A National Cancer Institute-designated Comprehensive Cancer Center

Make an appointment: 800-826-HOPE
Pfeifer, Gerd, Ph.D. Bookmark and Share

Laboratory of Gerd Pfeifer, Ph.D.

The laboratory studies biological mechanisms involved in human cancer. Our goal is to determine the molecular mechanisms that are involved in formation of genetic changes (gene mutations) and epigenetic changes (DNA methylation and histone modifications) in the human genome.

The main research topic in the laboratory is epigenetic gene regulation in development and disease. Many genes are silenced by DNA methylation and by other repressive epigenetic mechanisms in human tumors. Methylated genes hold great promise not only as functionally relevant silenced genes involved in tumorigenesis but also as biomarkers for cancer diagnosis. We developed a sensitive method for analysis of DNA methylation on a genome-wide scale, the methylated-CpG island recovery assay (MIRA). MIRA is used to identify new commonly methylated genes in human tumors. Homeobox genes, known to be involved in developmental processes and tissue specification, are very frequently methylated in lung cancers and many other human tumors. We found that the mechanisms of cancer-specific DNA hypermethylation often involves targeting of specific DNA sequences, in particular homeobox genes, by the Polycomb repression complex and this pathway is already prevalent in inflamed tissue predisposing epithelial cells to malignant transformation. Using bioinformatics approaches, we are trying to uncover mechanisms dependent on DNA sequence features and DNA binding proteins that determine the specificity of DNA methylation changes in human cancers. We are also investigating changes in the epigenome in response to exposure of cells to environmental carcinogens including ultraviolet and ionizing radiation. Another project will attempt to establish a link between tissue aging and malignant transformation based on common changes in epigenetic regulation that underlie these processes. Very recently, previously unrecognized DNA bases, including 5-hydroxymethylcytosine, 5-formyl-, and 5-carboxy-cytosine, have been detected in certain mammalian tissues and cell types. We developed methodology to determine the sequence location of 5-hydroxymethylcytosine in mammalian DNA and found that it is targeted to promoters and gene bodies. In collaboration with Piroska Szabó’s lab, we showed that 5-methylcytosine is oxidized to 5-hydroxymethylcytosine selectively in the paternal genome of fertilized oocytes as part of a transgenerational epigenetic reprogramming mechanism. We showed that 5-hydroxymethylcytosine is strongly depleted in human cancers and could therefore be used as a biomarker for malignancy. Future work will focus on the distribution patterns and on the enzymology of 5-hydroxymethylcytosine formation and removal and its biological function in normal and malignant tissues.
 
For more information on Dr. Pfeifer, please click here.

5-hydroxymethylcytosine

 
5-methylcytosine (5mC) can be oxidized enzymatically by the TET family of proteins to form 5-hydroxymethylcytosine (5hmC). This process occurs genome-wide in the sperm-derived paternal genome shortly after fertilization (Iqbal et al., 2011). One popular model proposes that 5hmC is a transient intermediate in DNA demethylation. However, this issue is still unresolved and needs to be investigated further. We found that 5hmC is strongly depleted in many types of human cancer and could be developed as a biomarker for malignant disease (Jin et al., 2011). One of our hypotheses is that defects in 5mC oxidation are responsible for altered DNA methylation patterns in tumors (and possibly other diseases). We have established and used methodology for precise quantification and genome-wide mapping of 5mC and 5hmC. Our goal is to determine the levels and the genomic distribution of 5hmC in normal human tissues and in malignant tumors. We will focus on several tumor types, including solid tumors and hematological malignancies, which are often characterized by mutations in one of the TET genes, TET2, a methylcytosine oxidase. We work on basic mechanistic studies of TET and TET-associated proteins (for example, CXXC domain containing proteins), their aberrations in cancer and on their functional roles in control of CpG island methylation and cell differentiation.
 
Iqbal, K., Jin, S.-G., Pfeifer, G.P., and Szabó, P.E. (2011) Reprogramming of the paternal genome upon fertilization involves genome-wide oxidation of 5-methylcytosine  Proc. Natl. Acad. Sci. USA 108, 3642-3647.
 
Jin, S.-G., Jiang, Y., Qiu, R., Rauch, T.A., Wang, Y., Schackert, G., Krex, D., Lu, Q., and Pfeifer, G.P. (2011) 5-hydroxymethylcytosine is strongly depleted in human cancers but its levels do not correlate with IDH1 mutations, Cancer Res. 71, 7360-7365.
 
