Archive for the ‘Cancer Informatics’ Category

New CRISPR-non Cas9 proteins

Posted in Cancer and Current Therapeutics, CANCER BIOLOGY & Innovations in Cancer Therapy, Cancer Informatics, Cell Biology, Chemical Genetics, Clinical & Translational, Computational Biology/Systems and Bioinformatics, CRISPR/Cas9 & Gene Editing, Curation, Genetics & Pharmaceutical, Genome Biology, Genomics Pharmacy, tagged CRISPR-Cas9, CRISPR/Cpf1, genetic engineering on October 27, 2015| Leave a Comment »

New CRISPR-non Cas9 proteins

Larry H. Bernstein, MD, FCAP, Curator

LPBI

 

More CRISPR Proteins Discovered

Researchers identify three new proteins that may serve as alternatives to Cas9.

By Jef Akst | October 23, 2015

http://www.the-scientist.com/?articles.view/articleNo/44323/title/More-CRISPR-Proteins-Discovered/

http://www.the-scientist.com/images/Nutshell/Sept2015/Cas9.jpg

Crystal structure of a Cas9 in complex with an RNA guide and a stretch of target DNAWIKIMEDIA, H. NISHIMASU ET AL.

Scouring genomic databases for sequences with similarity to the components of the CRISPR/Cas9 system and the recently identified CRISPR/Cpf1 system, researchers from the National Center for Biotechnology Information (NCBI), MIT, and Rutgers University have discovered three novel CRISPR systems that could one day provide new gene-editing tools to supplement the currently used CRISPR/Cas9 system. The newly discovered CRISPR systems contain three new proteins, C2c1, C2c2, and C2c3 (named for “Class 2 candidate x”), one of which may cleave RNA.

“This work shows a path to discovery of novel CRISPR/Cas systems with diverse properties, which are demonstrated here in direct experiments,” coauthor Eugene Koonin of NCBI told GenomeWeb. “The most remarkable aspect of the story is how evolution has achieved a broad repertoire of biological activities, a feat we can take advantage of for new genome manipulation tools.” The group published its results yesterday (October 22) in Molecular Cell.

Using such sequence-based techniques, the researchers predict that there are even more CRISPR systems to be discovered, added study coauthor Konstantin Severinov of Rutgers. “There are multiple ways to modify the search algorithm. So more exciting and distinct CRISPR/Cas mechanisms should be expected soon.”

 

Using CRISPR as a High-Throughput Cancer Screening and Modeling Tool

http://www.genengnews.com/gen-news-highlights/using-crispr-as-a-high-throughput-cancer-screening-and-modeling-tool/81251901/

http://www.genengnews.com/Media/images/GENHighlight/thumb_97219_large9423718917.jpg

 

Using CRISPR/Cas9, scientists created a new high-throughput screening tool for studying the development and progression of liver cancer in mice. [Ernesto del Aguila III, NHGRI]

• A contingent of researchers from the UK, Germany, and Spain have recently developed a novel CRISPR/Cas9 system that they believe can be utilized as a multiplexed screening approach to study and model cancer development in mice. In the current study, the investigators directly mutated genes within adult mouse livers to elucidate their role in cancer development and progression—simultaneously uncovering the gene combinations that coordinate to cause liver cancer.
• “We reasoned that, by targeting mutations directly to adult liver cells using CRISPR/Cas9, we could better study and understand the biology of this important cancer,” explained co-author Mathias Friedrich, Ph.D., research scientist at the Wellcome Trust Sanger Institute. “Other approaches to engineer mutations in mice, such as stem cell manipulation, are limited by the laborious process, the long time frames and large numbers of animals needed. And, our method better mimics important aspects of human cancer biology than many “classic” mouse models: as in most human cancers, the mutations occur in the adult and only affect a few cells”.
• The findings from this study were published online recently in PNAS through an article entitled “CRISPR/Cas9 somatic multiplex-mutagenesis for high-throughput functional cancer genomics in mice.”
• This new approach is rapid, scalable, and extremely efficient, allowing the researchers to examine an array of genes or large regions of the genome concurrently. Moreover, this methodology affords scientists the ability to distinguish between cancer driver mutations and passenger mutations—those that occur as side-effects of cancer development.
• The research team developed a list of up to eighteen genes with known or unknown evidence for their importance in two forms of liver cancer. They then introduced the CRISPR/Cas9 molecules, targeting various combinations of these genes into mice, which subsequently developed liver or bile duct cancer within a few months.
• “Our approach enables us to simultaneously target multiple putative genes in individual cells,” noted co-author Roland Rad, Ph.D., project leader at the Technical University of Munich and the German Cancer Research Center Heidelberg. “We can now rapidly and efficiently screen which genes are cancer-causing and which ones are not. And, we can study how genes work together to cause cancers—a crucial piece of the puzzle we must solve to understand and tackle the disease.”
• The investigators were able to confirm that a set of DNA-binding proteins called ARID (AT-rich interactive domain), influence the organization of chromosomes and are important for liver cancer development. Furthermore, mutations in a second protein, TET2, were found to be causative in bile duct cancer: although TET2 has not been found to be mutated in human biliary cancers, the proteins that it interacts with have been, showing that the CRISPR/Cas9 method can identify human cancer genes that are not mutated, but whose function is disturbed by other events.
• “The new tools of targeting genes in combination and inducing insertions or deletions in chromosomes change our ability to identify new cancer-causing genes and to understand their role in cancer,” stated senior group leader and co-author Allan Bradley, Ph.D., director emeritus from the Sanger Institute. “Our results show that this approach is feasible and productive in liver cancer; we will now continue to study our new findings and try to extend the approach to other cancer types.”
• This CRISPR/Cas9 approach may also be favorable for an in-depth examination of genomic deserts —regions within the human genome that appear to be devoid of genes. Yet, recent data from the ENCODE Project suggests that deserts can be populated, if not by genes, then by DNA regulatory regions that influence the activity of genes.
• “Liver cancer has many DNA alterations in regions lacking genes: we don’t know which of these might be important for the disease,” said Dr. Rad. “However, we could show that it is now possible to delete such regions to systematically determine their role in liver cancer development.”

 

Additional CRISPR Enzymes Found Bioinformatically

http://www.genengnews.com/gen-news-highlights/additional-crispr-enzymes-found-bioinformatically/81251889/

• Three newly discovered enzymes—provisionally named C2c1, C2c3, and C2c3—promise to expand the CRISPR genome-editing toolbox beyond the well-known Cas9. They had been hiding inside NIH genomic databases, but they were eventually found out, thanks to the application of computational approaches developed by two groups of researchers. These researchers also initiated experimental work to explore the function of the bioinformatically identified enzymes.

