Proliferative cells are labeled by means of immunohistochemical staining with the use of a cross-reactive polyclonal antiserum against Taenia solium GP50 antigens, shown in Panel A, and in situ hybridization with the use of a cestode 18S ribosomal DNA probe, shown in Panel B, with an absence of proliferative-cell labeling on in situ hybridization with a human Alu probe, which labels the surrounding human cells, shown in Panel C. Scale bars in Panels A, B, and C correspond to 50 μm. Panel D shows a phylogenetic analysis of the 391-bp H. nana CO1 nucleotide sequence in the patient (KT362138), together with all available H. nana sequences; the scale bar corresponds to a genetic distance of 0.02 substitutions per site. 
 
 Confirmation of H. nana Infection. Proliferative cells are labeled by means of immunohistochemical staining with the use of a cross-reactive polyclonal antiserum against Taenia solium GP50 antigens, shown in Panel A, and in situ hybridization with the use of a cestode 18S ribosomal DNA probe, shown in Panel B, with an absence of proliferative-cell labeling on in situ hybridization with a human Alu probe, which labels the surrounding human cells, shown in Panel C. Scale bars in Panels A, B, and C correspond to 50 μm. Panel D shows a phylogenetic analysis of the 391-bp H. nana CO1 nucleotide sequence in the patient (KT362138), together with all available H. nana sequences; the scale bar corresponds to a genetic distance of 0.02 substitutions per site. 
 
 Anteroposterior and axial CT scans in Panels A and B, respectively, show the presence of lung nodules. Panel C shows a biopsy specimen from a cervical lymph node containing firm, solid masses. Panel D shows small, atypical cells in an air-dried lymph-node touch preparation stained with Diff-Quik. Hematoxylin and eosin staining of a lymph-node histologic section shows invasive, irregular nests of proliferative cells (asterisk) in Panel E, monomorphic cellular features and multinucleated syncytia (arrowheads) on a higher-power field in Panel F, and cytologic atypia with occasional large, pleomorphic nuclei and multiple nucleoli (arrowheads) in Panel G. The transmission electron micrograph in Panel H shows ribosome-rich cytoplasm with scattered mitochondria (arrowhead) and a nucleus with a conspicuous central nucleolus (asterisk). Scale bars correspond to 1 cm in Panel C, 10 μm in Panels D through G, and 1 μm in Panel H. 
 
 Radiographic and Pathological Features of Malignant Hymenolepis nana. Anteroposterior and axial CT scans in Panels A and B, respectively, show the presence of lung nodules. Panel C shows a biopsy specimen from a cervical lymph node containing firm, solid masses. Panel D shows small, atypical cells in an air-dried lymph-node touch preparation stained with Diff-Quik. Hematoxylin and eosin staining of a lymph-node histologic section shows invasive, irregular nests of proliferative cells (asterisk) in Panel E, monomorphic cellular features and multinucleated syncytia (arrowheads) on a higher-power field in Panel F, and cytologic atypia with occasional large, pleomorphic nuclei and multiple nucleoli (arrowheads) in Panel G. The transmission electron micrograph in Panel H shows ribosome-rich cytoplasm with scattered mitochondria (arrowhead) and a nucleus with a conspicuous central nucleolus (asterisk). Scale bars correspond to 1 cm in Panel C, 10 μm in Panels D through G, and 1 μm in Panel H. 
 
 Neoplasms occur naturally in invertebrates but are not known to develop in tapeworms. We observed nests of monomorphic, undifferentiated cells in samples from lymph-node and lung biopsies in a man infected with the human immunodeficiency virus (HIV). The morphologic features and invasive behavior of the cells were characteristic of cancer, but their small size suggested a nonhuman origin. A polymerase-chain-reaction (PCR) assay targeting eukaryotes identified Hymenolepis nana DNA. Although the cells were unrecognizable as tapeworm tissue, immunohistochemical staining and probe hybridization labeled the cells in situ. Comparative deep sequencing identified H. nana structural genomic variants that are compatible with mutations described in cancer. Invasion of human tissue by abnormal, proliferating, genetically altered tapeworm cells is a novel disease mechanism that links infection and cancer. 
 
