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It is a form of cancer that is very subtle in it’s early stages with the symptoms often continuing unnoticed. Most ovarian cancers arise from the surface of the ovary, but research has suggested that the fallopian tubes may be responsible for some instances of ovarian cancer. If you find yourself with the symptoms of ovarian cancer more than 10 times a month, then it is time to have yourself examined for ovarian cancer. Less common symptoms can include back pain, general tiredness, involuntary weight loss and an abdominal mass. If you have a family member who has experienced ovarian cancer, your chances of experiencing the illness are twice as high. Infertile women also have a higher risk of experiencing ovarian cancer as are women with endometriosis and women who have had estrogen replacement therapy. Research has found that oral contraceptive pills are a protective factor against ovarian cancer. Women who also had their first pregnancy at a young age also have a lower risk of contracting ovarian cancer, and women who have had their fallopian tubes blocked surgically also have lower risk.
Because the ovaries produce the estrogen and progesterone hormones that some cancers require to grow, ovary removal can halt or slow cancers that occur specifically in women (such as breast cancer). In terms of genetic risk factors, carriers of some BRCA mutations have an increased risk of ovarian cancer. Initially your doctor will do a physical examination to determine if there are any masses or fluid buildup in the abdominal cavity. For the diagnosis to be confirmed, surgery must be undertaken to take biopsies and inspect the abdominal cavity. Tubal ligation will drastically reduce the risk of ovarian cancer and some women who have a long family history of ovarian cancer may take this option. Regular screening and being attentive to the symptoms of ovarian cancer is one of the best ways to prevent the disease taking hold. Chemotherapy is often used after surgery to treat any tumors that are not easily removed during surgery and to stop any cancer cells spreading.
Radiation may be effective in the early stages of the illness, but due to the location of the ovaries it is not safe to use a high dose. Unfortunately because of the difficulty in spotting the symptoms of ovarian cancer early on, prognosis is generally not good for ovarian cancer. Lung cancer is the most common cancer diagnosed in men and women in the United States, and is the leading cause of cancer death.
Over 160,000 individuals died as a result of lung cancer in 2008.[1] This number amounted to more than the number of deaths from colon, breast, and prostate cancers combined. To reduce the rate of distant metastases, adjuvant platinum-based chemotherapy is now considered the standard of care for patients with stages IIA to IIIA NSCLC and may be considered an option for select patients with stage IB disease. Adjuvant ChemotherapyPrior to discussing neoadjuvant chemotherapy, a brief review of adjuvant NSCLC chemotherapy is needed. Both the American Society of Clinical Oncology and National Comprehensive Cancer Network guidelines recommend the use of adjuvant chemotherapy for patients with resectable stage IIA to IIIA NSCLC. Neoadjuvant ChemotherapyThe role of neoadjuvant chemotherapy has also been explored in patients with early-stage NSCLC. In the 1990s, two small randomized trials sparked further interest in neoadjuvant chemotherapy in patients with resectable NSCLC because they demonstrated a survival benefit to platinum-based therapy (Table 2).[10,11] These trials had their limitations, which included relatively small patient numbers, unexpectedly poor outcome in the control arm, and inhomogeneous study populations.
Gilligan et al developed a randomized trial that compared neoadjuvant cisplatin-based chemotherapy to surgery alone. At the 2007 annual meeting of the American Society of Clinical Oncology (ASCO), the results of the Southwest Oncology Group (SWOG) 9900 trial were updated. It is a type of blood cancer that includes every type of lymphoma except the Hodgkin lymphoma. The signs and symptoms of colorectal cancer depend on the location of the tumor in the bowel, and whether it has spread elsewhere in the body (metastasis).
Those with a family history in two or more first-degree relatives (such as a parent or sibling) have a two to threefold greater risk of disease and this group accounts for about 20% of all cases. Colorectal cancer is a disease originating from the epithelial cells lining the colon or rectum of the gastrointestinal tract, most frequently as a result of mutations in the Wnt signaling pathway that increase signaling activity. Beyond the defects in the Wnt signaling pathway, other mutations must occur for the cell to become cancerous. Other proteins responsible for programmed cell death that are commonly deactivated in colorectal cancers are TGF-? and DCC (Deleted in Colorectal Cancer). Comprehensive, genome-scale analysis has revealed that colorectal carcinomas can be categorized into hypermutated and non-hypermutated tumor types.[34] In addition to the oncogenic and inactivating mutations described for the genes above, non-hypermutated samples also contain mutated CTNNB1, FAM123B, SOX9, ATM, and ARID1A.
However, in most cancer research, as pointed out by Rubin[40] "The vast majority of studies in cancer research has been done on well-defined tumors in vivo, or on discrete neoplastic foci in vitro. Epigenetic alterations are much more frequent in colon cancer than genetic (mutational) alterations.
