Cancers Tumors Cysts
Cysts, various cancer, tumors, lesions
“In many of my [Lyme] patients, cysts are found not uncommonly in various locations: thyroid, breast, liver, bone, ovary, skin, pineal gland, and kidney. … LD can cause an interstitial cystis leading to bladder pain relieved by urination. A neurogenic bladder can develop with either hesitancy, frequency, loss of bladder awareness, urinary retention, incontinence or the symptoms of UTI (urinary tract infection).” Bleiweiss, J. MD. When To Suspect Lyme Disease, 1994. http://thehumansideoflyme.net/viewarticle.php?aid=65
“Infections provoke an immune response from the body. Part of this response is inflammation. Inflamed tissues swell, redden, and leak fluids full of chemical signals to the immune system. … But Karin stresses the observation that more than one in five cancers worldwide is linked to long-term infections. … Eric Jacobs, PhD, senior epidemiologist for the American Cancer Society in Atlanta, agrees that several kinds of cancer are linked to infections.” By Denoon, Daniel J. Missing Link Ties Cancer to Chronic Infection Major Finding Could Lead to 20% Drop in Cancers Health News Aug. 5, 2004 http://www.webmd.com/cancer/news/20040805/missing-link-ties-cancer-to-chronic-infection
“A growing body of research suggests that a number of viruses, bacteria, and parasites cause cancer in humans, thus providing new possibilities for treatment and prevention of cancer. In 1997, the World Health Organization estimated that up to 84% of cases of some cancers are attributable to viruses, bacteria, and parasites and that more than 1.5 million (15%) new cases each year could be avoided by preventing the infectious disease associated with them. … The pathogenic mechanisms by which infectious agents cause cancer have not been resolved but they appear to be diverse. … This finding not only suggests a causal role but that treatment of a bacterial infection can actually result in regression of cancer.” Cassell, GH. Infectious Causes of Chronic Inflammatory Diseases and Cancer Emerging Infectious Diseases. National Center for Infectious Diseases. Centers for Disease Control and Prevention, Atlanta, GA. Vol 4, #3, July-September 1998. http://www.cdc.gov/ncidod/eid/vol4no3/cassell.htm
“We concluded that women with endometriosis are more likely to have chronic fatigue syndrome, systemic lupus erythematous, Sjögren's syndrome, rheumatoid arthritis, multiple sclerosis, and other autoimmune inflammatory and endocrine diseases. A review of the literature confirms the uniqueness of the co-existence of Lyme disease in women with endometriosis in these cases.” I. M. Matalliotakis, et al. Endometriosis-associated Lyme. Department of Obstetrics and Gynecology, University of Crete, Heraklion, Crete, Greece
“Infection by bacteria, parasites or viruses and tissue inflammation such as gastritis, hepatitis and colitis are recognized risk factors for human cancers at various sites. … Studies on the type of tissue and DNA damage produced by NO and by other reactive oxygen species are shedding new light on the molecular mechanisms by which chronic inflammatory processes may initiate or enhance carcinogenesis in humans.” Ohshima H, Bartsch H. Chronic infections and inflammatory processes as cancer risk factors: possible role of nitric oxide in carcinogenesis. Unit of Environmental Carcinogens and Host Factors, International Agency for Research on Cancer, Lyon, France. Mutat Res. 1994 Mar 1;305(2):253-64.
“A surfeit of PGE-2, free radicals, altered fat metabolism and general immunosuppression by LD may contribute to a predilection (stimulate or predispose) for oncogenesis (forming cancer). Carcinomas are not unknown in LD: melanoma, thyroid cancer, and lymphoma have been published. Free radicals, by engendering connective tissue cross-linking, could be responsible for intra-abdominal adhesions to form, and for some LD patients to appear older than their stated age, or have a haggard facial appearance.” Bleiweiss, J. MD. When To Suspect Lyme Disease, 1994. http://thehumansideoflyme.net/viewarticle.php?aid=65
“Chronic infection leads to inflammation, and chronic inflammation promotes cancer growth.” Sat Dharam Kaur. The Link Between Infection, Chronic Inflammation and Cancer, February 2006.
“At the present time, the etiology of epithelial ovarian cancer is poorly understood. It has recently been recognized that certain chronic infectious agents may contribute to carcinogenesis by inducing a state of persistent inflammation. Since the female upper genital tract is a frequent site of chronic infections, we propose various strategies that may be useful for determining the potential role of chronic infection and persistent inflammation in the pathogenesis of epithelial ovarian cancer.” Quirk JT, Kupinski JM. Chronic infection, inflammation, and epithelial ovarian cancer. Department of Cancer Prevention, Epidemiology and Biostatistics, Roswell Park Cancer Institute, Buffalo, New York 14263, USA. Med Hypotheses. 2001 Oct;57(4):426-8.