One of the groups was led by Eugene Koonin, Ph.D., senior investigator at the National Center for Biotechnology Information (NCBI), National Library of Medicine (NLM), part of the NIH. The other group was led by Feng Zhang, Ph.D., of the MIT-Harvard Broad Institute.

According to the researchers, the three newly discovered enzymes are all naturally occurring, and all share some features with Cas9. In addition, these three enzymes have unique properties that could be exploited for novel genome-editing applications.

“This work shows a path to discovery of novel CRISPR-Cas systems with diverse properties, which are demonstrated here in direct experiments,” said Dr. Koonin. “The most remarkable aspect of the story is how evolution has achieved a broad repertoire of biological activities, a feat we can take advantage of for new genome-manipulation tools.”

This comment highlights how the researchers’ work, which appeared October 22 in the journal Molecular Cell, included information about potential evolutionary pathways. The researchers also emphasized that their work might lead to additional enzyme discoveries.

“There are multiple ways to modify the search algorithm, so more exciting and distinct CRISPR-Cas mechanisms should be expected soon,” said Konstantin Severinov, Ph.D., one of the researchers. He is affiliated with Rutgers and the Skolkovo Institute of Science and Technology. “These new mechanisms will undoubtedly attract the attention of basic and applied scientists alike.”

The Koonin and Zhang groups also recently collaborated on a project that resulted in the characterization of Cpf1, a class II CRISPR endonuclease, like Cas9. This work was described last month in an article, published in Cell, suggesting that the newly found enzyme’s distinct features pointed to unique genome-editing possibilities.

In his comments about this earlier work, Dr. Zhang made a point that presaged the current work: “Our goal is to develop tools that can accelerate research and eventually lead to new therapeutic applications. We see much more to come, even beyond Cpf1 and Cas9, with other enzymes that may be repurposed for further genome-editing advances.”

 

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Cancer Immunotherapy

Posted in Cancer and Current Therapeutics, CANCER BIOLOGY & Innovations in Cancer Therapy, Cancer Informatics, Clinical & Translational, Clinical Diagnostics, Computational Biology/Systems and Bioinformatics, Curation, Disease Biology, Genetics & Innovations in Treatment, Genetics & Pharmaceutical, Genome Biology, Human Immune System in Health and in Disease, Immuno-Oncology & Genomics, Immunology, tagged Cancer immunotherapy, immune tolerance, PDL1/PD1 pathway on October 27, 2015| Leave a Comment »

Cancer Immunotherapy

Curator: Larry H. Bernstein, MD, FCAP, Curator

 

 

Research explains limits of cancer immunotherapy drugs

Finding offers possibility to improve response to therapies

http://www.uofmhealth.org/news/archive/201510/research-explains-limits-cancer-immunotherapy-drugs

 

A new study from the University of Michigan Comprehensive Cancer Center reveals molecular changes within the tumor that are preventing the immunotherapy drugs from killing off the cancer.

Clinical trials with PD-L1 and PD-1 blockade suggested that tumors with a high number of inflammation-causing T cells were more responsive to the immunotherapy-based PD-L1 and PD-1 inhibitors. Tumors with low inflammation, or low T cells, were less responsive. But what controls T cells in the tumor microenvironment is poorly understood.

http://www.uofmhealth.org/sites/default/files/styles/large/public/Immunotherapy.png?itok=_oihl0jj

 

“We defined a molecular mechanism to explain why some tumors are inflamed and others are not – and consequently why some patients will be responsive to therapy and others not,” says senior author Weiping Zou, M.D., Ph.D.

“If we can reprogram this epigenetic mechanism, then the therapy might work for more patients,” says Zou, Charles B. de Nancrede Professor of Surgery, Immunology and Biology at the University of Michigan Medical School.

Zou’s group was the first to show PD-L1 expression, regulation and functional blockade in dendritic cells in the human cancer microenvironment.

In this study, published in Nature, researchers studied human and mouse models of ovarian cancer cells. They applied epigenetic drugs and found that the numbers of T cells in the tumor increased. They also saw that the epigenetic drugs synergized the anti-tumor effect of PD-L1 blockade in their models.

“We hope this could be developed into a clinical trial testing a combination of PD-L1 and PD-1 blockade with epigenetic therapy. We want to see if we can make the responders more responsive and turn the non-responders into responders,” Zou says.

Additional authors: From U-M: Dongjun Pen, Ilona Kryczek, Nisha Nagarsheth, Lili Zhao, Shuang Wei, Weimin Wang, Yuqing Sun, Ende Zhao, Linda Vatan, Wojciech Szeliga, Yali Dou, Kathleen Cho, Rebecca Liu; from Medical University in Lublin, Poland: Jan Kotarski, Rafal Tarkowski; from Henry Ford Health System: Sharon Hensley-Alford, Adnan Munkarah

Funding: National Institutes of Health grants CA190176, CA123088, CA099985, CA193136, CA152470, CA171306, 5P30 CA46592; Rivkin Ovarian Cancer Center, Ovarian Cancer Research Fund, Barbara and Don Leclair

Cancer immunotherapy research is evolving to more targeted strategies

Discoveries in immune pathway research have helped refine cancer immunotherapy strategies to become more targeted.^1,2

 

http://www.researchcancerimmunotherapy.com/overview/targeted-cancer-research

• CAR=chimeric antigen receptor;
• CSF-1R=colony-stimulating factor 1; CTLA4=cytotoxic
• T-lymphocyte antigen-4; IDO=indoleamine
• 2,3-dioxygenase; PD-1=programmed death-1; PD-L1=programmed death-ligand 1.

http://www.researchcancerimmunotherapy.com/images/overview/evolution-research/history-of-immunotherapy.png

 

 

Engaging the immune response: a unique approach to cancer management

Cancer immunotherapy strategies are designed to engage the immune system against tumors. This approach is unique in the oncology setting and introduces new considerations for cancer management.^1,2

• 

  TARGETED

  to tumor-specific antigens

• 

  RAPID

  activation of the immune response

• 

  ADAPTABLE

  as the tumor mutates and evolves

• 

  SELF-PROPAGATING

  with each revolution of the cancer immunity cycle

• 

  DURABLE

  response over time

 

CONSIDERATIONS FOR CANCER IMMUNOLOGY

Duration of response

The immune response has the ability to adapt with cancer as it evolves, and can become self-propagating once the cancer immunity cycle is initiated. Immune-directed strategies aim to leverage these attributes, with the goal of inducing a durable antitumor effect.^3-5