 QUICK TAKE VIDEO SUMMARY Parasite-Derived Cancer 
 
 H. nana, the dwarf tapeworm, is the most common human tapeworm; up to 75 million persons are estimated to be carriers, and the prevalence among children is as high as 25% in some areas.1 Infections are typically asymptomatic. H. nana is unique among tapeworms in that it can complete its life cycle in the small intestine, without the need for an intermediate host. Such autoinfection can persist for years and lead to a high parasite burden, particularly in immunocompromised hosts. Infections are generally limited to the gastrointestinal tract, where eggs released in the small bowel by adult tapeworms hatch. The embryos (oncospheres) invade the host intestinal villi, where they are transformed into larvae (cysticercoids) before breaking out and reattaching to the mucosal lining. Extraintestinal H. nana infections are rare. Here we describe a man with HIV infection in whom samples from lymph-node and lung biopsies revealed monomorphic, undifferentiated cells. The proliferative cells had overt features of a malignant process, but their small size suggested a nonhuman origin. Proliferation in the immunosuppressed host may have allowed somatic mutations to accumulate in the H. nana stem-cell population, ultimately leading to malignant transformation. 
 
 Case Report In January 2013, a 41-year-old man in Medellín, Colombia, presented with fatigue, fever, cough, and weight loss of several months’ duration. He had received a diagnosis of HIV infection in 2006 and was nonadherent to therapy; the most recent CD4 cell count was 28 per cubic millimeter, and the viral load was 70,000 copies per milliliter. Stool examination revealed H. nana eggs and Blastocystis hominis cysts. Computed tomographic imaging showed lung nodules ranging in size from 0.4 to 4.4 cm (Figure 1A and 1BFigure 1 Radiographic and Pathological Features of Malignant Hymenolepis nana.Anteroposterior and axial CT scans in Panels A and B, respectively, show the presence of lung nodules. Panel C shows a biopsy specimen from a cervical lymph node containing firm, solid masses. Panel D shows small, atypical cells in an air-dried lymph-node touch preparation stained with Diff-Quik. Hematoxylin and eosin staining of a lymph-node histologic section shows invasive, irregular nests of proliferative cells (asterisk) in Panel E, monomorphic cellular features and multinucleated syncytia (arrowheads) on a higher-power field in Panel F, and cytologic atypia with occasional large, pleomorphic nuclei and multiple nucleoli (arrowheads) in Panel G. The transmission electron micrograph in Panel H shows ribosome-rich cytoplasm with scattered mitochondria (arrowhead) and a nucleus with a conspicuous central nucleolus (asterisk). Scale bars correspond to 1 cm in Panel C, 10 μm in Panels D through G, and 1 μm in Panel H. ), as well as liver and adrenal nodules and cervical, mediastinal, and abdominal lymphadenopathy. Excisional biopsy of a cervical lymph node and core-needle biopsy of the lung were performed. The Centers for Disease Control and Prevention (CDC) was initially consulted by means of telediagnosis, with digital images sent to the Web-based DPDx diagnostic laboratory; paraffin-embedded tissues were subsequently submitted to the CDC. The patient received three doses of albendazole as empirical treatment, and antiretroviral medications were reinstated. The disease progressed, and a second cervical lymph-node biopsy was performed in April 2013, with fresh tissue sent to the CDC for evaluation. The lymph nodes were grossly abnormal, solid, nodular masses (Figure 1C), from which a touch preparation showed small, atypical cells with scant cytoplasm and prominent nucleoli (Figure 1D). Histologic examination showed effacement of normal architecture by irregular, crowded nests of small, atypical cells (Figure 1E). Syncytia containing atypical nuclei were present at the periphery of the nests (Figure 1F). The individual cells had scant cytoplasm and measured 5 to 6 μm in diameter (slightly smaller than a human red cell), with nuclei that were approximately 2 to 3 μm in diameter. Occasional cells were markedly enlarged, with pleomorphic nuclei containing multiple nucleoli (Figure 1G). Mitotic figures, angiolymphatic invasion, and necrosis were also observed. Similar cells were present in the sample from the core-needle biopsy of the lung (see Fig. S1 in the Supplementary Appendix, available with the full text of this article at NEJM.org). Transmission electron microscopy showed that the cytoplasm was ribosome-rich and contained scattered mitochondria (Figure 1H). Other than syncytia formation, no feature of differentiation, including formation of microvilli, was seen (Fig. S2 in the Supplementary Appendix). Immunohistochemical staining of these cells was negative for human cytokeratin and vimentin (often expressed in cancer cells), as well as for free-living amebas. This case posed a diagnostic conundrum. The proliferative cells had overt features of a malignant process — they invaded adjacent tissue, had a crowded and disordered growth pattern, and were monomorphic, with morphologic features that are characteristic of stem cells (a high nucleus-to-cytoplasm ratio) — but the small cell size (<10 μm in diameter) suggested infection with an unfamiliar, possibly unicellular, eukaryotic organism. Infection with a plasmodial slime mold (phylum, Amoebozoa; class, Myxogastria) was considered because of the prominent syncytia formation. Although many cestode tissues are syncytial — notably, their tegument — a tapeworm infection was initially considered less likely because of the primitive appearance of the atypical cells, the complete absence of architecture that was identifiable as tapeworm tissue, and the rarity of previously reported cases of invasive cestodiasis.2,3 During our laboratory investigations, the lesions of the lung, liver, and adrenal glands remained stable, but the lymph nodes (particularly in the neck) increased to a maximum of 5 cm in diameter, and over the course of 4 months, the patient’s clinical condition deteriorated. The patient was receiving tenofovir for the treatment of HIV infection and amphotericin B for histoplasmosis, and renal failure developed. The patient declined hemodialysis, and the delivery of palliative care was begun in May 2013. A molecular diagnosis was provided 72 hours before he died, and specific treatment was not attempted. A postmortem examination was not performed. Before he died, the patient provided written informed consent for studies to be performed and for publication of the results. 
 
