Advanced searches left 3/3
Search only database of 8 mil and more summaries

Metastatic carcinoma

Summarized by PlexPage
Last Updated: 28 September 2020

* If you want to update the article please login/register

General | Latest Info

Metastasis is a word used to describe the spread of cancer. Unlike normal cells, cancer cells have the ability to grow outside of the place in the body where they originate. When this happen, it is called metastatic cancer. Nearly all types of cancer have the ability to metastasize, but whether they do depends on a variety of individual factors. Metastases can occur in three ways: they can grow directly into tissue surrounding tumor; Cells can travel through the bloodstream to distant locations; or cells can travel through the lymph system to nearby or distant lymph nodes. The most common sites for cancers to metastasize include the brain, bones, lungs and liver. Other places can include adrenal gland, lymph nodes, skin and other organs. Sometimes, metastasis will be found without known primary cancer. In this situation, extensive search is done to look for primary cancer source. If none can be find, it is considered a case of cancer of unknown primary. Some people will have no or minimal symptoms of metastatic cancer. If there are cancer symptoms, they are based on the location of metastasis. If a tumor has metastasized to the brain, symptoms may include headache, dizziness, visual problems, speech problems, nausea, difficulty walking or confusion. Bone metastasis may or may not cause pain. Occasionally, first sign of bone metastasis is when the bone breaks with minor injury or no injury. * Severe back pain accompanied by leg numbness or difficulty with bowel or bladder control, must be evaluated by a doctor immediately. Cancer symptoms of lung metastasis are usually very vague and can be related to other problems that are unrelated to cancer. They can include cough, coughing up blood, chest pain or shortness of breath. Liver metastasis can cause pain, weight loss, nausea, loss of appetite, abdominal fluid or jaundice. There is no one test to check for metastasis. Various tests will reveal different things. Tests that are done are determined by type of primary cancer and / or any symptoms that need to be investigate. Routine blood tests such as liver enzymes may be elevated in presence of liver metastasis. However, these blood tests are often normal, even in people with advanced disease. Some cancers have specific blood tests that can be helpful in following disease AFTER it has been diagnose. If these levels rise, it can be an indication that disease is active or progressing. Some examples are: colon cancer: CEA ovarian cancer: CA - 125 Prostate cancer: PSA testes cancer: AFP HCG. There are several tumor markers that are less specific, and therefore, not used as tool for diagnosing metastasis. There are many tests that are designed to take pictures of various parts of the inside of the body. The type of tests do will depend on symptoms and / or type of cancer. An Ultrasound is one way to evaluate the abdomen if mass is suspect.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

What Is Metastatic Cancer?

The main reason that cancer is so serious is its ability to spread in the body. Cancer cells can spread locally by moving into nearby normal tissue. Cancer can also spread regionally, to nearby lymph nodes, tissues, or organs. And it can spread to distant parts of the body. When this happen, it is called Metastatic Cancer. For many types of cancer, it is also called stage IV Cancer. The process by which cancer cells spread to other parts of the body is called metastasis. When observed under a microscope and tested in other ways, Metastatic Cancer cells have features like those of Primary Cancer and not like cells in places where cancer is find. This is how doctors can tell that it is cancer that has spread from another part of the body. Metastatic Cancer has the same name as Primary Cancer. For example, breast cancer that spreads to the lungs is called Metastatic Breast Cancer, not lung Cancer. It is treated as stage IV Breast Cancer, not as lung Cancer. Sometimes when people are diagnosed with Metastatic Cancer, doctors cannot tell where it start. This type of cancer is called Cancer of Unknown Primary origin, or CUP. See Carcinoma of Unknown Primary page for more information. When new Primary Cancer occurs in a person with a history of cancer, it is known as second Primary Cancer. Second, primary cancers are rare. Most of time, when someone who has had cancer has cancer again, it means the first Primary Cancer has return.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