Pseudo-progression

T-cell infiltration to the tumor site may cause an apparent increase in tumor size or the appearance of new lesions. This inflammatory effect can be misinterpreted as progressive disease, as it can be difficult to differentiate the different cell types in radiographic imaging. New criteria have been developed to better capture immune-related response patterns, and may guide evaluation of immunotherapies in clinical trials, and potentially in clinical care.^1,2,6

REFERENCES

1. Chen DS, Mellman I. Oncology meets immunology: the cancer-immunity cycle. Immunity. 2013;39:1-10. PMID: 23890059
2. Mellman I, Coukos G, Dranoff G. Cancer immunotherapy comes of age. Nature. 2011;480:480-489. PMID: 22193102
3. Hanahan D, Weinberg RA. Hallmarks of cancer: the next generation. Cell. 2011;144:646-674. PMID: 21376230

Immune-related adverse events

While the goal of cancer immunotherapy research is to understand how to activate specific components of the immune response, the potential for off-target effects exists. Adverse event profiles may vary among different immune-directed strategies. As strategies grow more targeted, the recognition and management of immune-related adverse events will evolve.^1,3

EVADING IMMUNE DESTRUCTION

EVOLUTION OF RESEARCH

REFERENCES

1. Mellman I, Coukos G, Dranoff G. Cancer immunotherapy comes of age. Nature. 2011;480:480-489. PMID: 22193102
2. Hoos A, Eggermont AM, Janetzki S, et al. Improved endpoints for cancer immunotherapy trials. J Natl Cancer Inst. 2010;102:1388-1397.PMID: 20826737
3. Chen DS, Mellman I. Oncology meets immunology: the cancer-immunity cycle. Immunity. 2013;39:1-10. PMID: 23890059
4. Topalian SL, Weiner GJ, Pardoll DM. Cancer immunotherapy comes of age. J Clin Oncol. 2011;29:4828-4836. PMID: 22042955
5. Chen DS, Irving BA, Hodi FS. Molecular pathways: next-generation immunotherapy—inhibiting programmed death-ligand 1 and programmed death-1. Clin Cancer Res. 2012;18:6580-6587. PMID: 23087408
6. Wolchok JD, Hoos A, O’Day S, et al. Guidelines for the evaluation of immune therapy activity in solid tumors: immune-related response criteria. Clin Cancer Res. 2009;15:7412-7420. PMID: 19934295

 

Tumors can evade immune destruction

By disrupting the processes of the cancer immunity cycle throughout the body, tumors can avoid detection by the immune system and limit the extent of immune destruction.^1-3

Tumor microenvironment

Disrupting antigen detection

http://www.researchcancerimmunotherapy.com/images/overview/evading-immune-destruction/tumor-microenv.png

 

Lymph node

Inhibiting T-cell activation by dendritic cells

http://www.researchcancerimmunotherapy.com/images/overview/evading-immune-destruction/lymph-node.png

Blood vessel

Blocking T-cell infiltration into tumor

http://www.researchcancerimmunotherapy.com/images/overview/evading-immune-destruction/blood-vessel.png

Tumor microenvironment

Suppressing cytotoxic T-cell activity

http://www.researchcancerimmunotherapy.com/images/overview/evading-immune-destruction/suppressing-tcell.png

 

EVADING IMMUNE DESTRUCTION IS AN EMERGING HALLMARK OF CANCER

http://www.researchcancerimmunotherapy.com/images/overview/evading-immune-destruction/hallmark-cancer.png

The growing body of research into the mechanisms of immune evasion has led to its addition as an emerging hallmark of cancer, a distinct biological capability that enables tumors to grow and metastasize.³ 

 

MUTATION RATE BY CANCER TYPE⁴

http://www.researchcancerimmunotherapy.com/images/tumor-types/immunogenic-cancer/immunogenic-cancer.png

REFERENCES

1. Chen DS, Mellman I. Oncology meets immunology: the cancer-immunity cycle. Immunity. 2013;39:1-10. PMID: 23890059
2. Chen DS, Irving BA, Hodi FS. Molecular pathways: next-generation immunotherapy—inhibiting programmed death-ligand 1 and programmed death-1. Clin Cancer Res. 2012;18:6580-6587. PMID: 23087408
3. Rajasagi M, Shokla SA, Fritsch EF, et al. Systematic identification of personal tumor-specific neoantigens in chronic lymphocytic leukemia.Blood. 2014;124:453-462. PMID: 24891321
4. Lawrence MS, Stojanov P, Polak P, et al. Mutational heterogeneity in cancer and the search for new cancer-associated genes. Nature.2013;499:214-218. PMID: 23770567

 

Atezolizumab (Anti-PDL1) clinical trials   

Atezolizumab clinical trials are being conducted for the following types of cancers: lung, bladder, kidney, hematological malignancies, and breast cancer. Please check back for updates or search clinicaltrials.gov with the search term “Atezolizumab.”

 

EXPLORING A MORE PERSONALIZED APPROACH TO CANCER IMMUNOTHERAPY RESEARCH

With the evolution to more targeted strategies, research is focusing on identifying predictors of individual immune response through specific tumor characteristics and factors in the tumor microenvironment, such as

• The presence of tumor-infiltrating immune cells⁸
  • The ability of immune cells to infiltrate the tumor microenvironment may be a key criterion for a variety of immune-directed strategies, and could indicate which tumors are more likely to respond
• Gene expression patterns in tumors, particularly the genes involved in immune response⁹
• Cell surface protein expression
  • PD-L1 expression on tumor cells and tumor-infiltrating immune cells^10,11
  • MUC1 expression on tumor cells¹²     