Hahn, M.A., Qiu, R., Wu, X., Li, A.X., Wang, J., Zhang, H., Jui, J., Jin, S.G., Jiang, Y., Pfeifer, G.P.,* and Lu, Q.* (2013) Dynamics of 5-hydroxymethylcytosine and chromatin marks in mammalian neurogenesis, Cell Reports 3, 291-300.
 
Pfeifer, G.P., Kadam, S., and Jin, S.-G. (2013) 5-hydroxymethylcytosine and its potential roles in development and cancer, Epigenetics Chromatin 6(1):10.
 

 
 

Aging and the unstable epigenome

Various hypotheses have been put forward to explain the aging process at both the cellular and organismal level. We investigate if and how alterations of the epigenome contribute to the aging process. We analyze several epigenetic marks including DNA CpG methylation and chromatin modifications in cells and tissues that undergo aging in vitro and in vivo. This work includes an in-depth analysis of the epigenome at the level of histone modifications, DNA methylation and gene expression during the time course of human in vivo aging and in premature aging syndromes. The data will allow an estimation of the extent and specificity of epigenetic changes that occur during aging.
 
 
 
 
 

DNA methylation and cancer

5-methylcytosine (5mC) is a modified DNA base that plays an important role in gene regulation. One major focus of the laboratory is to study DNA methylation patterns in normal and cancer tissues (Rauch et al., 2008; Hahn et al., 2008; Rauch et al., 2009; Wu et al., 2010; Kalari, Jung et al., 2013). Despite of thousands of reports in the literature describing hypermethylation of specific genes in almost every type of human cancer, the mechanisms and biological significance of CpG island hypermethylation in tumors have remained obscure. Our work focuses on studies that will investigate the molecular pathways leading to DNA methylation changes in tumors. Our general hypothesis is that CpG island hypermethylation is driven by specific mechanisms, either by exogenous or endogenous carcinogenic agents, by inflammation, by oncogene activation leading to epigenetic changes, and/or by targeted mechanisms involving the Polycomb repression complex.
 
Rauch, T.A., Zhong,, X., Wu,, X., Wang,, M., Kernstine,, K.H., Wang,, Z., Riggs,, A.D., and Pfeifer, G.P. (2008) High-resolution mapping of DNA hypermethylation and hypomethylation in lung cancer, Proc. Natl. Acad. Sci. USA 105, 252-257.
 
Hahn, M.A., Hahn, T., Lee, D.-H., Esworthy, R.S., Kim, B.-W., Riggs, A.D., Chu, F.F., and Pfeifer, G.P. (2008) Methylation of Polycomb target genes in intestinal cancer is mediated by inflammation, Cancer Res. 68, 10280-10289.
 
Rauch, T.A., Wu, X., Zhong, X., Riggs, A.D., and Pfeifer, G.P. (2009) A human B cell methylome at 100 bp resolution, Proc. Natl. Acad. Sci. USA 106, 671-678.
 
Wu, X., Rauch, T.A., Zhong, X., Bennett, W.P., Latif, F., Krex, D., and Pfeifer, G.P. (2010) CpG island hypermethylation in human astrocytomas, Cancer Res. 70, 2718-2727.
 
Kalari, S., Jung, M., Kernstine, K.H., Takahashi, T., and Pfeifer, G.P. (2013) The DNA methylation landscape of small cell lung cancer suggests a differentiation defect of neuroendocrine cells, Oncogene 32, 3559-3568.
 
 

Mammalian neurogenesis

In collaboration with Dr. Qiang Lu, City of Hope, we are investigating changes in DNA cytosine modification and histone modifications in the developing mouse brain. The focus is on how these epigenetic events orchestrate gene expression patterns during neurogenesis (Hahn et al., 2013).
 
Hahn, M.A., Qiu, R., Wu, X., Li, A.X., Wang, J., Zhang, H., Jui, J., Jin, S.G., Jiang, Y., Pfeifer, G.P.,* and Lu, Q.* (2013) Dynamics of 5-hydroxymethylcytosine and chromatin marks in mammalian neurogenesis, Cell Reports 3, 291-300.
 