How Cancer Spreads

Cancer cells spread through the body in a series of steps. These steps include: Growing into, or invading, nearby normal tissue Moving through walls of nearby lymph nodes or blood vessels Traveling through lymphatic system and bloodstream to other parts of the body Stopping in small blood vessels at distant location, invading blood vessel walls, and Moving into surrounding tissue Growing in this tissue until tiny tumor forms Causing new blood vessels to grow, which create blood supply that allow tumor to continue Growing most of time, spreading Cancer cells die at some point in this process. But, as long as conditions are favorable for cancer cells at every step, some of them are able to form new tumors in other parts of the body. Metastatic Cancer cells can also remain inactive at distant sites for many years before they begin to grow again, if at all.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Finding Support

For many people with cancer, goal of treatment is to try to cure cancer. This means getting rid of cancer and never having it come back. With metastatic cancer, curing cancer may not be a realistic goal. However, it might still be hope or dream. It is reasonable to ask your doctor if curing cancer is the goal. If curing cancer is not the goal of treatment, goal is to help person live as well as possible for as long as possible. Getting more specific, this goal can be broken into 4 parts: To have fewest possible side effects from cancer To have fewest possible side effects from cancer treatment for person with cancer To have the best quality of life for person with cancer To live as long as possible with cancer each person value these items differently. It is important to tell your health care team what is important to you. Getting treatment for metastatic cancer can help you live longer and feel better. But getting treatment is always your decision. Learn more about making decisions about cancer treatment. These recommendations include information on treating many types of metastatic cancer.


Treatment and Side Effects

Coping with side effects of treatment can be one of the hardest parts of cancer. It can be scary to read through long lists of side effects. This can be especially upsetting when you think about being in treatment off and on for the rest of your life. It helps to plan in advance and talk with your health care team. Before you start treatment, ask your health care team about side effects of treatment you are considering. Find out how to manage them. After you start treatment, keep track of how you feel. Write down when you notice a problem, how long it last, and if there is anything that will make it better. Let your health care team know. You probably wo have all the symptoms or side effects you read on list. Your health care team can help you manage symptoms and side effects. Your health care team only knows what you tell them. Hormone therapy - Hot flashes, vaginal discharge or dryness, post - menopausal symptoms, joint stiffness, weight gain, and pain or soreness at injection site. Chemotherapy - Nausea and vomiting, fatigue, hair loss, mouth sores, cognitive changes, low blood counts, numbness or tingling in feet, nail and skin changes, diarrhea, loss of appetite, and skin rash. Target therapy - Skin rash, diarrhea, fatigue, mild nausea and vomiting, low blood counts, hair loss, mouth sores, abnormal liver or blood tests, and risks of bleeding. Refer to our Treatment for Metastatic Breast Cancer booklet for the most common side effects associated with specific drugs. Chapter 4 of our Metastatic Breast Cancer book also includes advice on how to manage side effects.


What is Metastatic Breast Cancer?

There are three major types of breast cancer that can become Metastatic: invasive ductal Breast Cancer - this type forms in ducts of the breast. Ducts are tubes that carry milk. This type may appear as lump you can feel. It is the most common type. Invasive lobular Breast Cancer - this type forms in the glands or lobules of the breast. Inflammatory Breast Cancer - this is a rare form of Breast Cancer. It may appear as rash. Your doctor will want to know as much about your cancer as possible. This means knowing subtype. Subtype is based on biomarkers. Biomarkers are signs in your blood or tissue. They help describe your cancer. Your cancer will be tested for: hormones: Breast Cancer can be estrogen receptor positive and / or progesterone receptor positive. This means that hormones play a role in cancer, and cancer may respond to anti - estrogen hormone therapy. Her2: Breast Cancer can be HER2 / neu positive. This means that a protein called human epidural growth factor receptor 2 is present in cancer. These cancers may be treated with targeted therapy. If cancer is Negative for both hormones and HER2, it is called Triple Negative Breast Cancer. There are fewer treatments that work against this subtype of cancer. Doctors are working hard to understand it better and find effective ways to treat it.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