However, by comparison, epigenetic alterations in colon cancers are frequent and affect hundreds of genes.
Changes in the level of miR-137 expression result in changed mRNA expression of the target genes by 2 to 20-fold and corresponding, though often smaller, changes in expression of the protein products of the genes.
In addition to epigenetic alteration of expression of miRNAs, other common types of epigenetic alterations in cancers that change gene expression levels include direct hypermethylation or hypomethylation of CpG islands of protein-encoding genes and alterations in histones and chromosomal architecture that influence gene expression.[47][48] As an example, 147 hypermethylations and 27 hypomethylations of protein coding genes were frequently associated with colorectal cancers. As summarized in the articles Carcinogenesis and Neoplasm, for sporadic cancers in general, a deficiency in DNA repair is occasionally due to a mutation in a DNA repair gene, but is much more frequently due to epigenetic alterations that reduce or silence expression of DNA repair genes. Diagnosis of colorectal cancer is via sampling of areas of the colon suspicious for possible tumor development typically done during colonoscopy or sigmoidoscopy, depending on the location of the lesion.
The microscopic cellular characteristics of the tumor are usually reported from the analysis of tissue taken from a biopsy or surgery. Cancers on the right side of the large intestine (ascending colon and cecum) tend to be exophytic, that is, the tumor grows outwards from one location in the bowel wall.
Adenocarcinoma is a malignant epithelial tumor, originating from superficial glandular epithelial cells lining the colon and rectum.
Most (50%) colorectal adenomas and (80-90%) colorectal cancer tumors are thought to over express the cyclooxygenase-2 (COX-2) enzyme.[55] This enzyme is generally not found in healthy colon tissue, but is thought to fuel abnormal cell growth. Appearance of the inside of the colon showing one invasive colorectal carcinoma (the crater-like, reddish, irregularly shaped tumor).
Gross appearance of a colectomy specimen containing two adenomatous polyps (the brownish oval tumors above the labels, attached to the normal beige lining by a stalk) and one invasive colorectal carcinoma (the crater-like, reddish, irregularly shaped tumor located above the label). Endoscopic image of colon cancer identified in sigmoid colon on screening colonoscopy in the setting of Crohn's disease.
Precancer — Tubular adenoma (left of image), a type of colonic polyp and a precursor of colorectal cancer. The colon cancer staging can be made according to the TNM staging system from the WHO organization, the UICC and the AJCC. Tumor budding in colorectal cancer is loosely defined by the presence of individual cells and small clusters of tumor cells at the invasive front of carcinomas. Fecal occult blood testing (FOBT) of the stool is typically recommended every two years and can be either guaiac based or immunochemical.[15] If abnormal FOBT results are found, participants are typically referred for a follow-up colonoscopy examination. Medical societies in the United States typically recommend screening between the age of 50 and 75 years with sigmoidoscopy every 5 years and colonoscopy every 10 years.

Some countries have national colorectal screening programs which offer FOBT screening for all adults within a certain age group, typically starting between age 50 and 60. If the cancer is found at a very early stage, it may be removed during a colonoscopy.[1] For people with localized cancer, the preferred treatment is complete surgical removal with adequate margins, with the attempt of achieving a cure.
In both cancer of the colon and rectum, chemotherapy may be used in addition to surgery in certain cases. In Stage I colon cancer, no chemotherapy is offered, and surgery is the definitive treatment. If cancer has spread to the lymph nodes or distant organs, which is the case with stage III and stage IV colon cancer respectively, adding chemotherapy agents fluorouracil, capecitabine or oxaliplatin increases life expectancy. The primary difference in the approach to low stage rectal cancer is the incorporation of radiation therapy. While a combination of radiation and chemotherapy may be useful for rectal cancer,[15] its use in colon cancer is not routine due to the sensitivity of the bowels to radiation.[86] Just as for chemotherapy, radiotherapy can be used in the neoadjuvant and adjuvant setting for some stages of rectal cancer.
In people with incurable colorectal cancer, palliative care can consist of procedures that relieve symptoms or complications from the cancer but do not attempt to cure the underlying cancer, thereby improving quality of life.
The aims of follow-up are to diagnose, in the earliest possible stage, any metastasis or tumors that develop later, but did not originate from the original cancer (metachronous lesions). Survival is directly related to detection and the type of cancer involved, but overall is poor for symptomatic cancers, as they are typically quite advanced.