“The observation of a Brucella-infected ovarian dermoid cyst, which has not been previously reported, illustrates the importance of localized brucellosis as a cause of persistent infection despite appropriate antimicrobial therapy.” M. Uwaydah1 , A. Khalil3, N. Shamsuddine2, F. Matar3 and G. F. Araj4 Brucella-infected ovarian dermoid cyst causing initial treatment failure in a patient with acute brucellosis. Journal of Obstetrics & Gynaecology. February 2010, Vol. 30, No. 2, Pages 184-186.
“Research suggests that a compromised immune system is a major contributor to the development of cancer…. Recent research has linked the presence of various infections as the trigger of cancer, for example HPV infections and cervical cancer, candida and breast cancer, and Chlamydia and Lymphoma. In these cases, infections are usually present because the immune system is compromised. Because a tumor grows into and disrupts surrounding tissue, decreased circulation to certain areas occur with provides the perfect low-oxygen environment where infections flourish. Data has shown that when the infection is treated, cancer progression stops.” Alternative Ovarian Cancer Facts & Information. Sunridge Medical Wellness Center, Scottsdale, AZ. http://www.sunridgemedical.com/Ovarian_Cancer
“More recently, Borrelia burgdorferi and Campylobacter jejuni have been linked to MALT-type lymphomas involving the skin and small intestine, respectively (4, 5). Jaffe ES. Common threads of mucosa-associated lymphoid tissue lymphoma pathogenesis: from infection to translocation. J Natl Cancer Inst. 2004 Apr 21;96(8):571-3.
“Specific DNA sequences of Borrelia burgdorferi were identified in cutaneous lesions from 9 patients (follicle center lymphoma: 3/20; immunocytoma: 3/4; marginal zone B-cell lymphoma: 2/20; diffuse large B-cell lymphoma: 1/6). Specificity was confirmed by Southern blot hybridisation in all positive cases. We could show that Borrelia burgdorferi DNA is present in skin lesions from a small proportion of patients (18%) with various types of CBCL. Our results may have therapeutic implications. In analogy to Helicobacter pylori-associated MALT-lymphomas, which in some cases can be cured by eradication of Helicobacter pylori infection, a proportion of CBCL may be cured with antibiotic therapy against Borrelia burgdorferi. Although yet speculative, adequate antibiotic treatment for patients with primary CBCL should be considered before more aggressive therapeutic options are applied, particularly in countries where infection by Borrelia burgdorferi is endemic. PCR analysis of Borrelia burgdorferi DNA is a fast test that should be performed in all patients with CBCL to identify those who more likely could benefit from an early antibiotic treatment.”
“In addition, serious signs of liver damage, like cirrhosis or cancer, may not appear until as long as 20 years after the infection began. … Near the end of the 20th century, researchers began to learn that microbes also contribute to many chronic diseases and conditions. Mounting scientific evidence strongly links them to some forms of cancer, coronary artery disease, diabetes, multiple sclerosis, autism, and chronic lung diseases.” Microbes in Sickness and in Health -- Publications, National Institute of Allergy and Infectious Diseases: NIAID. National Institutes of Health Bethesda, MD 20892
Cerroni L, Zochling N, Putz B, Kerl H. Infection by Borrelia burgdorferi and cutaneous B-cell lymphoma. J Cutan Pathol 1997;24:457–61.[CrossRef][Web of Science][Medline]
“These results show that, at least in some instances, PCBCL arises from chronically stimulated lymphoid tissue acquired in the skin in response to B. burgdorferi infection. This may have significant therapeutic implications and warrant further studies on the extent of this association.” Goodlad JR, Davidson MM, Hollowood K, Batstone P, Ho-Yen DO. Borrelia burgdorferi-associated cutaneous marginal zone lymphoma: a clinicopathological study of two cases illustrating the temporal progression of B. burgdorferi-associated B-cell proliferation in the skin. Histopathology. 2000 Dec;37(6):501-8.
“B. burgdorferi-specific DNA was detected in seven of 20 lymphoma cases (five of 12 marginal zone lymphomas, one of five primary cutaneous follicle center cell lymphomas, one of three diffuse, large B-cell lymphomas of the leg) and in one melanoma reexcision patient of 40 control subjects. The relationship between B. burgdorferi and PCBCL was significant when compared with the control groups separately (p <0.05) or in combination (p <0.01). These results provide strong evidence to support the concept of B. burgdorferi-driven lymphomagenesis in the skin.” Goodlad JR, Davidson MM, Hollowood K, Ling C, MacKenzie C, Christie I, Batstone PJ, Ho-Yen DO. Primary cutaneous B-cell lymphoma and Borrelia burgdorferi infection in patients from the Highlands of Scotland. Am J Surg Pathol. 2000 Sep;24(9):1279-85.