 Methods Cell Culture We performed cell culture with the use of culture methods for free-living amebas and Myxogastria, including agar plates and tissue cultures of human lung fibroblasts. (The complete details of these and other methods are provided in the Supplementary Appendix.) PCR Assays DNA was extracted from the tissue specimens with the use of standard methods. For the initial molecular studies, we used Myxogastria and panfungal PCR and sequencing assays targeting the 18S ribosomal RNA (rRNA) gene and internal transcribed spacer regions (525 bp and approximately 650 bp, respectively).4,5 A subsequent cestode-specific PCR assay targeted a 206-bp fragment of the 18S rRNA gene,2 and a hymenolepidid-species–specific PCR assay targeted a 391-bp fragment of the gene encoding cytochrome c oxidase (CO1)6 (see the Methods section and Table S1 in the Supplementary Appendix). Immunohistochemical Studies and In Situ Hybridization Immunohistochemical studies were performed with the use of a polymer-based indirect immunoalkaline phosphatase detection system and fast-red chromogen. Polyclonal rabbit antiserum against Taenia solium GP50 antigens was used at a 1:250 dilution, which labels the T. solium cysticercus bladder epithelium, H. nana adult tegument, and H. diminuta cysticercoids (see the Methods section and Fig. S3 in the Supplementary Appendix). Digoxigenin-labeled DNA probes targeting a 206-bp fragment of the H. nana 18S rRNA gene and a 224-bp conserved area of human Alu sequences were prepared with the use of standard methods (see the Methods section and Table S1 in the Supplementary Appendix). Phylogenetic Analysis The product of the PCR assay of the H. nana CO1 gene described above was bidirectionally sequenced, and a repeat PCR assay and sequencing reaction were used to confirm the results (National Center for Biotechnology Information [NCBI] number, KT362138). Together with H. nana sequences available in GenBank, nucleotide data were aligned with the use of MUSCLE software, and a phylogenetic tree was estimated by means of the neighbor-joining method (MEGA software, version 5.2). Genomic Sequencing and Comparative Analysis DNA from the specimen from the patient’s second cervical lymph-node biopsy and DNA from cryopreserved H. nana reference-strain specimens were used to construct sequencing libraries and were sequenced with the use of the MiSeq system (Illumina). The contaminating human reads were filtered with the use of CLC Genomics Workbench, version 7.0.4 (CLC bio), by mapping to the reference human genome (Genome Reference Consortium human genome build 37). Next, the remaining sequencing reads (NCBI number, SRP061937) were mapped to the unannotated H. nana laboratory reference-strain genome (http://parasite.wormbase.org). The relatively incomplete genome coverage allowed for qualitative analysis of copy-number and structural variants.7 Insertional mutations were detected on the basis of nearby left and right sequencing reads with abrupt changes in sequence (split reads). Deletions, inversions, and point mutations were not formally examined. Genes were predicted by means of homology with the use of the annotated H. microstoma genome.8,9 The complete details are provided in the Methods section in the Supplementary Appendix. 
 