How metastases develop

Macrophages are among the most versatile cells of the body with respect to their ability to migrate, to change shape, and to secrete growth factors and cytokines. 14 39 71 - 73 these Macrophage behaviors also recognize behaviors of metastatic cells. 14 Macrophages manifest two distinct polarization phenotypes: classically activated and alternatively activate. Macrophages acquire the M1 phenotype in response to pro - inflammatory molecules and release inflammatory cytokines, reactive oxygen species, and nitric oxide. 30 46 48 74 - 76 in contrast, macrophages acquire the M2 phenotype in response to anti - inflammatory molecules such as IL - 4, IL 13, IL - 10 and To apoptotic cells. 46 77 M2 Macrophages promote tissue remodeling and repair, but are immunosuppressive and poor antigen presenters. 48 Although M1 and M2 Macrophages play distinct roles during Tumor initiation and malignant progression, Macrophage - epithelial cell fusions can involve either activation state. M1 Macrophages facilitate early stages of tumorigenesis through creation of an inflammatory microenvironment that can produce nuclear and mitochondrial damage. 50 78 However, TAM can also undergo phenotypic switch to M2 phenotype during Tumor progression. The 46 78 TAM population comprising M2 Macrophages scavenges cellular debris, promotes Tumor growth, and enhances angiogenesis. M2 Macrophages also fuse with Tumor cells, thus, expressing characteristics of both cell types. It has always been difficult to know for certain, however, whether TAM are part of normal stroma or are part of malignant cell population. 28 55 this is especially case in human cancers. 56 increasing evidence suggests that many of myeloid / macrophage cells seen within human tumors are also part of the malignant cell population. Aichel first proposed over a century ago that tumor progression involves fusion between leukocytes and somatic cells. 1 - 5 Several human metastatic cancers express multiple molecular and behavioral characteristics of Macrophages including phagocytosis, cell - cell fusion, and antigen expression. Tarin also considers expression of osteopontin and CD44 as important for regulatory gene group / network associated with metastasis. 1 This is interesting as there is strong evidence that both osteopontin and CD44 are expressed in monocytes and macrophages under various physiological and pathological states. 79 - 81 We argue that the origin of metastatic cancer from myeloid cells could account for many mesenchymal properties of metastatic cancers. 14 28 It is not, therefore, necessary to invoke EMT to account for Metastasis. Interestingly, Macrophages express most hallmarks of metastatic Tumor cells when responding to tissue injury or disease. For example, monocytes extravasate from vasculature and are recruited to wound via cytokines released from damaged tissue. 28 30 Within wound, monocytes differentiate into alternatively - activate macrophages and dendritic cells where they release a variety of pro - angiogenic molecules including vascular endothelial growth factor, fibroblast growth factor, and platelet derive growth factor. 30 82 83 M2 Macrophages also actively phagocytize dead cells and cellular debris. 30 73 on occasion, macrophages undergo homotypic fusion resulting in multinucleated giant cells with increased phagocytic capacity.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Copy Number Analysis

1 School of Life Science and Technology, Harbin Institute of Technology, Harbin, China 2 Department of Neurology, First Affiliated Hospital of Harbin Medical University, Harbin, China. Clear - cell renal cell carcinoma is the most common and lethal subtype of kidney cancer. Vhl and PBRM1 are the top two significantly mutated genes in ccRCC specimens, while the genetic mechanism of VHL / PBRM1 - negative ccRCC remains to be elucidate. Here we carried out comprehensive analysis of single - cell genomic copy number variations in VHL / PBRM1 - negative ccRCC. Genomic CNVs were identified at single - cell level, and tumor cells show widespread amplification and deletion across the whole genome. Functional enrichment analysis indicates that amplified genes are significantly enriched in cancer - related signaling transduction pathways. Besides, receptor protein tyrosine kinase genes also show widespread copy number variations in cancer cells. Our studies indicate that genomic CNVs in RTK genes and downstream signaling transduction pathways may be involved in VHL / PBRM1 - negative ccRCC pathogenesis and progression, and highlight the role of comprehensive investigation of genomic CNVs at single - cell level in both clarifying pathogenic mechanism and identifying potential therapeutic targets in cancers.