 

RASSF1 and the Hippo pathway

The biological significance of aberrant methylation in cancer (“driver” versus “passenger” methylation) is unclear (Kalari et al., 2010). Earlier, we identified and characterized the gene RASSF1A (Dammann et al., 2000). This gene undergoes methylation silencing in almost every type of human tumor (~1000 publications in PubMed). In the face of increasing numbers of cancer genome sequencing studies identifying mutations in critical genes, researchers are loosing sight of the breadth and significance of cancer-associated promoter hypermethylation. The RASSF1A pathway is a prime example highlighting the importance of epigenetic silencing events in tumors in the absence of frequent mutation of a gene. We identified RASSF1A as an upstream regulator of the Hippo tumor suppressor pathway (Guo et al., 2007). Interestingly, the one component of the Hippo pathway most frequently affected in human cancer is RASSF1A, which is silenced by promoter methylation in over 90% of human liver tumors, for example. Therefore, this promoter methylation is of high significance and we continue to study the biochemical function of RASSF1A and its related family members in the mammalian Hippo pathway and other tumor-relevant processes.
 
Dammann, R., Li, C., Yoon, J.-H., Chin, P.L., Bates, S., and Pfeifer, G.P. (2000) Epigenetic inactivation of a RAS association domain family protein from the lung tumour suppressor locus 3p21.3, Nature Genet. 25, 315-319.
 
Guo, C., Tommasi, S., Liu, L., Yee, J.-K., Dammann, R., and Pfeifer, G.P. (2007) The RASSF1A tumor suppressor protein is a component of a mammalian complex analogous to the Drosophila Hippo/Salvador/Lats tumor suppressor network, Curr. Biol. 17, 700-705.
 
Kalari, S., and Pfeifer, G.P. (2010) Identification of driver and passenger DNA methylation in cancer by epigenomic analysis, Adv. Genet. 70, 277-308.
 
Pfeifer, G.P., Dammann, R., and Tommasi, S. (2010) RASSF proteins, Curr. Biol. 20, R344-R345.
 

 
 

UV damage and repair

Exposure to ultraviolet (UV) causes melanoma and non-melanoma skin cancer in humans and UV-specific mutation patterns can be found in tumor genomes (Pfeifer and Hainaut, 2011). This work is an ongoing project supporting studies on UV-induced DNA damage, repair and mutagenesis. Part of the current work is aimed at investigating mechanisms of epigenetic changes induced by different types of UV radiation (Lahtz et al., 2013). One main goal is to obtain high-resolution DNA damage maps of UV-induced cyclobutane pyrimidine dimers (CPDs), the main DNA lesion induced by UVB radiation. We are currently developing methodology for base-resolution mapping of CPDs thus allowing a precise assessment of genomic UV damage and its relationship to features of DNA sequence and chromatin. Another goal is to study epigenetic changes in melanoma and relate them to genetic changes in the same tumors.
 
Pfeifer, G.P. and Hainaut, P., (2011) Next generation sequencing: emerging lessons on the origins of human cancer, Curr. Opin. Oncol. 23, 62–68.
 
Lahtz, C., Kim, S.I., Bates, S.E., Li, A.X., Wu, X., and Pfeifer, G.P. (2013) UVB irradiation does not directly induce detectable changes of DNA methylation in human keratinocytes, F1000Research, v1, online Feb 13, 2013. http://f1000r.es/np.

 
 

Gerd Pfeifer, Ph.D. Lab Members

Maria Hahn
Staff Scientist
626-256-4673 ext. 65610
mhahn@coh.org
 
Seung-Gi Jin
Staff Scientist
626-256-4673 ext. 65926
sjin@coh.org
 
Marc Jung
Postdoctoral Fellow
626-256-4673 ext. 63792
mjung@coh.org
 
Sang-In Kim
Research Associate II
626-256-4673 ext. 62342
Skim@coh.org
 
Wenying Xiong
Senior Research Associate
626-256-4673 ext. 64638
wxiong@coh.org
 
Xiaoying Zhang
Postdoctoral Fellow
626-256-4673 ext. 2342
xiazhang@coh.org
 

Pfeifer, Gerd, Ph.D.

Laboratory of Gerd Pfeifer, Ph.D.