 Results Cell Culture Cell culture was attempted from the fresh tissue. However, no growth occurred after 4 weeks of incubation. Molecular Identification and Confirmation We performed Myxogastria and panfungal PCR assays in an attempt to target an unknown eukaryote, but these assays unexpectedly identified H. nana with 99% sequence identity. The presence of H. nana DNA in the specimen was confirmed by cestode- and hymenolepidid-species–specific PCR testing and sequencing. The molecular findings were surprising, since there was no recognizable tapeworm tissue architecture; thus, to confirm that the cells originated from a tapeworm, we performed immunohistochemical studies and in situ hybridization, which localized cestode antigen and nucleic acid markers (Figure 2A, 2B, and 2CFigure 2 Confirmation of H. nana Infection.Proliferative cells are labeled by means of immunohistochemical staining with the use of a cross-reactive polyclonal antiserum against Taenia solium GP50 antigens, shown in Panel A, and in situ hybridization with the use of a cestode 18S ribosomal DNA probe, shown in Panel B, with an absence of proliferative-cell labeling on in situ hybridization with a human Alu probe, which labels the surrounding human cells, shown in Panel C. Scale bars in Panels A, B, and C correspond to 50 μm. Panel D shows a phylogenetic analysis of the 391-bp H. nana CO1 nucleotide sequence in the patient (KT362138), together with all available H. nana sequences; the scale bar corresponds to a genetic distance of 0.02 substitutions per site. ). Phylogenetic and Mitochondrial DNA Analysis The CO1 sequence obtained from the patient was grouped within the clade of known H. nana sequences (Figure 2D). An unexpected feature of the patient-derived sequence was the presence of three single-nucleotide insertions within a span of 12 bp in a highly conserved domain (NCBI Conserved Domain Database, cd01663) (Fig. S4 in the Supplementary Appendix), which was compatible with a deleterious mutation. Comparative Genomic Analysis Deep sequencing of the specimen from the patient generated 10.2 million 150-bp, paired-end reads. Removal of contaminating human sequences resulted in 1.7 million remaining reads, of which 1.4 million mapped onto the H. nana reference genome, with 53% coverage, at an average coverage of 2.4 times per base (excluding zero-coverage regions). From the H. nana control specimen, 7.1 million reads were mapped, with 93% coverage, at an average coverage of 7.0 times per base. Amplifications were detected by evaluating genomic regions that had increased coverage in the biopsy specimen as compared with the control specimen. Both exons of the gene encoding lysosome-associated membrane protein 2 (LAMP2), predicted on the basis of homology with the annotated H. microstoma genome,8,9 were present in two of the top four overrepresented contigs and scaffolds (increased by a factor of 13 in one case and 25 in the other) (Figure 3A, 3B, and 3CFigure 3 Structural Genomic Alterations in H. nana.Panel A shows sequencing coverage in the biopsy specimen from the patient as compared with the H. nana control, along the length of H. nana scaffold 1. Panels B and C show complex copy-number alterations in conserved genomic regions containing both exons 1 and 2 of LAMP2. Arrowheads indicate split-read sequences that are present in the specimen from the patient but not in the control specimen, findings that are compatible with chromosomal breakpoints. Panel D shows insertion mutation–associated genes, with H. microstoma gene expression data comparing expression levels in larvae with those in various adult tissues; asterisks indicate expression levels in adult tissues that differ significantly from the level of expression in larval tissue.8 FPKM denotes fragments per kilobase of transcript per 1 million mapped reads. ). Multiple split-read sequences within these conserved regions were present in the specimen from the patient but not in the control specimen, findings that are compatible with complex genomic rearrangement and amplification. Similar alterations were seen in other regions without predicted homologous genes. Insertion-site analysis identified six insertional mutations (Table S2 in the Supplementary Appendix), of which five were associated with protein-coding genes predicted on the basis of homology with H. microstoma. The predicted genes were the transcriptional regulator PHF10/BAF45a (implicated in development), the gene encoding protein kinase ULK2 (implicated in autophagy), a putative C2H2 zinc-finger transcription factor, the gene encoding the actin-binding protein IPP, and a gene encoding a novel protein. Mammalian homologues of three of these genes — PHF10, ULK2, and IPP — have been studied in cancer (Table S3 in the Supplementary Appendix). Furthermore, four of the five H. microstoma genes are differentially expressed between larval and adult tissues (Figure 3D). 
 