DISCUSSION

The significant morbidity of colorectal cancer is largely due to metastatic dissemination of primary tumor. These distant metastatic deposits may have very different molecular landscape to primary disease as they may have arisen from minor clones of primary disease or have undergone molecular changes through selective pressures during the metastatic process. However, actionable biomarkers used for informing therapeutic regimens for metastatic disease are usually based on the molecular status of the primary tumor sample alone. Here, we perform SNP arrays to investigate copy number profiles between pair of primary and metastatic colorectal cancer samples to better understand global differences that may occur between these two disease states. When comparing primary tumors to paired metastatic samples, almost quarter of genomes contain copy number differences. Whole genome duplication occurs in 4 primary tumors and their paired metastases. In another 5 pair samples, WGD was identified in metastasis but not in primary tumor. There were no paired samples where only primary tumor had undergone WGD. Recent reports reveal that the majority of esophageal adenocarcinoma undergo WGD and that tumors with WGD had different patterns of genomic alterations with more frequent oncogenic amplifications and less frequent inactivation of tumor suppressors. Dewhurst et al. Show that in colorectal cancer, WGD allows for a higher rate of chromosomal instability, resulting in poor relapse - free survival. These studies are consistent with our finding of greater rates of WGD in metastases compared to primary tumours. Further studies are now required to determine whether WGD is associated with distinctive clinical or molecular features. In colorectal cancer patients with liver metastases, it has recently been reported that intra - tumoral heterogeneity is more common in patients previously exposed to chemotherapy compared with patients who are chemotherapy - naive. A similar finding is seen in patients with urothelial carcinoma metastases. Understanding how selective pressure from chemotherapy is involved in evolution from primary tumor to metastasis is a central biological question with clinical implications. In our study, LOH events unique to primary tumor were commonly observed in therapy naive cases, which likely reflect reduced clonal complexity of secondary tumor due to metastasis and expansion of single primary tumor clone. By contrast, we predominantly observe acquisition of LOH events in metastases following chemotherapy, suggesting therapy has driven an increase in genomic complexity. For colorectal cancer, mutation status of KRAS and BRAF is critical for directing choice of therapy. Here we have demonstrated a case where the primary tumor was KRAS mutant but was wildtype in metastatic sample following chemotherapy. This suggests that mutant allele were either lost from metastatic tumor or metastatic deposit arisen from KRAS wildtype clone in primary tumor and highlights the importance of assessing clinically actionable markers in metastatic rather than primary tumor sample. In this case, targeting metastatic disease with an anti - EGFR agent may have improved the outcome for this patient.


