in the lung and is not called lung cancer.

Lung cancer comprises a group of different types of tumors. Lung cancers usually are divided into two main groups that account for about 95% of all cases.

  • The division into groups is based on the type of cells that make up the cancer.
  • The two main types of lung cancer are characterized by the cell size and cell type of the tumor when viewed under the microscope. They are called small cell lung cancer (SCLC) and non-small cell lung cancer (NSCLC). NSCLC includes several subtypes of tumors.
  • SCLCs are less common, but they grow more quickly and are more likely to metastasize than NSCLCs. Often, SCLCs have already spread to other parts of the body when the cancer is diagnosed.
  • About 5% of lung cancers are of rare cell types, including carcinoid tumor, lymphoma, and others.

The specific types of primary lung cancers are as follows:

  • Adenocarcinoma (an NSCLC) is the most common type of lung cancer, making up 30%-40% of all cases. A subtype of adenocarcinoma is called bronchoalveolar cell carcinoma, which creates a pneumonia-like appearance on chest X-rays.
  • Squamous cell carcinoma (an NSCLC) is the second most common type of lung cancer, making up about 30% of all cases.
  • Large cell cancer (another NSCLC) makes up 10% of all cases.
  • SCLC makes up 20% of all cases.
  • Carcinoid tumors account for 1% of all cases.

Medically Reviewed by a Doctor on 4/10/2015

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Li-Fraumeni Syndrome Awareness

Li-Fraumeni Syndrome is a rare inherited hereditary cancer disorder that greatly increases one’s risk of developing cancer during their lifetime. Sometimes, people with LFS develop multiple tumors or multiple cancers, often in childhood or as young adults. In 1969, Dr. Joseph Fraumeni noticed groups of families with a higher number of childhood cancers and adult early onset cancers. With the help of Dr. Frederick Li, they found increased numbers of sarcomas, leukemias, adrenal cancer, and breast cancer in these families than would normally be expected. This ‘familial cancer syndrome’ ultimately became known as Li-Fraumeni Syndrome. In 1990 researchers found that LFS is most often caused by a gene mutation in the p53 tumor suppressor gene. When this p53 gene is mutated, it doesn’t work properly to stop cell growth and tumors develop. LFS diagnosis can also result from CHK2 mutations.

Cancers associated with LFS include:

  • adrenocortical cancer
  • brain tumors
  • soft tissue sarcomas
  • osteosarcomas
  • genetic breast cancer
  • genetic leukemia
  • lymphoma
  • glioblastoma
  • rhabdomyosarcoma

We now know that numerous other cancers have been seen in LFS families, often occurring at younger ages than expected. Due to the complexity of this disorder, it is recommended that families with LFS undergo Li-Fraumeni genetic testing. Those with a family history of cancer, multiple cancers or childhood cancers, and patients with LFS should seek input from providers experienced in caring for patients with Li-Fraumeni Syndrome.

Learn More About Li-Fraumeni Syndrome