“Neuroborreliosis was suspected due to epidemiologic history (a tick bite, erythema migrans), general symptoms (fatigue, hypersomnia, apathy, dysmnesia, concentration disorders) and neurological symptoms, seropositive tests for Borrelia burgdorferi in serum and cerebrospinal fluid (IgG), increased protein concentration in cerebrospinal fluid. Owing to the fact that the serologic criteria of neuroborreliosis were not fulfilled, and other symptoms (loss of consciousness) appeared, CT was done. The CT showed the presence of a tumor in the longitudinal fissure of the brain, which, after intraoperative and histopathological examination, was defined as meningioma.”Biesiada G, Kalinowska-Nowak A. [The coexistence of an intracranial tumor and a positive epidemiologic history of Lyme borreliosis as the reason for diagnostic problems--case report] Przegl Lek. 1999;56(10):682-3.
“Data were recorded on a total of 1797 individual patients: …The 30 most commonly treated complaints were… psoriatic arthropathy; urticaria; ovarian cancer…” Thompson EA, et al. Towards standard setting for patient-reported outcomes in the NHS homeopathic hospitals. Bristol Homeopathic Hospital, Bristol, UK.
“In conclusion there appears to be a clustering of positive serology for Lyme disease Borrelias in PCBCL patients possibly related to an ethiopathogenic relationship. Mechanisms of Borrelia escape from immunosurveillance mechanisms, persistence of both their mitogenic and antigenic stimuli for B-cells, and SALT formation may be involved in the pathogenesis of a subset of PCBCL.” Positive serology for Lyme disease borrelias in primary cutaneous B-cell lymphoma: a study in 22 patients; is it a fortuitous finding? Jelić S, Filipović-Ljesković I. Hematol Oncol. 1999 Sep;17(3):107-16.
“As novel pathogens and previously described pathogens are revealed as the causative agents for some of these conditions, new diagnostic, preventive, and therapeutic modalities may emerge, transforming some diseases from idiopathic and chronic, to infectious and curable.” Infectious agents and the etiology of chronic idiopathic diseases. Fredricks DN, Relman DA. Curr Clin Top Infect Dis. 1998;18:180-200.
“We report two patients with low-grade malignant primary cutaneous B cell lymphoma in association with Borrelia burgdorferi infection.” Kütting B, Bonsmann G, Metze D, Luger TA, Cerroni L. Borrelia burgdorferi-associated primary cutaneous B cell lymphoma: complete clearing of skin lesions after antibiotic pulse therapy or intralesional injection of interferon alfa-2a. J Am Acad Dermatol. 1997 Feb;36(2 Pt 2):311-4.
“The modern data concerning major factors of the Bartonellae virulence and host-bacteria interactions were considered and discussed in this article. The induction of the type IV secretion system, effector protein transmission, inhibition of the endothelial cells apoptosis, and induction of their proliferation lead to formation of new blood vessels and tumors.” [Interaction of bacteria of the genus Bartonella with the host: inhibition of apoptosis, induction of proliferation, and formation of tumors]. Il'ina TS, Bashkirov VN. Mol Gen Mikrobiol Virusol. 2008;(3):3-11.
“We present a 60-year-old man with chronic lymphocytic leukemia and neutropenic fever caused by bacillary angiomatosis.” Bacillary angiomatosis in a patient with chronic lymphocytic leukemia. Petersen K, Earhart KC, Wallace MR. Infection. 2008 Oct;36(5):480-4. Epub 2007 Dec 28.
“Most remarkably, bartonellae can trigger massive proliferation of endothelial cells, leading to vascular tumour formation. The recent availability of infection models and bacterial molecular genetic techniques has fostered research on the pathogenesis of the bartonellae and has advanced our understanding of the virulence mechanisms that underlie the host-cell tropism, the subversion of host-cell functions during bacterial persistence, as well as the formation of vascular tumours by these intriguing pathogens.” Bartonella-host-cell interactions and vascular tumour formation. Dehio C. Nat Rev Microbiol. 2005 Aug;3(8):621-31.
“An analogy for the existence of these individual steps is considered in connection with the development of cancer. The transformations of eukaryotic cells occur in particular in the type IV secretion system, i.e. involving the simultaneous transmission of DNA and protein from bacterial cells to eukaryotic cells. Thus, transfected cells facilitate the indefinite growth of tissue cells and additionally produce growth factors, triggering further bacterial multiplication. The higher numbers of bacteria then produce more transfection and the cycle repeats as long as the host lives. The main limiting factor is the frequency of bacterial infection, while the secondary rate-limiting factors are the levels of transforming growth factors and factors triggering bacteria growth. CONCLUSIONS: Analogous processes are probably responsible for the tumor induction by the three different bacterial species; however, the critical points for eradication are different. The early eradication or limitation of B. henselae or H. pylori can prevent hemangiomas, stomach cancer and malignant cell proliferation. The crown gall formation by A. tumefaciens can only be avoided by prevention of the transforming activity of a single bacterial infection.” Bacterial models for tumor development. Mini-review. Gyémánt N, Molnár A, Spengler G, Mándi Y, Szabó M, Molnár J. Acta Microbiol Immunol Hung. 2004;51(3):321-32.