Introduction

Metastatic breast Cancer remains the leading cause of Cancer - related death among women 1 2. Of 1. 7 million new cases of breast cancer are diagnosed annually worldwide, approximately 30% of patients diagnosed with localized disease eventually present with metastatic lesions in distant organs. While non - metastatic breast Cancer has a 5 - year survival rate of 99%, metastatic disease reduces 5 - year survival to only 25% 2. Therapeutic strategies to treat localized disease such as molecular profiling and target therapy have been increasingly successful, but patients with disseminated disease continue to face much worse outcomes, as metastases are largely insensitive to such treatments 3 4. Therefore, to improve outcomes for patients with advanced cancer, specific metastasis - target strategies will need to be develop, as will deeper understanding of unique biological processes that occur during disease progression 4 - 6. Despite the importance of this process, relatively little is known regarding somatic events that drive metastatic cascade. The most commonly accepted hypothesis of tumour progression postulates that mutations are acquired over time, resulting in heterogeneous primary tumour tissue composed of distinct subclones 7. According to this hypothesis, metastatic capability is induced when subclone acquire all of the necessary secondary genomic alterations to intravasate into circulation, survive in circulation, arrest and extravasate at a distant site, and colonize that distant organ 7 8. However, while primary tumour genetic heterogeneity predicted by this model is widely accept, evidence of somatic metastasis - driving mutations is lacking 9 - 11. Large - scale projects such as Cancer Genome Atlas 12 have provided detailed inventory of oncogenic driver mutations, but no equivalent data set currently exists for metastatic disease. Furthermore, data from our lab and work of others suggest that metastasis may instead be driven by dynamic epigenetic variation of gene expression programs 13 - 17 and there is increasing evidence to favour model of early metastatic dissemination, which is inconsistent with somatic evolutionary hypothesis 18 - 20. The difficulty of targeting such dynamic gene expression programs and preventing dissemination of cells from clinically undetectable tumours obliges deeper assessment of the existence of targetable metastasis - driving mutations. In this study, we have shown that recurrent single nucleotide variants and copy number variants, but not gene fusion events, occur spontaneously in the absence of therapeutic pressures and drive breast cancer metastasis. Of note, we identified recurrent mutations in Ras signalling pathway that specifically promote metastasis in vivo.


Results

Surgical samples of primary colorectal tumors and a pair of liver metastases from 16 patients were analyze. A pair of normal control samples were obtained for each patient from macroscopically normal mucosa adjacent to the primary tumor. In all 16 patients, primary CRC tissue was taken prior to chemotherapy. Nine patients had synchronous liver metastasis at time of diagnosis and 7 patients developed liver metastasis metachronously. Metastatic tissue was taken after exposure to chemotherapy in 6 patients, which included 5 metachronous patients and 1 synchronous patient who had neoadjuvant chemotherapy prior to liver surgery and was concordant between all primary tumors and paired metastases.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Systemic Radionuclide Therapy

The first application of bone - seeking radiopharmaceutical strontium - 89 - chloride was described by Pecher in 1940 / 41, followed by the first report of pain palliation in patients with bone metastases from breast carcinoma using phosphorous - 32 by Friedell. In Europe, strontium - chloride is approved for bone pain palliation in patients with bone metastases of prostate cancer, whereas samarium - ethylenediaminetetrameth - ylenephosphonate is approved for treatment of pain from all osteoblastic bone metastases. Phosphor - orthophosphate is used in several other countries. 89 Sr is calcium analog and is incorporated into the newly formed hydroxyapatite of bone matrix. 153 Sm is radiolabeled to bisphosphonate and adsorbed onto hydroxyapatite surface of metabolically active bone by the same mechanism as technetium - label bisphosphonates used for diagnostic bone scintigraphy. Selective uptake depends on the degree of metabolic response elicited in normal bone by the presence of metastatic tissue. An increase in bone turnover leads to enhanced incorporation of bone - seeking radiopharmaceuticals at metastatic sites, by comparison with normal bone, and can therefore deliver high, target local radiation dose. Skeletal uptake of radiolabeled bisphosphonate 153 Sm - EDTMP is in order at 48% of administered activity. The effective half life of 89 Sr in bone metastases is greater than 50 days, compared with 14 days in normal bone table. 32 P as sodium phosphate is no longer approved in many countries because of documented myelotoxocity associated with therapeutic administration. More recently, clinical trial comparing 89 Sr and 32 P in patients suffering from bone metastases reported slightly higher toxicity in the 32 P group but comparable efficacy in terms of pain palliation. Further research will be necessary to confirm these results, particularly in heavily pretreated patients WHO may have limited bone marrow reserves. Clinical trials are in progress evaluating the therapeutic potential of other radionuclides for bone pain palliation. These include: tin - diethylenetriaminopentaacetate, sodium - phosphate, Rhenium - hydroxye - thylidenediphosphonate, lutetium - EDTMP, and radium - chloride. In addition to clinical variables such as skeletal metastatic burden, disease distribution, and prior treatment, Myelosuppression resulting from systemic bone - seeking radiopharmaceutical therapy reflects effective half - life, particle energy and particle range of radionuclide use. Use of low - energy beta - emitting radionuclides would be expected to deliver high absorb dose to bone surface, but negligible dose to hematopoietic bone marrow. Theoretical dose calculations predict a 3 - 6fold advantage in terms of myelotoxicity risk if 33 P were substituted for 32 P, for example. The same is true for conversion electons of 117m Sn or alpha - emitters like 223 Ra. To reduce myelotoxicity, therapeutic potential of conversion electron - emitting radiolabels such as 117m Sn - DTPA has been report. Conversion electrons ejected during decay of this nuclear have 1. 7 - 5. 5 times lower energy than beta - particles conventionally used for systemic treatment for pain palliation. But the limiting factor of this compound used in Phase I / II clinical study was not Radiation Dose to marrow but the high amount of DTPA in current formulation, in 20 - fold molar excess over tin. More recently, new 1: 1 chelate was synthesize.