According to American Cancer Society statistics in 2006,[100] over 20% of people with colorectal cancer come to medical attention when the disease is already advanced (stage IV), and up to 25% of this group will have isolated liver metastasis that is potentially resectable. In 2 Chronicles 21, Jehoram of Judah is cursed because of his evil deeds with an incurable disease of the bowels which left him in great agony and eventually his bowels came out. Some other factors that increase the risk of lung cancer are the age at which the person started smoking, the period for which the person has been smoking and how many cigarettes he smoked. Please note that we are unable to respond back directly to your questions or provide medical advice.
As the name implies, it is a form of cancer that affects women’s ovaries and it affects mostly older women. So for example if you suddenly experience pelvic soreness on 5 days, have difficulty eating on 3 days, experience bloating on 4 days and are older than 50 you should seek diagnosis immediately.
The bloating and pelvic pain are usually caused by a buildup of fluid in the abdominal cavity. Long term studies have shown that women who used oral contraception for 10 years have a 50%+ reduction in their chance of contracting ovarian cancer. A blood test for ovarian cancer markers will also be conducted, that specifically looks for CA-125.
Cancer cells will most likely be found in the abdominal fluid if a patient has ovarian cancer.
More than 50% of women presenting with ovarian cancer are already stage III or stage IV (stage I and II being early development). For those with resectable disease, the use of neoadjuvant chemotherapy has the potential to reduce tumor volume, address micrometastatic disease early, and improve outcomes. The majority of lung cancer cases are non–small-cell lung cancer (NSCLC), and the poor outcomes are attributed to the high rate of metastases associated with this disease. This article will review the neoadjuvant chemotherapy data and explore what role, if any, neoadjuvant chemotherapy plays in patients with resectable NSCLC. Three large trials and two meta-analyses have demonstrated that platinum-based chemotherapy can result in a survival benefit when given in the adjuvant setting. The rationale for further investigations was the hope of decreasing micrometastases at distant sites and tumor burden preoperatively to increase resectability rates and overall survival. The Depierre et al study randomized 355 patients with stage IB to IIIA to two cycles of preoperative cisplatin, ifosfamide, and mitomycin compared with primary surgery.[13] Patients who responded to chemotherapy (64%) received an additional two cycles postoperatively. This study, which spanned four countries and randomized 588 participants with resectable stage I to III disease, failed to demonstrate a statistically significant improvement in overall survival at 5 years (44% vs 45%, hazard ratio = 1.02). The trial randomized 388 participants to surgery alone vs three cycles of preoperative carboplatin and paclitaxel. A gene that appears to contribute to the potential for metastatic disease, metastasis associated in colon cancer 1 (MACC1), has been isolated.[25] It is a transcriptional factor that influences the expression of hepatocyte growth factor. The mutations can be inherited or acquired, and most probably occur in the intestinal crypt stem cell.[28][29][30] The most commonly mutated gene in all colorectal cancer is the APC gene, which produces the APC protein. The p53 protein, produced by the TP53 gene, normally monitors cell division and kills cells if they have Wnt pathway defects. For example, genes encoding the proteins KRAS, RAF, and PI3K, which normally stimulate the cell to divide in response to growth factors, can acquire mutations that result in over-activation of cell proliferation. Plus a schematic diagram indicating a likely field defect (a region of tissue that precedes and predisposes to the development of cancer) in this colon segment. As described by Vogelstein et al.,[42] an average cancer of the colon has only 1 or 2 oncogene mutations and 1 to 5 tumor suppressor mutations (together designated “driver mutations”), with about 60 further “passenger” mutations. For instance, there are types of small RNAs called microRNAs that are about 22 nucleotides long.
Other microRNAs, with likely comparable numbers of target genes, are even more frequently epigenetically altered in colonic field defects and in the colon cancers that arise from them. The extent of the disease is then usually determined by a CT scan of the chest, abdomen and pelvis. It invades the wall, infiltrating the muscularis mucosae layer, the submucosa, and then the muscularis propria. The Astler-Coller classification (1954) or the Dukes classification (1932) are now less used. The decision on which aim to adopt depends on various factors, including the person's health and preferences, as well as the stage of the tumor.[83] When colorectal cancer is caught early, surgery can be curative. Sometimes chemotherapy is used before surgery to shrink the cancer before attempting to remove it. The decision to add chemotherapy in management of colon and rectal cancer depends on the stage of the disease.
The role of chemotherapy in Stage II colon cancer is debatable, and is usually not offered unless risk factors such as T4 tumor or inadequate lymph node sampling is identified.
Often, it is used in conjunction with chemotherapy in a neoadjuvant fashion to enable surgical resection, so that ultimately as colostomy is not required.
Surgical options may include non-curative surgical removal of some of the cancer tissue, bypassing part of the intestines, or stent placement. National Comprehensive Cancer Network and American Society of Clinical Oncology provide guidelines for the follow-up of colon cancer.[92][93] A medical history and physical examination are recommended every 3 to 6 months for 2 years, then every 6 months for 5 years. In epidemiological studies, exercise may decrease colorectal cancer-specific mortality and all-cause mortality.