REFERENCES

1. Chen DS, Mellman I. Oncology meets immunology: the cancer-immunity cycle. Immunity. 2013;39:1-10. PMID: 23890059
2. Mellman I, Coukos G, Dranoff G. Cancer immunotherapy comes of age. Nature. 2011;480:480-489. PMID: 22193102
3. Lesterhuis WJ, Haanen JB, Punt CJ. Cancer immunotherapy—revisited. Nat Rev Drug Discov. 2011;10:591-600. PMID: 21804596
4. National Institutes of Health ClinicalTrials.gov. https://clinicaltrials.gov/ct2/show/NCT01494688. Accessed March 4, 2015.
5. National Institutes of Health ClinicalTrials.gov. https://clinicaltrials.gov/ct2/show/NCT00739609. Accessed March 4, 2015.
6. Glienke W, Esser R, Priesner C, et al. Advantages and applications of CAR-expressing natural killer cells. Front Pharmacol. 2015;6:21. doi: 10.3389/fphar.2015.00021. PMID: 25729364
7. National Institutes of Health ClinicalTrials.gov. https://clinicaltrials.gov/ct2/show/NCT01303705. Accessed March 4, 2015.
8. Gajewski TF, Schreiber H, Fu YX. Innate and adaptive immune cells in the tumor microenvironment. Nat Immunol. 2013;14:1014-1022.PMID: 24048123
9. Ji RR, Chasalow SD, Wang L, et al. An immune-active tumor microenvironment favors clinical response to ipilimumab. Cancer Immunol Immunother. 2012;61:1019-1031. PMID: 22146893
10. Taube JM, Anders RA, Young GD, et al. Colocalization of inflammatory response with B7-h1 expression in human melanocytic lesions supports an adaptive resistance mechanism of immune escape. Sci Transl Med. 2012;4:127ra37. PMID: 22461641
11. Chen DS, Irving BA, Hodi FS. Molecular pathways: next-generation immunotherapy—inhibiting programmed death-ligand 1 and programmed death-1. Clin Cancer Res. 2012;18:6580-6587. PMID: 23087408
12. Stojnev S, Ristic-Petrovic A, Velickovic LJ, et al. Prognostic significance of mucin expression in urothelial bladder cancer. Int J Clin Exp Pathol. 2014;7:4945-4958. PMID: 25197366
13. Pardoll DM. The blockade of immune checkpoints in cancer immunotherapy. Nat Rev Cancer. 2012;12:252-264. PMID: 22437870
14. Taylor RC, Patel A, Panageas KS, Busam KJ, Brady MS. Tumor-infiltrating lymphocytes predict sentinel lymph node positivity in patients with cutaneous melanoma. J Clin Oncol. 2007;25:869-875. PMID: 17327608

 

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Metabolic Genomics and Pharmaceutics, Vol. 1 of BioMed Series D available on Amazon Kindle

Posted in Academic Publishing, Amino acids, Anaerobic Glycolysis, Biochemical pathways, Biological Networks, Biomarkers & Medical Diagnostics, Bone Disease and Musculoskeletal Disease, Ca2+ triggered activation, Cachexia, Calcium, Calcium Signaling, Calmodulin, Calmodulin Kinase and Contraction, Cancer and Current Therapeutics, CANCER BIOLOGY & Innovations in Cancer Therapy, Cancer Informatics, Cardiac & Vascular Repair Tools Subsegment, Cardiac and Cardiovascular Surgical Procedures, Cardiac muscle regeneration, Cardiomyopathy, Cardiovascular Pharmacogenomics, Cardiovascular Research, Cell Biology, Chemical Biology and its relations to Metabolic Disease, Clinical & Translational, Clinical Diagnostics, Clinical Genomics, Competition in regenerative stem cell science, Curation, Curation methodology, Cytoskeleton, Dehydrogenase, Diabetes Mellitus, Discovery process, Disease Biology, Endocrine Diseases, Enzyme Induction, Enzymes and isoenzymes, Explanatory, Fatty acids, Folate and B12, Frontiers in Cardiology and Cardiovascular Disorders, Gene Regulation, Gene Regulation and Evolution, Genome Biology, Genomic Endocrinology, Genomic Expression, Glycobiology: Biopharmaceutical Production, Health Economics and Outcomes Research, Hexokinase, Historical relevance, Inosine nucleotides, Interviews with Scientific Leaders, Iron deficiency, Kinase, Lipid metabolism, Lipids, Liver & Digestive Diseases Research, Loss of function gene, Metabolism, Metabolomics, Methylation, Mg++, Molecular Genetics & Pharmaceutical, mtDNA, Mutant Gene Expression, Myelodysplasia, Myelofibrosis, Myocardial Ischemia, Myocardial Metabolism, Na-K-ATPase, Neurodegenerative Diseases, Neurohumoral Transmission, Nitric Oxide in Health and Disease, Nutrigenomics, Nutrition, Nutrition and Phytochemistry, Nutrition Disorders, Nutritional Supplements: Atherogenesis, Open Access Journals, Oxidative phosphorylation, Pentose monophosphate shunt, Phosphatase, Phosphorylase, Phosphorylation, PKC, Plant extract, Proteins, Proteomics, Pyridine nucleotide transhydrogenase, Pyridine nucleotides, Pyruvate Kinase, Reproductive Andrology, Embryology, Genomic Endocrinology, Preimplantation Genetic Diagnosis and Reproductive Genomics, RNA Biology, S-nitrosylation, Signaling, Signaling & Cell Circuits, Skeletal muscle regeneration, Small Molecules in Development of Therapeutic Drugs, Theoretic convergence, Transcriptomics, Translational Science, Ubiquitinylation, Warburg effect, tagged ATP, Aviva Lev-Ari, Biology, Cell Biology, cell metabolic regulation, energy metabolism, gene, genetics, health, Heart disease, Larry H. Bernstein, Lipid metabolism, metabolic analysis, metabolic disorders, Metabolomics, Proteomics, research, science on August 15, 2015| Leave a Comment »

Metabolic Genomics and Pharmaceutics, Vol. 1 of BioMed Series D available on Amazon Kindle

Reporter: Stephen S Williams, PhD

Article ID #180: Metabolic Genomics and Pharmaceutics, Vol. 1 of BioMed Series D available on Amazon Kindle. Published on 8/15/2015

WordCloud Image Produced by Adam Tubman

Leaders in Pharmaceutical Business Intelligence would like to announce the First volume of their BioMedical E-Book Series D:

Metabolic Genomics & Pharmaceutics, Vol. I

which is now available on Amazon Kindle at

http://www.amazon.com/dp/B012BB0ZF0.

This e-Book is a comprehensive review of recent Original Research on  METABOLOMICS and related opportunities for Targeted Therapy written by Experts, Authors, Writers. This is the first volume of the Series D: e-Books on BioMedicine – Metabolomics, Immunology, Infectious Diseases.  It is written for comprehension at the third year medical student level, or as a reference for licensing board exams, but it is also written for the education of a first time baccalaureate degree reader in the biological sciences.  Hopefully, it can be read with great interest by the undergraduate student who is undecided in the choice of a career. The results of Original Research are gaining value added for the e-Reader by the Methodology of Curation. The e-Book’s articles have been published on the Open Access Online Scientific Journal, since April 2012.  All new articles on this subject, will continue to be incorporated, as published with periodical updates.

We invite e-Readers to write an Article Reviews on Amazon for this e-Book on Amazon.