 Discussion Although extraintestinal H. nana infections are rare, cysticercoids have been reported in whole-blood preparations from glucocorticoid-treated children,10 and a case of fatal invasive H. nana infection with atypical morphologic features was described in an HIV-positive man.2,3 H. nana is known to develop abnormal, enlarged, ballooned cysticercoids in immunosuppressed mice.11,12 Normal tapeworm development probably requires signals from immune responses of normal hosts,13 as is further suggested by in vitro cultures of hydatid tapeworms.14 Atypical proliferative infections with other tapeworm species have also been reported in humans2,15 and in other animals, including orangutans16 and cats.17 In contrast to the current case, all previously reported cases of invasive cestodiasis showed recognizable metazoan tissue architecture. Neoplastic cellular proliferations occur in invertebrates18,19 and have been described in free-living flatworms,20 but to our knowledge, such proliferations have not previously been documented in multicellular parasites, including tapeworms. In this case, proliferating cells with monomorphic morphologic features, cytologic atypia, and genetic alterations fulfill working definitions of neoplasia, and the presence of tissue invasion and metastasis is characteristic of a malignant process. Although the genomic variability of H. nana in human populations is unknown, the observed genetic alterations are compatible with mutations seen in mammalian cancer. These include deleterious mitochondrial gene mutations (which occur in up to 70% of colorectal carcinomas21), complex genomic rearrangements, and a predominance of intragenic as compared with intergenic insertional mutations.22 H. microstoma homologues of the insertion-associated genes appear to be functionally important and are differentially expressed in larval tissues. These data suggest that the insertional mutations we observed were nonrandom, were likely to have been selected for during cellular proliferation, and may promote cellular growth. In contrast to mammalian stem cells, pluripotent stem cells in flatworms (called neoblasts) are the only cells with proliferative capacity, and differentiated cells do not divide.23 Cestode stem cells were recently characterized in detail in the hydatid tapeworm Echinococcus multilocularis.24 The mitotic activity, small size, ribosome-rich cytoplasm, comparatively large nuclei, and prominent nucleoli of the cells from the patient described here are entirely consistent with tapeworm stem cells. We hypothesize that continued proliferation in the immunosuppressed host allowed somatic mutations to accumulate in the H. nana stem-cell population, ultimately leading to malignant transformation. Malignant transformation of H. nana may be misdiagnosed as human cancer, particularly in underdeveloped countries in which HIV and H. nana infections are widespread. Typical gastrointestinal H. nana infection is treated with praziquantel or nitazoxanide, and albendazole is the drug of choice for tissue-invasion stages of larval cestodes. However, the efficacy of albendazole against clonal proliferations of tapeworm stem cells as opposed to whole organisms is questionable. Preliminary data from in vitro studies using cultured cestode stem cells25 suggest that albendazole is ineffective (Brehm K: personal communication). Invasive H. nana cellular proliferations may therefore present a new challenge to therapy. Infectious agents, such as human papillomavirus and Schistosoma haematobium, contribute to human cancer worldwide. Transmissible clones of cancer cells circulate naturally within populations of Tasmanian devils and domestic dogs.26 In humans, cancer cells are infrequently transmitted through organ transplantation or from mother to fetus during pregnancy. Human disease caused by parasite-derived cancer cells is a novel finding. Multicellular parasites that live in host tissue generally possess cellular mechanisms for host tissue invasion and immune evasion; these mechanisms could potentially be co-opted during malignant transformation within the host. The host–parasite interaction that we report should stimulate deeper exploration of the relationships between infection and cancer. 
 
 Disclosure forms provided by the authors are available at NEJM.org. The views expressed in this article are those of the authors and do not necessarily represent the official position of the Centers for Disease Control and Prevention. We thank the physicians of the internal medicine and radiology services at Clínica Universitaria Bolivariana. ||||| 
 
 This common parasite, known as the hymenolepis nana or the dwarf tapeworm, may carry cancer cells that may take root in people with weakened immune systems. The malignant cells are pictured here. (Centers for Disease Control and Prevention) 
 
 Scientists from the Centers for Disease Control and Prevention have identified a puzzling and unsettling new cancer-like condition in a 41-year-old man, who is believed to have become ill through a common stomach bug. 
 
 The case — the first known transmission of cancer cells from a parasite to a human — involves an HIV patient from Colombia who developed multiple, large tumors in various parts of his body. Local doctors biopsied those tumors and found that the cells acted like cancer cells in their destructiveness but were strange in other respects. For one, they were about 10 times smaller than normal human cancer cells. The doctors contacted the CDC for help. 
 
 Atis Muehlenbachs, an agency pathologist in the special unit that investigates unexplained mystery illnesses and deaths, wasn't sure what to make of the cell samples when he and his team received them in 2013. The cells' growth pattern was cancer-like, they noticed, with overcrowding and a high rate of multiplication. But the cells also fused together, which is rare for human cells. 
 
 One early theory, Muehlenbachs said in an interview Wednesday, was that they could be a new type of infectious organism. But after performing dozens of tests, the team discovered the cells contained DNA snippets of a dwarf tapeworm, Hymenolepis nana. That analysis was verified by a researcher and tapeworm expert at the Natural History Museum in London. 
 
 "In the initial months, we wondered if this was a weird human cancer or some unusual, bizarre emerging protozoa-amoeba-like infection," he recalled. "Discovering these cells had tapeworm DNA was a big surprise — a really big surprise." 
 
 The CDC researchers, who published their findings Wednesday in the New England Journal of Medicine, now think the Colombian man may have ingested some microscopic tapeworm eggs, most likely in food contaminated by mouse droppings, insects or human feces. Because of the man's compromised immune system, the tapeworms multiplied rapidly inside his gastrointestinal tract and the cells invaded other parts of his body. It's unclear whether the cells in the tapeworm eggs exhibited cancer-like properties before they entered the man's body or whether some interaction between the parasite and his body then caused them to become cancerous. 
 