Introduction

The incidence rate of many common primary tumors is still rising and, due to progression in efficacious treatment, many patients survive for longer time. Because the skeleton is a potential metastatic target for the majority of malignant extracranial tumors, increasing number of patients will suffer from painful bone metastases, which can significantly impair patient's health. Postmortem studies indicate that approximately 80% of all patients with prostate cancer and 75% of breast carcinoma patients develop bone metastases, which together account for approximately 80% of all skeletal metastases. By comparison, bone metastases occur in approximately 20 - 40% of patients with lung or renal cancer. World Health Organization data suggest that approximately 4 million people worldwide experience daily pain due to malignant disease; in half of these people, metastatic bone discomfort is the dominant source of symptoms. The majority of patients with bone metastases develop severe pain as their disease progress, resulting in a considerable reduction in their quality of life. A multidisciplinary approach to symptom palliation is recommend, tailoring treatment to individual need, with the aim of individualized treatment being to add life to years, not years to life. Uptake of bone - seeking radiotracers used for radionuclide therapy of bone metastases depends on osteoblastic activity and calcification of tumor tissue. In the past, morphology of bone metastases arising from primary prostate cancer was typically characterized as mainly osteoblastic, whereas plasmocytoma and renal cell carcinoma have been associated with predominantly osteolytic bone lesions. Mixed patterns of osteoblastic and osteolytic metastases are more common in breast, lung, colorectal and pancreatic malignancies. More recently, when comparing the morphology of breast cancer metastases by computed tomography in the time period 1996 - 2000 versus 2001 - 2005, higher prevalence of osteosclerosis was observed in the later period. This may be due to the application of systematic adjuvant bisphosphonate treatment. Approximately 75% of patients with bone metastases complain of pain as their main symptom and the dominant reason for decreased quality of life. Appropriate pain management may be difficult, particularly in case of poorly localized discomfort. The prognosis of patients with metastases confined to skeleton is usually superior to that of patients with soft - tissue metastases, in lungs, liver or lymph nodes, for example, and therefore merits careful consideration. In addition to analgesic drugs, local external - beam radiation therapy, and surgical interventions, especially in locally restricted disease,s several radiopharmaceuticals have been developed for systemic palliation of bone pain with more multilocular skeletal involvement.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