All forthcoming BioMed e-Book Titles can be viewed at:

http://pharmaceuticalintelligence.com/biomed-e-books/

Leaders in Pharmaceutical Business Intelligence, launched in April 2012 an Open Access Online Scientific Journal is a scientific, medical and business multi expert authoring environment in several domains of  life sciences, pharmaceutical, healthcare & medicine industries. The venture operates as an online scientific intellectual exchange at their website http://pharmaceuticalintelligence.com and for curation and reporting on frontiers in biomedical, biological sciences, healthcare economics, pharmacology, pharmaceuticals & medicine. In addition the venture publishes a Medical E-book Series available on Amazon’s Kindle platform.

Analyzing and sharing the vast and rapidly expanding volume of scientific knowledge has never been so crucial to innovation in the medical field. WE are addressing need of overcoming this scientific information overload by:

• delivering curation and summary interpretations of latest findings and innovations on an open-access, Web 2.0 platform with future goals of providing primarily concept-driven search in the near future
• providing a social platform for scientists and clinicians to enter into discussion using social media
• compiling recent discoveries and issues in yearly-updated Medical E-book Series on Amazon’s mobile Kindle platform

This curation offers better organization and visibility to the critical information useful for the next innovations in academic, clinical, and industrial research by providing these hybrid networks.

Table of Contents for Metabolic Genomics & Pharmaceutics, Vol. I

Chapter 1: Metabolic Pathways

Chapter 2: Lipid Metabolism

Chapter 3: Cell Signaling

Chapter 4: Protein Synthesis and Degradation

Chapter 5: Sub-cellular Structure

Chapter 6: Proteomics

Chapter 7: Metabolomics

Chapter 8:  Impairments in Pathological States: Endocrine Disorders; Stress

                   Hypermetabolism and Cancer

Chapter 9: Genomic Expression in Health and Disease 

 

Summary 

Epilogue

 

 

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Cancer Biology and Genomics for Disease Diagnosis (Vol. I) Now Available for Amazon Kindle

Posted in Academic Publishing, Biochemical pathways, Cancer and Current Therapeutics, CANCER BIOLOGY & Innovations in Cancer Therapy, Cancer Informatics, Cancer Prevention: Research & Programs, Cancer Screening, Cancer Surgery of the Heart, Cell Biology, Clinical & Translational, Clinical Diagnostics, Clinical Genomics, Curation, Curation methodology, De novo synthesis, Discovery process, Disease Biology, Drug Delivery Platform Technology, Enzymes and isoenzymes, Evolutionary cognition, Experimental validation, Explanatory, FDA, FDA Regulatory Affairs, Health Economics and Outcomes Research, HealthCare IT, Historical relevance, International Global Work in Pharmaceutical, Interventional Oncology: Radiofrequency Ablation, Transarterial Chemoembolization, Microwave Ablation and Irreversible Electroporation (IRE), Interviews with Scientific Leaders, Metabolism, Metabolomics, Molecular Genetics & Pharmaceutical, Open Access Journals, Personal Health Applications: Tech Innovations serves HealhCare, Pharmaceutical R&D Informatics, Pharmaceutical R&D Investment, Proteomics, REAL TIME Conference Coverage Twitter's Hashtags and Handles per Presentation/session, Scientific & Biotech Conferences: Press Coverage, Signaling & Cell Circuits, Small Molecules in Development of Therapeutic Drugs, Technology Advance Assessment of, Theoretic convergence, tagged Amazon Kindle, anti-cancer drugs, Aviva Lev-Ari, breast cancer, breast cancer genes, Cancer - General, cancer patient management, cancer risk, Cell Biology, Chemotherapy, Clinical trial, Conditions and Diseases, Content Curation, Curation, Curation methodology, DNA, DNA Sequencing, Food and Drug Administration, genetics, genome, genomics, Harvard Medical School, health outcomes research, Larry H. Bernstein, Medical imaging, Metabolomics, National Institutes of Health, personalised medicine, Personalized medicine, Prostate cancer, research, RNA, science, Stem cell on August 14, 2015| Leave a Comment »

Cancer Biology and Genomics for Disease Diagnosis (Vol. I) Now Available for Amazon Kindle

Reporter: Stephen J Williams, PhD

Article ID #179: Cancer Biology and Genomics for Disease Diagnosis (Vol. I) Now Available for Amazon Kindle. Published on 8/14/2015

WordCloud Image Produced by Adam Tubman

Leaders in Pharmaceutical Business Intelligence would like to announce the First volume of their BioMedical E-Book Series C: e-Books on Cancer & Oncology

Volume One: Cancer Biology and Genomics for Disease Diagnosis

which is now available on Amazon Kindle at                          http://www.amazon.com/dp/B013RVYR2K.

This e-Book is a comprehensive review of recent Original Research on Cancer & Genomics including related opportunities for Targeted Therapy written by Experts, Authors, Writers. This ebook highlights some of the recent trends and discoveries in cancer research and cancer treatment, with particular attention how new technological and informatics advancements have ushered in paradigm shifts in how we think about, diagnose, and treat cancer. The results of Original Research are gaining value added for the e-Reader by the Methodology of Curation. The e-Book’s articles have been published on the Open Access Online Scientific Journal, since April 2012.  All new articles on this subject, will continue to be incorporated, as published with periodical updates.

We invite e-Readers to write an Article Reviews on Amazon for this e-Book on Amazon. All forthcoming BioMed e-Book Titles can be viewed at:

http://pharmaceuticalintelligence.com/biomed-e-books/

Leaders in Pharmaceutical Business Intelligence, launched in April 2012 an Open Access Online Scientific Journal is a scientific, medical and business multi expert authoring environment in several domains of  life sciences, pharmaceutical, healthcare & medicine industries. The venture operates as an online scientific intellectual exchange at their website http://pharmaceuticalintelligence.com and for curation and reporting on frontiers in biomedical, biological sciences, healthcare economics, pharmacology, pharmaceuticals & medicine. In addition the venture publishes a Medical E-book Series available on Amazon’s Kindle platform.

Analyzing and sharing the vast and rapidly expanding volume of scientific knowledge has never been so crucial to innovation in the medical field. WE are addressing need of overcoming this scientific information overload by:

• delivering curation and summary interpretations of latest findings and innovations
• on an open-access, Web 2.0 platform with future goals of providing primarily concept-driven search in the near future
• providing a social platform for scientists and clinicians to enter into discussion using social media
• compiling recent discoveries and issues in yearly-updated Medical E-book Series on Amazon’s mobile Kindle platform

This curation offers better organization and visibility to the critical information useful for the next innovations in academic, clinical, and industrial research by providing these hybrid networks.

Table of Contents for Cancer Biology and Genomics for Disease Diagnosis

Preface

Introduction  The evolution of cancer therapy and cancer research: How we got here?