 [5 important things you need to know about tapeworm cancer in humans] 
 
 "This is the first time we've seen parasite-derived cancer cells spreading within an individual," Muehlenbachs said. "This is a very unusual, very unique illness." 
 
 The case study is worrisome for numerous reasons. 
 
 We know that many creatures, such as various sea animals, are susceptible to cancer, while others, like elephants, are almost immune to it. But until now, scientists had not believed that any human parasite could harbor cancer cells or transfer them to people. 
 
 We've also known that certain parasitic infections may put people at higher risk for specific cancers — such as flatworms for bile duct cancer or a river creature called schistosoma haematobium for bladder cancer, according to the American Cancer Society. But the reason was wholly different, namely a hyper-immune response that may weaken an individual. 
 
 
 
 A cross-section of a chest scan of the 41-year-old man shows large tumors. (Courtesy Pontifical Bolivarian University) 
 
 The presence of cancerous cells in tapeworms also raises numerous questions about where the mutant cells originated — from something in the environment? — and whether other organisms that live inside or on people that could transmit cancer cells. In recent years, many scientists have emphasized that the human body's ecosystem is only made up of 10 percent human cells but 90 percent microbial cells. 
 
 "We didn’t believe that cells from a human parasite could become malignant and then invade human tissue. … It's just very unusual that the parasite’s cells became cancerous inside a human and then invaded into human tissue," Bobbi Pritt, director of clinical parasitology at the Mayo Clinic, said in an interview. 
 
 Yet the idea of tapeworms also being vulnerable to cancer makes some sense, Pritt said, as "every living animal is made up of cells that divide and could become cancerous." 
 
 
 
 A dwarf tapeworm. (Photo courtesy Peter D. Olson/Natural History Museum in London) 
 
 Cancer is generally not considered to be a transmittable disease, although there have been very rare cases of humans passing on malignant cells to other humans through organ transplants or from mother to fetus during pregnancy. There are also some animal species -- such as Tasmanian devils and domestic dogs -- that are known to have transmissible cancer cells circulating within their populations. The CDC does not believe there is any risk of the tapeworm cancer cells being spread directly from one person to another. 
 
 It's unclear how common this type of tapeworm cancer illness is in humans, but experts like Pritt believe it's likely that there are more cases out there: "H. nana is a very common tapeworm infection in humans, and therefore I would expect there to be other cases like the one described…that were misdiagnosed or went undetected." 
 
 Matthew B. Laurens, an associate professor at the University of Maryland School of Medicine who specializes in infectious diseases, said the findings highlight our need to strengthen cancer diagnosis and data collection in developing countries. 
 
 “We could just be scratching the surface of something that could be very important,” Laurens said. 
 
 Peter D. Olson, a researcher at the Natural History Museum in London who helped the CDC interpret its results, said that the finding represents "an enormous advance in our knowledge and raises questions about the conditions under which cells may become cancerous." 
 
 
 
 Another CT scan, this one of the front of the man's chest, shows another view of the tumors. (Courtesy Pontifical Bolivarian University) 
 
 The Colombian man came to the attention of researchers at the Pontifical Bolivarian University in his home town of Medellin when he sought care because of fatigue, fever, a cough and weight loss. 
 
 The patient had been living with HIV for at least seven years and had not been adhering to therapy. A CT scan showed tumors ranging in size from 0.4 to 4.4 centimeters in his neck, lymph nodes, lungs and liver. Stool samples showed tapeworms inside his body. 
 
 Tapeworm infections are very common worldwide, especially in the developing world, with an estimated 75 million people infected with H. nana at any given time. Most do not show symptoms and clear the parasites quickly. But in people with compromised immune systems, tapeworms tend to thrive and can live in their hosts for years. 
 
 By the time the CDC researchers figured out what was going on, the man's condition had deteriorated and he was in hospice care. He died 72 hours later, without any opportunity for treatment. His official cause of death was HIV/AIDS, with cancer a contributor to his weakened state. 
 
 Muehlenbachs said further study was limited by the patient's death and the fact that researchers have been unable to grow tapeworm cancer cells in the lab. 
 
 Muehlenbachs said he's not sure the current arsenal of treatments could have helped given the nature of the man's tumors. He said traditional drugs to treat tapeworm infection -- which target the whole organism at the larval stage - might not have been effective against tapeworm cancer cells, and it's also unclear whether chemotherapy for normal human cancer cells could have helped shrink the tumors. 
 
 In fact, the pathologist is cautious about calling the Colombian's illness "cancer" because those cells were different from normal human cancer cells, even though they behaved similarly. Instead, Muehlenbachs referred to it as "an infection with parasite-derived cancer which causes a cancer-like illness." 
 
 He said the CDC investigation's findings are so unexpected that we lack the precise terminology to describe it: "Can you say a worm has cancer? That’s a philosophical question how you define this." 
 
