The biology of Hodgkin's lymphoma

Küppers, Ralf

doi:10.1038/nrc2542

Cited by 620 publications

(488 citation statements)

References 150 publications

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“…Numerous kinds of tumors can be initiated by the revelation to various infective agents, bacteria or viruses, for instance cervical cancer linked to human papilloma virus (HPV) infection (Zur Hausen, 2002), hepatocellular carcinoma to hepatitis B virus (Blumberg and London, 1985), adult T-cell leukemia/lymphoma (ATL) to HTVL-1 (Matsuoka and Jeang, 2007), Burkett lymphomas to Epstein-Barr virus (Kuppers, 2009), gastric carcinoma to Helicobacter pylori (Burnett-Hartman, Newcomb, & Potter, 2008), and lately XMRV, a member of Retroviridae family, has been allied with prostatic carcinoma (Urisman et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

HPV and the Development of Colorectal Cancer

Khabaz¹

2016

GJHS

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Over the past two decades, many studies reported that around (20%) of the worldwide malignant tumors problem can be related to viral infections. Some publications recently have described a relationship between malignant colorectal tumors and human papilloma virus (HPV), but these findings are still debatable. The purpose of this report is to evaluate the existence of the genetic sequences and the proteins of HPV in the transformed cells of colorectal cancer in Saudi Arabia. Extracted DNA from eighty three archival colorectal tumor samples were examined for HPV DNA types 16 and 18 and their protein products using polymerase chain reaction (PCR) technique in addition to immunohistochemical staining. All colorectal cancer and control cases were found negative for both 16 and 18 HPV types by using PCR. Moreover, immunostaining did not detect any nuclear expression of HPV proteins in all examined cases. Our outcomes supports the statement that HPV is not engaged in the initiation and progression of colorectal carcinomas especially in the Western province of Saudi Arabia.

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Section: Introductionmentioning

confidence: 99%

HPV and the Development of Colorectal Cancer

Khabaz¹

2016

GJHS

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“…In BL, the proliferation is sustained by the constitutive c-myc expression as a result of the Ig/myc translocation (16). For survival and proliferation of the EBV-carrying type IIa cells, inter-actions with the microenvironment are required (17). Results from our laboratory have shown that a number of cytokines (interleukin-4 [IL-4], IL-13, and IL-21) contribute to the induction of expression of LMP1 (18)(19)(20) and probably help the survival and proliferation of latency IIa cells in vivo.…”

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confidence: 99%

T Cells Modulate Epstein-Barr Virus Latency Phenotypes during Infection of Humanized Mice

Heuts

Rottenberg

Salamon

et al. 2014

J Virol

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“…HodgkinReed-Sternberg (HRS) cells, the genuine tumor cells of HL, originate from germinal center (GC) B cells (1) and PEL cells originate from GC or post-GC B cells (2). In 25% of cases of classical HL, crippling mutations in the immunoglobulin genes (Ig) of HRS cells destroy the coding capacity of a functional B cell receptor (BCR) (3).…”

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confidence: 99%

K1 and K15 of Kaposi's Sarcoma-Associated Herpesvirus Are Partial Functional Homologues of Latent Membrane Protein 2A of Epstein-Barr Virus

Steinbrück

Gustems

Medele

et al. 2015

J Virol

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The human herpesviruses Epstein-Barr virus (EBV) and, supporting an essential role of EBV in HL lymphomagenesis (1). EBV ϩ HRS cells express the viral protein latent membrane protein 2A (LMP2A), which can functionally replace the BCR because Ig-negative B cells can only survive if infected with EBV but not with an LMP2A-negative EBV mutant (4). BCR and LMP2A both contain an immunoreceptor tyrosine-based activation motif (ITAM) (5, 6), which is central for the induction of BCR signaling cascades. In contrast to the BCR, LMP2A is thought to be constitutively active and independent of any ligand or antigen encounter (references 7 and 8 and references therein). EBV also encodes LMP1, a constitutive CD40 receptor mimic that provides a second survival signal for B cells. LMP1 together with LMP2A activates HRS cells, protects them from apoptosis, and induces their proliferation (1, 9).PEL tumor cells are infected with KSHV, and ca. 80% are EBV ϩ , although LMP1 and LMP2A are barely expressed (10,11

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The biology of Hodgkin's lymphoma

Cited by 620 publications

References 150 publications

HPV and the Development of Colorectal Cancer

HPV and the Development of Colorectal Cancer

T Cells Modulate Epstein-Barr Virus Latency Phenotypes during Infection of Humanized Mice

K1 and K15 of Kaposi's Sarcoma-Associated Herpesvirus Are Partial Functional Homologues of Latent Membrane Protein 2A of Epstein-Barr Virus

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