Part I. Historical Perspective of Cancer Demographics, Etiology, and Progress in Research

Chapter 1:  The Occurrence of Cancer in World Populations

Chapter 2.  Rapid Scientific Advances Changes Our View on How Cancer Forms

Chapter 3:  A Genetic Basis and Genetic Complexity of Cancer Emerge

Chapter 4: How Epigenetic and Metabolic Factors Affect Tumor Growth

Chapter 5: Advances in Breast and Gastrointestinal Cancer Research Supports Hope for Cure

Part II. Advent of Translational Medicine, “omics”, and Personalized Medicine Ushers in New Paradigms in Cancer Treatment and Advances in Drug Development

Chapter 6:  Treatment Strategies

Chapter 7:  Personalized Medicine and Targeted Therapy

Part III.Translational Medicine, Genomics, and New Technologies Converge to Improve Early Detection

Chapter 8:  Diagnosis                                     

Chapter 9:  Detection

Chapter 10:  Biomarkers

Chapter 11:  Imaging In Cancer

Chapter 12: Nanotechnology Imparts New Advances in Cancer Treatment, Detection, &  Imaging                                 

Epilogue by Larry H. Bernstein, MD, FACP: Envisioning New Insights in Cancer Translational Biology

 

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Treatment for Chronic Leukemias [2.4.4B]

Posted in Academic Publishing, Automated Cell Processing, BioIT: BioInformatics, Cancer and Current Therapeutics, CANCER BIOLOGY & Innovations in Cancer Therapy, Cancer Informatics, Cancer Screening, Clinical & Translational, Clinical Genomics, Curation, Diagnostics and Lab Tests, Discovery process, Disease Biology, Experimental validation, Explanatory, Gene Regulation, Genetics & Innovations in Treatment, Genetics & Pharmaceutical, Genomic Expression, Hematopoiesis, Historical relevance, Human Immune System in Health and in Disease, Molecular Genetics & Pharmaceutical, Mutant Gene Expression, Myelodysplasia, Myelofibrosis, Neutrophilia, Pharmaceutical Analytics, Pharmaceutical Drug Discovery, Platelet count disorder, Regulated Clinical Trials: Design, Methods, Components and IRB related issues, Technology Advance Assessment of, tagged Chemotherapy, chronic lymphocytic leukemia, Chronic myelogenous leukemia, myelodyspalstic syndromes on August 11, 2015| Leave a Comment »

Treatment for Chronic Leukemias [2.4.4B]

Larry H. Bernstein, MD, FCAP, Author, Curator, Editor

http://pharmaceuticalintelligence.com/2015/8/11/larryhbern/Treatment-for-Chronic-Leukemias-[2.4.4B]

2.4.4B1 Treatment for CML

Chronic Myelogenous Leukemia Treatment (PDQ®)

http://www.cancer.gov/cancertopics/pdq/treatment/CML/Patient/page4

Treatment Option Overview

Key Points for This Section

There are different types of treatment for patients with chronic myelogenous leukemia.

Six types of standard treatment are used:

1. Targeted therapy
2. Chemotherapy
3. Biologic therapy
4. High-dose chemotherapy with stem cell transplant
5. Donor lymphocyte infusion (DLI)
6. Surgery

New types of treatment are being tested in clinical trials.

Patients may want to think about taking part in a clinical trial.

Patients can enter clinical trials before, during, or after starting their cancer treatment.

Follow-up tests may be needed.

There are different types of treatment for patients with chronic myelogenous leukemia.

Different types of treatment are available for patients with chronic myelogenous leukemia (CML). Some treatments are standard (the currently used treatment), and some are being tested in clinical trials. A treatment clinical trial is a research study meant to help improve current treatments or obtain information about new treatments for patients with cancer. When clinical trials show that a new treatment is better than the standard treatment, the new treatment may become the standard treatment. Patients may want to think about taking part in a clinical trial. Some clinical trials are open only to patients who have not started treatment.

Six types of standard treatment are used:

Targeted therapy

Targeted therapy is a type of treatment that uses drugs or other substances to identify and attack specific cancer cells without harming normal cells. Tyrosine kinase inhibitors are targeted therapy drugs used to treat chronic myelogenous leukemia.

Imatinib mesylate, nilotinib, dasatinib, and ponatinib are tyrosine kinase inhibitors that are used to treat CML.

See Drugs Approved for Chronic Myelogenous Leukemia for more information.

Chemotherapy

Chemotherapy is a cancer treatment that uses drugs to stop the growth of cancer cells, either by killing the cells or by stopping them from dividing. When chemotherapy is taken by mouth or injected into a vein or muscle, the drugs enter the bloodstream and can reach cancer cells throughout the body (systemic chemotherapy). When chemotherapy is placed directly into the cerebrospinal fluid, an organ, or a body cavity such as the abdomen, the drugs mainly affect cancer cells in those areas (regional chemotherapy). The way the chemotherapy is given depends on the type and stage of the cancer being treated.

See Drugs Approved for Chronic Myelogenous Leukemia for more information.

Biologic therapy

Biologic therapy is a treatment that uses the patient’s immune system to fight cancer. Substances made by the body or made in a laboratory are used to boost, direct, or restore the body’s natural defenses against cancer. This type of cancer treatment is also called biotherapy or immunotherapy.

See Drugs Approved for Chronic Myelogenous Leukemia for more information.

High-dose chemotherapy with stem cell transplant

High-dose chemotherapy with stem cell transplant is a method of giving high doses of chemotherapy and replacing blood-forming cells destroyed by the cancer treatment. Stem cells (immature blood cells) are removed from the blood or bone marrow of the patient or a donor and are frozen and stored. After the chemotherapy is completed, the stored stem cells are thawed and given back to the patient through an infusion. These reinfused stem cells grow into (and restore) the body’s blood cells.

See Drugs Approved for Chronic Myelogenous Leukemia for more information.

Donor lymphocyte infusion (DLI)

Donor lymphocyte infusion (DLI) is a cancer treatment that may be used after stem cell transplant.Lymphocytes (a type of white blood cell) from the stem cell transplant donor are removed from the donor’s blood and may be frozen for storage. The donor’s lymphocytes are thawed if they were frozen and then given to the patient through one or more infusions. The lymphocytes see the patient’s cancer cells as not belonging to the body and attack them.