 While he believes this type of case is rare, no one knows for sure. Muehlenbachs said further investigation is needed to determine whether it is limited to tapeworms or whether the situation is worse — that there's some "underlying biological phenomena" that might lead to transmissible cancer cells developing in other creatures that can pass them along to humans. 
 
 This post has been updated. 
 
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 For more health news, you can sign up for our weekly newsletter here. ||||| A man developed tumors that were actually cancer cells from a tapeworm living inside him. Above, an image of the tapeworm cancer cells from a biopsy of the man's tumor. 
 
 A Colombian man's lung tumors turned out to have an extremely unusual cause: The rapidly growing masses weren't actually made of human cells, but were from a tapeworm living inside him, according to a report of the case. 
 
 This is the first known report of a person becoming sick from cancer cells that developed in a parasite, the researchers said. 
 
 "We were amazed when we found this new type of disease — tapeworms growing inside a person, essentially getting cancer, that spreads to the person, causing tumors," said study researcher Dr. Atis Muehlenbachs, a staff pathologist at the Centers for Disease Control and Prevention's Infectious Diseases Pathology Branch (IDPB). 
 
 The man had HIV, which weakens the immune system and likely played a role in allowing the development of the parasite cancer, the researchers said. Although the man's case is probably a rare one, the researchers noted that both tapeworms and HIV affect millions of people worldwide, "so there may be more cases that are unrecognized," Muehlenbachs said. [10 Deadly Diseases That Hopped Across Species] 
 
 The 41-year-old man first went to doctors in Colombia after experiencing a fever, cough and weight loss for several months. The man had been diagnosed with HIV more than 10 years earlier, but was not taking his medications. 
 
 A CT scan showed tumors in his lung and lymph nodes, but biopsies of these tumors revealed bizarre cells, leading Colombian doctors to contact the CDC for assistance in diagnosing the man. 
 
 The cells, when examined under a microscope, acted like cancer cells — they multiplied quickly and crowded together. But the cells didn't appear to be human, they were 10 times smaller than human cancer cells. 
 
 After a number of tests, the researchers found DNA from a type of tapeworm called H. nana in the man's tumor. This result was surprising, the researchers said, because the cells did not look at all like tissue from a tapeworm. But further tests confirmed that the cells were indeed from H. nana. 
 
 The researchers hypothesized that, because the man had HIV, the tapeworm kept growing in the body, unchecked by the immune system. Eventually, mutations developed in the tapeworm's cells that turned the cells cancerous. 
 
 The patient died just 72 hours after researchers determined that the tumors were caused by H. nana. 
 
 H. nana is the most common tapeworm in humans, infecting up to 75 million people worldwide at any given time. 
 
 If researchers do find other cases like the Colombian man's, it's not clear what type of treatment would help. Drugs that treat tapeworm infections may not be able to treat cancer cells from tapeworms, the researchers said. But it's possible that human cancer treatment might also work against parasite cancer cells. 
 
 The study is published in today's (Nov. 5) issue of the New England Journal of Medicine. 
 
 Follow Rachael Rettner @RachaelRettner. Follow Live Science @livescience, Facebook & Google+. Original article on Live Science. ||||| A Man In Colombia Got Cancer And It Came From A Tapeworm 
 
 Enlarge this image toggle caption Courtesy Peter Olson, Natural History Museum, London Courtesy Peter Olson, Natural History Museum, London 
 
 In January 2013, a 41-year-old man came to a hospital in Medellin, Colombia. He was in bad shape. He'd lost weight, had a fever, a tapeworm infestation and also had trouble breathing. He had HIV but had stopped taking his medications a few months before. 
 
 It turned out to be a very strange medical case, published Wednesday in the New England Journal of Medicine. 
 
 When doctors tried to find out why his breathing was labored, they came across what looked like tumors on his lungs, but the samples looked really weird. 
 
 "It looked like cancer, but the tumors were composed of cells that were not human," says Dr. Atis Muehlenbachs, a pathologist at the Centers for Disease Control and Prevention and the lead author on the report. 
 
 Doctors in Colombia had sent Muehlenbachs samples from the patient's lesions, which he says, looked like sheets and clumps of cells that were much smaller than human cells. At first, he thought it was a slime mold. 
 
 Eventually — and, Muehlenbachs says, pretty much by accident — DNA tests confirmed the tumors were made of tapeworm cells. They had formed blobs on the man's lungs, liver and adrenal glands. Lymph nodes had swollen in the patient's neck to the size of golf balls, making it hard for him to move his head. 
 
 "We knew invertebrates can grow tumors, but the fact that one can invade and disseminate in a human and make them sick just really, really defied belief," says Muehlenbachs. 
 