The laboratory studies biological mechanisms involved in human cancer. Our goal is to determine the molecular mechanisms that are involved in formation of genetic changes (gene mutations) and epigenetic changes (DNA methylation and histone modifications) in the human genome.

The main research topic in the laboratory is epigenetic gene regulation in development and disease. Many genes are silenced by DNA methylation and by other repressive epigenetic mechanisms in human tumors. Methylated genes hold great promise not only as functionally relevant silenced genes involved in tumorigenesis but also as biomarkers for cancer diagnosis. We developed a sensitive method for analysis of DNA methylation on a genome-wide scale, the methylated-CpG island recovery assay (MIRA). MIRA is used to identify new commonly methylated genes in human tumors. Homeobox genes, known to be involved in developmental processes and tissue specification, are very frequently methylated in lung cancers and many other human tumors. We found that the mechanisms of cancer-specific DNA hypermethylation often involves targeting of specific DNA sequences, in particular homeobox genes, by the Polycomb repression complex and this pathway is already prevalent in inflamed tissue predisposing epithelial cells to malignant transformation. Using bioinformatics approaches, we are trying to uncover mechanisms dependent on DNA sequence features and DNA binding proteins that determine the specificity of DNA methylation changes in human cancers. We are also investigating changes in the epigenome in response to exposure of cells to environmental carcinogens including ultraviolet and ionizing radiation. Another project will attempt to establish a link between tissue aging and malignant transformation based on common changes in epigenetic regulation that underlie these processes. Very recently, previously unrecognized DNA bases, including 5-hydroxymethylcytosine, 5-formyl-, and 5-carboxy-cytosine, have been detected in certain mammalian tissues and cell types. We developed methodology to determine the sequence location of 5-hydroxymethylcytosine in mammalian DNA and found that it is targeted to promoters and gene bodies. In collaboration with Piroska Szabó’s lab, we showed that 5-methylcytosine is oxidized to 5-hydroxymethylcytosine selectively in the paternal genome of fertilized oocytes as part of a transgenerational epigenetic reprogramming mechanism. We showed that 5-hydroxymethylcytosine is strongly depleted in human cancers and could therefore be used as a biomarker for malignancy. Future work will focus on the distribution patterns and on the enzymology of 5-hydroxymethylcytosine formation and removal and its biological function in normal and malignant tissues.
 
For more information on Dr. Pfeifer, please click here.

5-hydroxymethylcytosine

5-hydroxymethylcytosine

 
5-methylcytosine (5mC) can be oxidized enzymatically by the TET family of proteins to form 5-hydroxymethylcytosine (5hmC). This process occurs genome-wide in the sperm-derived paternal genome shortly after fertilization (Iqbal et al., 2011). One popular model proposes that 5hmC is a transient intermediate in DNA demethylation. However, this issue is still unresolved and needs to be investigated further. We found that 5hmC is strongly depleted in many types of human cancer and could be developed as a biomarker for malignant disease (Jin et al., 2011). One of our hypotheses is that defects in 5mC oxidation are responsible for altered DNA methylation patterns in tumors (and possibly other diseases). We have established and used methodology for precise quantification and genome-wide mapping of 5mC and 5hmC. Our goal is to determine the levels and the genomic distribution of 5hmC in normal human tissues and in malignant tumors. We will focus on several tumor types, including solid tumors and hematological malignancies, which are often characterized by mutations in one of the TET genes, TET2, a methylcytosine oxidase. We work on basic mechanistic studies of TET and TET-associated proteins (for example, CXXC domain containing proteins), their aberrations in cancer and on their functional roles in control of CpG island methylation and cell differentiation.
 
Iqbal, K., Jin, S.-G., Pfeifer, G.P., and Szabó, P.E. (2011) Reprogramming of the paternal genome upon fertilization involves genome-wide oxidation of 5-methylcytosine  Proc. Natl. Acad. Sci. USA 108, 3642-3647.
 
Jin, S.-G., Jiang, Y., Qiu, R., Rauch, T.A., Wang, Y., Schackert, G., Krex, D., Lu, Q., and Pfeifer, G.P. (2011) 5-hydroxymethylcytosine is strongly depleted in human cancers but its levels do not correlate with IDH1 mutations, Cancer Res. 71, 7360-7365.
 