Surgery

Splenectomy

What`s new in chronic myeloid leukemia research and treatment?

http://www.cancer.org/cancer/leukemia-chronicmyeloidcml/detailedguide/leukemia-chronic-myeloid-myelogenous-new-research

Combining the targeted drugs with other treatments

Imatinib and other drugs that target the BCR-ABL protein have proven to be very effective, but by themselves these drugs don’t help everyone. Studies are now in progress to see if combining these drugs with other treatments, such as chemotherapy, interferon, or cancer vaccines (see below) might be better than either one alone. One study showed that giving interferon with imatinib worked better than giving imatinib alone. The 2 drugs together had more side effects, though. It is also not clear if this combination is better than treatment with other tyrosine kinase inhibitors (TKIs), such as dasatinib and nilotinib. A study going on now is looking at combing interferon with nilotinib.

Other studies are looking at combining other drugs, such as cyclosporine or hydroxychloroquine, with a TKI.

New drugs for CML

Because researchers now know the main cause of CML (the BCR-ABL gene and its protein), they have been able to develop many new drugs that might work against it.

In some cases, CML cells develop a change in the BCR-ABL oncogene known as a T315I mutation, which makes them resistant to many of the current targeted therapies (imatinib, dasatinib, and nilotinib). Ponatinib is the only TKI that can work against T315I mutant cells. More drugs aimed at this mutation are now being tested.

Other drugs called farnesyl transferase inhibitors, such as lonafarnib and tipifarnib, seem to have some activity against CML and patients may respond when these drugs are combined with imatinib. These drugs are being studied further.

Other drugs being studied in CML include the histone deacetylase inhibitor panobinostat and the proteasome inhibitor bortezomib (Velcade).

Several vaccines are now being studied for use against CML.

2.4.4.B2 Chronic Lymphocytic Leukemia

Chronic Lymphocytic Leukemia Treatment (PDQ®)

General Information About Chronic Lymphocytic Leukemia

Key Points for This Section

1. Chronic lymphocytic leukemia is a type of cancer in which the bone marrow makes too many lymphocytes (a type of white blood cell).
2. Leukemia may affect red blood cells, white blood cells, and platelets.
3. Older age can affect the risk of developing chronic lymphocytic leukemia.
4. Signs and symptoms of chronic lymphocytic leukemia include swollen lymph nodes and tiredness.
5. Tests that examine the blood, bone marrow, and lymph nodes are used to detect (find) and diagnose chronic lymphocytic leukemia.
6. Certain factors affect treatment options and prognosis (chance of recovery).
7. Chronic lymphocytic leukemia is a type of cancer in which the bone marrow makes too many lymphocytes (a type of white blood cell).

Chronic lymphocytic leukemia (also called CLL) is a blood and bone marrow disease that usually gets worse slowly. CLL is one of the most common types of leukemia in adults. It often occurs during or after middle age; it rarely occurs in children.

http://www.cancer.gov/images/cdr/live/CDR755927-750.jpg

Anatomy of the bone; drawing shows spongy bone, red marrow, and yellow marrow. A cross section of the bone shows compact bone and blood vessels in the bone marrow. Also shown are red blood cells, white blood cells, platelets, and a blood stem cell.

Anatomy of the bone. The bone is made up of compact bone, spongy bone, and bone marrow. Compact bone makes up the outer layer of the bone. Spongy bone is found mostly at the ends of bones and contains red marrow. Bone marrow is found in the center of most bones and has many blood vessels. There are two types of bone marrow: red and yellow. Red marrow contains blood stem cells that can become red blood cells, white blood cells, or platelets. Yellow marrow is made mostly of fat.

Leukemia may affect red blood cells, white blood cells, and platelets.

Normally, the body makes blood stem cells (immature cells) that become mature blood cells over time. A blood stem cell may become a myeloid stem cell or a lymphoid stem cell.

A myeloid stem cell becomes one of three types of mature blood cells:

1. Red blood cells that carry oxygen and other substances to all tissues of the body.
2. White blood cells that fight infection and disease.
3. Platelets that form blood clots to stop bleeding.

A lymphoid stem cell becomes a lymphoblast cell and then one of three types of lymphocytes (white blood cells):

1. B lymphocytes that make antibodies to help fight infection.
2. T lymphocytes that help B lymphocytes make antibodies to fight infection.
3. Natural killer cells that attack cancer cells and viruses.

Blood cell development. CDR526538-750

http://www.cancer.gov/images/cdr/live/CDR526538-750.jpg

Blood cell development; drawing shows the steps a blood stem cell goes through to become a red blood cell, platelet, or white blood cell. A myeloid stem cell becomes a red blood cell, a platelet, or a myeloblast, which then becomes a granulocyte (the types of granulocytes are eosinophils, basophils, and neutrophils). A lymphoid stem cell becomes a lymphoblast and then becomes a B-lymphocyte, T-lymphocyte, or natural killer cell.

Blood cell development. A blood stem cell goes through several steps to become a red blood cell, platelet, or white blood cell.

In CLL, too many blood stem cells become abnormal lymphocytes and do not become healthy white blood cells. The abnormal lymphocytes may also be called leukemia cells. The lymphocytes are not able to fight infection very well. Also, as the number of lymphocytes increases in the blood and bone marrow, there is less room for healthy white blood cells, red blood cells, and platelets. This may cause infection, anemia, and easy bleeding.

This summary is about chronic lymphocytic leukemia. See the following PDQ summaries for more information about leukemia:

• Adult Acute Lymphoblastic Leukemia Treatment.
• Childhood Acute Lymphoblastic Leukemia Treatment.
• Adult Acute Myeloid Leukemia Treatment.
• Childhood Acute Myeloid Leukemia/Other Myeloid Malignancies Treatment.
• Chronic Myelogenous Leukemia Treatment.
• Hairy Cell Leukemia Treatment

Older age can affect the risk of developing chronic lymphocytic leukemia.

Anything that increases your risk of getting a disease is called a risk factor. Having a risk factor does not mean that you will get cancer; not having risk factors doesn’t mean that you will not get cancer. Talk with your doctor if you think you may be at risk. Risk factors for CLL include the following:

• Being middle-aged or older, male, or white.
• A family history of CLL or cancer of the lymph system.
• Having relatives who are Russian Jews or Eastern European Jews.

Signs and symptoms of chronic lymphocytic leukemia include swollen lymph nodes and tiredness.

Usually CLL does not cause any signs or symptoms and is found during a routine blood test. Signs and symptoms may be caused by CLL or by other conditions. Check with your doctor if you have any of the following:

• Painless swelling of the lymph nodes in the neck, underarm, stomach, or groin.
• Feeling very tired.
• Pain or fullness below the ribs.
• Fever and infection.
• Weight loss for no known reason.

Tests that examine the blood, bone marrow, and lymph nodes are used to detect (find) and diagnose chronic lymphocytic leukemia.