 This video explains how the tapeworm is thought to have spread its cancer to a human. New England Journal of Medicine YouTube 
 
 Peter Olson, a biologist at the Natural History Museum in London who took part in the research, says the dwarf tapeworm lives in the guts of some 75 million people. It's most common in areas with poor sanitation. 
 
 "But it doesn't typically cause problems," he says. 
 
 Of the about 9,000 described tapeworm species, the dwarf tapeworm is the only one that's known to be able to live and reproduce entirely in the human gut, producing new generations in the host's stool. 
 
 "We think that was one of the things that allowed this to happen," says Olson, because "you can get a large buildup of parasites without having to be re-exposed from the environment." 
 
 It sounds gross, though an otherwise healthy person with the tapeworm might not have any symptoms at all. But Olson has published on a couple of rare cases where, like this one, things went south. 
 
 He says one was a patient with AIDS in California, and another was on immuno-suppressive drugs because he was receiving an organ transplant. Both died. In each case, the patients suffered from a double whammy: a tapeworm infestation and a downed immune system. 
 
 "When your immune system gets compromised, you're in for all sorts of trouble," Olson says. 
 
 In this case, he says, the worm multiplied in the man's weakened gut, each generation offering a new chance for mutations to crop up. Eventually, enough mutations must have accumulated, leading some larval stem cells to go awry. Instead of dividing rapidly to create a new, adult tapeworm, the cells proliferated as cancer. 
 
 To find out what happened, the researchers compared normal tapeworm genes to those in the tumor, looking for spots where the cancerous ones differed. "There were structural abnormalities or breaks in a small number of genes," says Olson. "You can just think of those as broken genes." 
 
 
 
 He says in three out of five of the cases, the "broken genes" were the same genes that get damaged in human cells, causing malignant human cancer. 
 
 "It speaks of the commonality across the biological world," says Olson. "So, it shows that malignant transformation ... whether that's involving our own cells or those of a parasitic worm, may be the result of mutations to the same genes." 
 
 If that happens and the patient's weak immune system can't contain the cells inside the gut, then the tapeworm cancer can spread in a human body. Muehlenbachs says that clinicians all over the world should be aware of this possibility. 
 
 "We don't know how rare this disease is," he says. "It's the most common tapeworm worldwide, and HIV is also very common. So we're very eager to learn about other cases and potentially those that we might have an opportunity to attempt treatment." 
 
 In this case, doctors never had a chance to treat the patient. 
 
 For months, the hospitalized man had asked what was going on in his body, says Dr. Carlos Agudelo, an infectious disease doctor at the Bolivariana University in Clinic in Medellin. 
 
 "He was very worried about his condition, and we didn't have answers for him," he says. The most Agudelo could do was show him the FedEx receipt to prove that they had sent his fresh tissue samples to the CDC for analysis. 
 
 Days before the CDC figured out that it was tapeworm cancer, the man slipped into a coma. His kidneys were failing and, after almost six months in the hospital, he had refused further treatment. 
 
 "When he was so sick and so tired, because he had spent several months at the hospital, he dropped all his hope," says Agudelo. 
 
 Within 72 hours after the diagnosis came in, he died. 
 
 
 
 "It was heartbreaking," says Muehlenbachs. 
 
 He says it's unclear what treatment would help in future cases — chemotherapy for human cancer or antibiotics to fight tapeworm infections. 
 
 "I'm afraid about the treatment that we can give a [future] patient if we discovered another," says Agudelo. He says if another doctor called him up for advice on a similar case, he wouldn't know what to say.
– Centers for Disease Control researchers say it is one of the strangest and most unsettling cases they have ever encountered. The researchers say that scans of a very ill man in Colombia revealed what "looked like cancer, but the tumors were composed of cells that were not human," NPR reports. The tumors had come from the man's resident tapeworm, which had developed cancer and somehow spread the disease to its host, according to the scientists, whose study published in the New England Journal of Medicine describes the "invasion of human tissue by abnormal, proliferating, genetically altered tapeworm cells" as a "novel disease mechanism." The man died 72 hours after researchers pinpointed the cause of the tumors, Live Science reports. The Colombian man had HIV, which meant the tapeworm's growth in his body was not halted the way it would have been by a healthy immune system, Live Science notes. A CDC pathologist tells the Washington Post that it took dozens of tests to reveal the cause of the illness, and finding tapeworm DNA in the tumors was a huge surprise. "This is the first time we've seen parasite-derived cancer cells spreading within an individual," he says. "This is a very unusual, very unique illness." The Post notes that the study raises questions about what other parasites dwelling in the human body can develop—and spread—cancer. (For more tapeworm horror, read about what caused this man's headache.)