Hahn, M.A., Qiu, R., Wu, X., Li, A.X., Wang, J., Zhang, H., Jui, J., Jin, S.G., Jiang, Y., Pfeifer, G.P.,* and Lu, Q.* (2013) Dynamics of 5-hydroxymethylcytosine and chromatin marks in mammalian neurogenesis, Cell Reports 3, 291-300.
 
Pfeifer, G.P., Kadam, S., and Jin, S.-G. (2013) 5-hydroxymethylcytosine and its potential roles in development and cancer, Epigenetics Chromatin 6(1):10.
 

 
 

Aging and the unstable epigenome

Aging and the unstable epigenome

Various hypotheses have been put forward to explain the aging process at both the cellular and organismal level. We investigate if and how alterations of the epigenome contribute to the aging process. We analyze several epigenetic marks including DNA CpG methylation and chromatin modifications in cells and tissues that undergo aging in vitro and in vivo. This work includes an in-depth analysis of the epigenome at the level of histone modifications, DNA methylation and gene expression during the time course of human in vivo aging and in premature aging syndromes. The data will allow an estimation of the extent and specificity of epigenetic changes that occur during aging.
 
 
 
 
 

DNA methylation and cancer

DNA methylation and cancer

5-methylcytosine (5mC) is a modified DNA base that plays an important role in gene regulation. One major focus of the laboratory is to study DNA methylation patterns in normal and cancer tissues (Rauch et al., 2008; Hahn et al., 2008; Rauch et al., 2009; Wu et al., 2010; Kalari, Jung et al., 2013). Despite of thousands of reports in the literature describing hypermethylation of specific genes in almost every type of human cancer, the mechanisms and biological significance of CpG island hypermethylation in tumors have remained obscure. Our work focuses on studies that will investigate the molecular pathways leading to DNA methylation changes in tumors. Our general hypothesis is that CpG island hypermethylation is driven by specific mechanisms, either by exogenous or endogenous carcinogenic agents, by inflammation, by oncogene activation leading to epigenetic changes, and/or by targeted mechanisms involving the Polycomb repression complex.
 
Rauch, T.A., Zhong,, X., Wu,, X., Wang,, M., Kernstine,, K.H., Wang,, Z., Riggs,, A.D., and Pfeifer, G.P. (2008) High-resolution mapping of DNA hypermethylation and hypomethylation in lung cancer, Proc. Natl. Acad. Sci. USA 105, 252-257.
 
Hahn, M.A., Hahn, T., Lee, D.-H., Esworthy, R.S., Kim, B.-W., Riggs, A.D., Chu, F.F., and Pfeifer, G.P. (2008) Methylation of Polycomb target genes in intestinal cancer is mediated by inflammation, Cancer Res. 68, 10280-10289.
 
Rauch, T.A., Wu, X., Zhong, X., Riggs, A.D., and Pfeifer, G.P. (2009) A human B cell methylome at 100 bp resolution, Proc. Natl. Acad. Sci. USA 106, 671-678.
 
Wu, X., Rauch, T.A., Zhong, X., Bennett, W.P., Latif, F., Krex, D., and Pfeifer, G.P. (2010) CpG island hypermethylation in human astrocytomas, Cancer Res. 70, 2718-2727.
 
Kalari, S., Jung, M., Kernstine, K.H., Takahashi, T., and Pfeifer, G.P. (2013) The DNA methylation landscape of small cell lung cancer suggests a differentiation defect of neuroendocrine cells, Oncogene 32, 3559-3568.
 
 

Mammalian neurogenesis

Mammalian neurogenesis

In collaboration with Dr. Qiang Lu, City of Hope, we are investigating changes in DNA cytosine modification and histone modifications in the developing mouse brain. The focus is on how these epigenetic events orchestrate gene expression patterns during neurogenesis (Hahn et al., 2013).
 
Hahn, M.A., Qiu, R., Wu, X., Li, A.X., Wang, J., Zhang, H., Jui, J., Jin, S.G., Jiang, Y., Pfeifer, G.P.,* and Lu, Q.* (2013) Dynamics of 5-hydroxymethylcytosine and chromatin marks in mammalian neurogenesis, Cell Reports 3, 291-300.
 