1 Introduction

Tumor metastasis is a highly inefficient process. It has been estimated that less than 0. 01% of tumor cells that enter circulation develop into metastases. Despite this inefficiency, metastases are responsible for more than 90% of all Cancer - related deaths. Metastasis selects highly aggressive tumor cells that acquire a number of cellular traits that allow them to disseminate from their tissue of origin and establish tumor growth at distant sites. Recent studies have characterized the molecular and phenotypic makeup of Metastatic Tumor cells. Additionally, it is now appreciated that cellular and molecular constituents of the tumor microenvironment also greatly affect Metastatic Tumor progression. In this chapter, we will describe cellular and molecular traits driving tumor metastasis and discuss how the tumor microenvironment influences this process. Most importantly, we will discuss how this knowledge is translated into current and future cancer therapies.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Conjunctival Metastatic Tumors

Metastatic tumors to conjunctiva are rare. In report of 1643 tumors of conjunctiva, 13 cases of conjunctival metastasis were describe. The most commonly reported primary cancers associated with metastasis are breast, lung, and cutaneous melanoma. Laryngeal cancer has also been report. 68 Rarely, bilateral conjunctival infiltrates may be the first sign of relapsed acute leukemia. 117 Most patients presenting with conjunctival metastasis have previously been diagnosed with primary malignancy, as conjunctival metastasis occurs at advanced stages of disease. Occasionally, it may be the first presenting sign of underlying systemic cancer that has not yet been diagnose. 118 means survival time after diagnosis of conjunctival metastasis is on order of months.


Treatment: General Guidelines

Conjunctival melanoma and Squamous Carcinoma can be difficult to treat if they are mulitfocal - occur in multiple spots on eye. In these cases, even surgical removal with freezing therapy may not control the tumor. Dr. Finger has found that Chemotherapy Eye - drops can be used for and are often better than surgery for most patients with Conjunctival cancers. Chemotherapy Eye - drops treat the entire surface of the eye, are less dependent upon defining tumors edges, and decrease the chance of scarring after surgery. Researchers at New York Eye Cancer Center recently published on treatment of Giant Conjunctival Squamous Carcinoma with Chemotherapy Eye drop alone. Systemic lymphoma can usually be treated with standard Chemotherapy that is also likely to cure malignant ocular lymphomas. If the eye is only site of malignant lymphoma, low dose external beam radiation therapy is commonly employ.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Clinical features

Metastatic tumors may occur anywhere in the uvea, including the iris, ciliary body, and choroid. The vast majority of metastatic tumors, however, develop in choroid, whereas metastases to iris are relatively rare. Metastasizing breast cancer accounts for more than half of all patients with clinical diagnosis of uveal metastasis, 5 and can even occur in men. 6 in quarter of all patients with Choroidal metastases cancer of lung is underlying primary tumor. Other primary tumors, such as carcinoid tumor, cancer of gastrointestinal tract, thyroid, prostrate, cutaneous melanoma, and renal cell carcinoma, rarely metastasize to uvea. Sarcomas only very exceptionally lead to uveal metastasis. Choroidal metastases usually occur in the setting of pre - existing primary tumor, eg in breast cancer. 5 It may also occur as initial manifestation of metastasizing primary tumor. 7 Choroidal metastases from unknown or undetectable primary tumor is uncommon, although some authors have reported frequency of one in five patients with uveal metastasis. 8 Evaluation of patients presenting with Choroidal metastasis as first symptom most frequently detects bronchial carcinoma as the primary tumor.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Sources

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

logo

Plex.page is an Online Knowledge, where all the summaries are written by a machine. We aim to collect all the knowledge the World Wide Web has to offer.

Partners:
Nvidia inception logo

© All rights reserved
2021 made by Algoritmi Vision Inc.

If you believe that any of the summaries on our website lead to misinformation, don't hesitate to contact us. We will immediately review it and remove the summaries if necessary.

If your domain is listed as one of the sources on any summary, you can consider participating in the "Online Knowledge" program, if you want to proceed, please follow these instructions to apply.
However, if you still want us to remove all links leading to your domain from Plex.page and never use your website as a source, please follow these instructions.