The following tests and procedures may be used:

Physical exam and history : An exam of the body to check general signs of health, including checking for signs of disease, such as lumps or anything else that seems unusual. A history of the patient’s health habits and past illnesses and treatments will also be taken.

Complete blood count (CBC) with differential : A procedure in which a sample of blood is drawn and checked for the following:

The number of red blood cells and platelets.

The number and type of white blood cells.

The amount of hemoglobin (the protein that carries oxygen) in the red blood cells.

The portion of the blood sample made up of red blood cells.

Results from the Phase 3 Resonate™ Trial

Significantly improved progression free survival (PFS) vs ofatumumab in patients with previously treated CLL

• Patients taking IMBRUVICA® had a 78% statistically significant reduction in the risk of disease progression or death compared with patients who received ofatumumab¹
• In patients with previously treated del 17p CLL, median PFS was not yet reached with IMBRUVICA® vs 5.8 months with ofatumumab (HR 0.25; 95% CI: 0.14, 0.45)¹

Significantly prolonged overall survival (OS) with IMBRUVICA® vs ofatumumab in patients with previously treated CLL

• In patients with previously treated CLL, those taking IMBRUVICA® had a 57% statistically significant reduction in the risk of death compared with those who received ofatumumab (HR 0.43; 95% CI: 0.24, 0.79; P<0.05)¹

Typical treatment of chronic lymphocytic leukemia

http://www.cancer.org/cancer/leukemia-chroniclymphocyticcll/detailedguide/leukemia-chronic-lymphocytic-treating-treatment-by-risk-group

Treatment options for chronic lymphocytic leukemia (CLL) vary greatly, depending on the person’s age, the disease risk group, and the reason for treating (for example, which symptoms it is causing). Many people live a long time with CLL, but in general it is very difficult to cure, and early treatment hasn’t been shown to help people live longer. Because of this and because treatment can cause side effects, doctors often advise waiting until the disease is progressing or bothersome symptoms appear, before starting treatment.

If treatment is needed, factors that should be taken into account include the patient’s age, general health, and prognostic factors such as the presence of chromosome 17 or chromosome 11 deletions or high levels of ZAP-70 and CD38.

Initial treatment

Patients who might not be able to tolerate the side effects of strong chemotherapy (chemo), are often treated with chlorambucil alone or with a monoclonal antibody targeting CD20 like rituximab (Rituxan) or obinutuzumab (Gazyva). Other options include rituximab alone or a corticosteroid like prednisione.

In stronger and healthier patients, there are many options for treatment. Commonly used treatments include:

• FCR: fludarabine (Fludara), cyclophosphamide (Cytoxan), and rituximab
• Bendamustine (sometimes with rituximab)
• FR: fludarabine and rituximab
• CVP: cyclophosphamide, vincristine, and prednisone (sometimes with rituximab)
• CHOP: cyclophosphamide, doxorubicin, vincristine (Oncovin), and prednisone
• Chlorambucil combined with prednisone, rituximab, obinutuzumab, or ofatumumab
• PCR: pentostatin (Nipent), cyclophosphamide, and rituximab
• Alemtuzumab (Campath)
• Fludarabine (alone)

Other drugs or combinations of drugs may also be also used.

If the only problem is an enlarged spleen or swollen lymph nodes in one region of the body, localized treatment with low-dose radiation therapy may be used. Splenectomy (surgery to remove the spleen) is another option if the enlarged spleen is causing symptoms.

Sometimes very high numbers of leukemia cells in the blood cause problems with normal circulation. This is calledleukostasis. Chemo may not lower the number of cells until a few days after the first dose, so before the chemo is given, some of the cells may be removed from the blood with a procedure called leukapheresis. This treatment lowers blood counts right away. The effect lasts only for a short time, but it may help until the chemo has a chance to work. Leukapheresis is also sometimes used before chemo if there are very high numbers of leukemia cells (even when they aren’t causing problems) to prevent tumor lysis syndrome (this was discussed in the chemotherapy section).

Some people who have very high-risk disease (based on prognostic factors) may be referred for possible stem cell transplant (SCT) early in treatment.

Second-line treatment of CLL

If the initial treatment is no longer working or the disease comes back, another type of treatment may help. If the initial response to the treatment lasted a long time (usually at least a few years), the same treatment can often be used again. If the initial response wasn’t long-lasting, using the same treatment again isn’t as likely to be helpful. The options will depend on what the first-line treatment was and how well it worked, as well as the person’s health.

Many of the drugs and combinations listed above may be options as second-line treatments. For many people who have already had fludarabine, alemtuzumab seems to be helpful as second-line treatment, but it carries an increased risk of infections. Other purine analog drugs, such as pentostatin or cladribine (2-CdA), may also be tried. Newer drugs such as ofatumumab, ibrutinib (Imbruvica), and idelalisib (Zydelig) may be other options.

If the leukemia responds, stem cell transplant may be an option for some patients.

Some people may have a good response to first-line treatment (such as fludarabine) but may still have some evidence of a small number of leukemia cells in the blood, bone marrow, or lymph nodes. This is known as minimal residual disease. CLL can’t be cured, so doctors aren’t sure if further treatment right away will be helpful. Some small studies have shown that alemtuzumab can sometimes help get rid of these remaining cells, but it’s not yet clear if this improves survival.

Treating complications of CLL

One of the most serious complications of CLL is a change (transformation) of the leukemia to a high-grade or aggressive type of non-Hodgkin lymphoma called diffuse large cell lymphoma. This happens in about 5% of CLL cases, and is known as Richter syndrome. Treatment is often the same as it would be for lymphoma (see our document called Non-Hodgkin Lymphoma for more information), and may include stem cell transplant, as these cases are often hard to treat.

Less often, CLL may transform to prolymphocytic leukemia. As with Richter syndrome, these cases can be hard to treat. Some studies have suggested that certain drugs such as cladribine (2-CdA) and alemtuzumab may be helpful.

In rare cases, patients with CLL may have their leukemia transform into acute lymphocytic leukemia (ALL). If this happens, treatment is likely to be similar to that used for patients with ALL (see our document called Leukemia: Acute Lymphocytic).

Acute myeloid leukemia (AML) is another rare complication in patients who have been treated for CLL. Drugs such as chlorambucil and cyclophosphamide can damage the DNA of blood-forming cells. These damaged cells may go on to become cancerous, leading to AML, which is very aggressive and often hard to treat (see our document calledLeukemia: Acute Myeloid).

CLL can cause problems with low blood counts and infections. Treatment of these problems were discussed in the section “Supportive care in chronic lymphocytic leukemia.”

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