 

RASSF1 and the Hippo pathway

RASSF1 and the Hippo pathway

The biological significance of aberrant methylation in cancer (“driver” versus “passenger” methylation) is unclear (Kalari et al., 2010). Earlier, we identified and characterized the gene RASSF1A (Dammann et al., 2000). This gene undergoes methylation silencing in almost every type of human tumor (~1000 publications in PubMed). In the face of increasing numbers of cancer genome sequencing studies identifying mutations in critical genes, researchers are loosing sight of the breadth and significance of cancer-associated promoter hypermethylation. The RASSF1A pathway is a prime example highlighting the importance of epigenetic silencing events in tumors in the absence of frequent mutation of a gene. We identified RASSF1A as an upstream regulator of the Hippo tumor suppressor pathway (Guo et al., 2007). Interestingly, the one component of the Hippo pathway most frequently affected in human cancer is RASSF1A, which is silenced by promoter methylation in over 90% of human liver tumors, for example. Therefore, this promoter methylation is of high significance and we continue to study the biochemical function of RASSF1A and its related family members in the mammalian Hippo pathway and other tumor-relevant processes.
 
Dammann, R., Li, C., Yoon, J.-H., Chin, P.L., Bates, S., and Pfeifer, G.P. (2000) Epigenetic inactivation of a RAS association domain family protein from the lung tumour suppressor locus 3p21.3, Nature Genet. 25, 315-319.
 
Guo, C., Tommasi, S., Liu, L., Yee, J.-K., Dammann, R., and Pfeifer, G.P. (2007) The RASSF1A tumor suppressor protein is a component of a mammalian complex analogous to the Drosophila Hippo/Salvador/Lats tumor suppressor network, Curr. Biol. 17, 700-705.
 
Kalari, S., and Pfeifer, G.P. (2010) Identification of driver and passenger DNA methylation in cancer by epigenomic analysis, Adv. Genet. 70, 277-308.
 
Pfeifer, G.P., Dammann, R., and Tommasi, S. (2010) RASSF proteins, Curr. Biol. 20, R344-R345.
 

 
 

UV damage and repair

UV damage and repair

Exposure to ultraviolet (UV) causes melanoma and non-melanoma skin cancer in humans and UV-specific mutation patterns can be found in tumor genomes (Pfeifer and Hainaut, 2011). This work is an ongoing project supporting studies on UV-induced DNA damage, repair and mutagenesis. Part of the current work is aimed at investigating mechanisms of epigenetic changes induced by different types of UV radiation (Lahtz et al., 2013). One main goal is to obtain high-resolution DNA damage maps of UV-induced cyclobutane pyrimidine dimers (CPDs), the main DNA lesion induced by UVB radiation. We are currently developing methodology for base-resolution mapping of CPDs thus allowing a precise assessment of genomic UV damage and its relationship to features of DNA sequence and chromatin. Another goal is to study epigenetic changes in melanoma and relate them to genetic changes in the same tumors.
 
Pfeifer, G.P. and Hainaut, P., (2011) Next generation sequencing: emerging lessons on the origins of human cancer, Curr. Opin. Oncol. 23, 62–68.
 
Lahtz, C., Kim, S.I., Bates, S.E., Li, A.X., Wu, X., and Pfeifer, G.P. (2013) UVB irradiation does not directly induce detectable changes of DNA methylation in human keratinocytes, F1000Research, v1, online Feb 13, 2013. http://f1000r.es/np.

 
 

Lab Members

Gerd Pfeifer, Ph.D. Lab Members

Maria Hahn
Staff Scientist
626-256-4673 ext. 65610
mhahn@coh.org
 
Seung-Gi Jin
Staff Scientist
626-256-4673 ext. 65926
sjin@coh.org
 
Marc Jung
Postdoctoral Fellow
626-256-4673 ext. 63792
mjung@coh.org
 
Sang-In Kim
Research Associate II
626-256-4673 ext. 62342
Skim@coh.org
 
Wenying Xiong
Senior Research Associate
626-256-4673 ext. 64638
wxiong@coh.org
 
Xiaoying Zhang
Postdoctoral Fellow
626-256-4673 ext. 2342
xiazhang@coh.org
 
Our Scientists

Our research laboratories are led by the best and brightest minds in scientific research.
 

Beckman Research Institute of City of Hope is internationally  recognized for its innovative biomedical research.
City of Hope is one of only 41 Comprehensive Cancer Centers in the country, the highest designation awarded by the National Cancer Institute to institutions that lead the way in cancer research, treatment, prevention and professional education.
Learn more about City of Hope's institutional distinctions, breakthrough innovations and collaborations.
Develop new therapies, diagnostics and preventions in the fight against cancer and other life-threatening diseases.
 
Support Our Research
By giving to City of Hope, you support breakthrough discoveries in laboratory research that translate into lifesaving treatments for patients with cancer and other serious diseases.
 
 
 
 
NEWS & UPDATES
  • Cancer research has yielded scientific breakthroughs that offer patients more options, more hope for survival and a higher quality of life than ever before. The 14.5 million cancer patients living in the United States are living proof that cancer research saves lives. Now, in addition to the clinic, hospital an...
  • Advances in cancer treatment, built on discoveries made in the laboratory then brought to the bedside, have phenomenally changed the reality of living with a cancer diagnosis. More than any other time in history, people diagnosed with cancer are more likely to survive and to enjoy a high quality of life. Howeve...
  • While health care reform has led to an increase in the number of people signing up for health insurance, many people remain uninsured or are not taking full advantage of the health benefits they now have. Still others are finding that, although their premiums are affordable, they aren’t able to see the do...
  • Kidney cancer rates and thyroid cancer rates in adults have continued to rise year after year. Now a new study has found that incidence rates for these cancers are also increasing in children — particularly in African-American children. The study, published online this month in Pediatrics, examined childhood ca...
  • Thyroid cancer has become one of the fastest-growing cancers in the United States for both men and women. The chance of being diagnosed with the cancer has nearly doubled since 1990. This year an estimated 63,000 people will be diagnosed with thyroid cancer in the United States and nearly 1,900 people will die ...
  • Older teenagers and young adults traditionally face worse outcomes than younger children when diagnosed with brain cancer and other central nervous system tumors. A first-of-its-kind study shows why. A team of researchers from the departments of Population Sciences and Pathology at City of Hope recently examine...
  • Cancer treatment can take a toll on the mouth, even if a patient’s cancer has nothing to do with the head or throat, leading to a dry mouth, or a very sore mouth, and making it difficult to swallow or eat. Here’s some advice from the National Cancer Institute (NCI)  on how to ease cancer-related dis...
  • Radiation oncology is one of the three main specialties involved in the successful treatment of cancer, along with surgical oncology and medical oncology. Experts in this field, known as radiation oncologists, advise patients as to whether radiation therapy will be useful for their cancer – and how it can best ...
  • There’s more to cancer care than simply helping patients survive. There’s more to cancer treatment than simple survival. Constant pain should not be part of conquering cancer,  insists Betty Ferrell, Ph.D., R.N., director of nursing research and education at City of Hope. She wants patients and caregivers...
  • Even its name is daunting. Systemic mastocytosis is a fatal disease of the blood with no known cure. But a new study suggests a bone marrow transplant may be the answer for some patients. While rare, systemic mastocytosis is resistant to treatment with drugs and, when aggressive, can be fatal within four years ...
  • Could what you eat affect the health of your chromosomes? The short answer is, “Yes.” Researchers led by Dustin Schones, Ph.D., assistant professor in the Department of Cancer Biology, and Rama Natarajan, Ph.D., director of the Division of Molecular Diabetes Research and the National Business Products Industry ...
  • September is Prostate Cancer Awareness Month. Here, Bertram Yuh, M.D., assistant clinical professor in the Division of Urology and Urologic Oncology at City of Hope, explains the importance of understanding the risk factors for the disease and ways to reduce those risks, as well as overall prostate health. “Wha...
  • ** Learn more about prostate health, plus prostate cancer research and treatment, at City of Hope. ** Learn more about getting a second opinion at City of Hope by visiting us online or by calling 800-826-HOPE (4673). City of Hope staff will explain what’s required for a consult at City of Hope and help yo...
  • Childhood cancer survival rates have increased dramatically over the past 40 years. More than 80 percent of children with cancer now survive five years or more, which is a tremendous feat. Despite the survival rate increase, cancer continues to be the No. 1 disease killer and second-leading cause of death in ch...
  • Although a stem cell transplant can be a lifesaving procedure for people diagnosed with a blood cancer or blood disorder, the standard transplant may not be appropriate for all patients. This is because the conditioning regimen (the intensive chemotherapy and/or radiation treatments preceding the transplant) is...