Survivors with tumors that expressed p27 and performed greater and equal to 18 MET hours per week were found to have reduced colorectal-cancer mortality survival compared to those with less than 18 MET hours per week.
Those symptoms are frequently found in conjunction with other illnesses so it is often difficult to diagnose early on.
The pressure on the stomach from this fluid buildup is usually what causes changes to apetite also. So if you have a mother or grandmother who experienced ovarian cancer, you should consult a doctor early on if you experience symptoms, and get screened regularly when you are over 50.

Modern medicine allows women to understand their genetic risk factors more comprehensively so discuss this with your doctor. The symptoms aren’t very useful in early stages of ovarian cancer because they can point to many other illnesses. By stage III and stage IV the cancer has already spread from the ovaries into other parts of the body. Randomized trials comparing neoadjuvant platinum-based regimens with surgery alone were able to demonstrate the feasibility and safety of this modality. Before these studies were published, adjuvant chemotherapy was not considered a standard therapy.
Although 31% of the patients in the chemotherapy arm were downstaged, there was no change in the planned surgery.[14] The investigators found no increase in surgical morbidity in the chemotherapy group. The most common of these is hereditary nonpolyposis colorectal cancer (HNPCC or Lynch syndrome) which is present in about 3% of people with colorectal cancer.[15] Other syndromes that are strongly associated with colorectal cancer include Gardner syndrome,[22] and familial adenomatous polyposis (FAP). This gene is associated with the proliferation, invasion and scattering of colon cancer cells in cell culture, and tumor growth and metastasis in mice. Eventually, a cell line acquires a mutation in the TP53 gene and transforms the tissue from an benign epithelial tumor into an invasive epithelial cell cancer. Likewise, epigenetic alterations present in tumors may have occurred in pre-neoplastic field defects.
The oncogenes and tumor suppressor genes are well studied and are described below under Pathogenesis. These microRNAs (or miRNAs) do not code for proteins, but they can target protein coding genes and reduce their expression. There are other potential imaging test such as PET and MRI which may be used in certain cases. The most common colon cancer cell type is adenocarcinoma which accounts for 98% of cases.[53] Other, rarer types include lymphoma and squamous cell carcinoma.
Left-sided tumors tend to be circumferential, and can obstruct the bowel lumen, much like a napkin ring, and results in thinner caliber stools. Tumor cells describe irregular tubular structures, harboring pluristratification, multiple lumens, reduced stroma ("back to back" aspect). Tumor budding is a well-established independent marker of a potentially poor outcome in colorectal carcinoma that may allow for dividing people into risk categories more meaningful than those defined by TNM staging, and also potentially guide treatment decisions, especially in T1 and T3 N0 (Stage II, Dukes’ B) colorectal carcinoma. It is also known that the patients who carry abnormalities of the mismatch repair genes do not benefit from chemotherapy. However, it may not be possible in low lying tumors, in which case, a permanent colostomy may be required.
Carcinoembryonic antigen blood level measurements follow the same timing, but are only advised for people with T2 or greater lesions who are candidates for intervention.
People with a tumor that has not breached the muscularis mucosa (TNM stage Tis, N0, M0) have a five-year survival rate of 100%, while those with invasive cancer of T1 (within the submucosal layer) or T2 (within the muscular layer) have an average five-year survival rate of approximately 90%.
These cause damage to the cells of the lungs and these damaged cells can turn into cancerous ones after some time.
The other causes of lung cancer include exposure to radiation and cancer causing substances.
These trials supported evidence found in phase II trials that utilized third-generation chemotherapies. These late stages are unresectable and have grave prognoses (1%–5% 5-year survival).[2,3] Even those with early-stage (stage I–IIIA), resectable disease are likely to succumb to recurrent disease.
In 1995, a meta-analysis of 52 randomized trials evaluating cytotoxic chemotherapy in patients with NSCLC was reported. Factors that may have contributed to the negative results included the fact that six different chemotherapy regimens were allowed in this study and the majority of study participants had stage I disease (61%), thus making it more difficult for the study to reach statistical significance. These studies suggest a role for induction chemotherapy for patients with stage II or IIIA NSCLC who are operable candidates.
Lymphocytes (white blood cells), where the tumor develops, are in the lymph nodes and other lymphoid tissues.Abdominal pain, swollen lymph nodes, fever and night sweats are some symptoms. For people with these syndromes, cancer almost always occurs and makes up 1% of the cancer cases.[23] A total proctocolectomy may be recommended for people with FAP as a preventative measure due to the high risk of malignancy. Without APC, ?-catenin accumulates to high levels and translocates (moves) into the nucleus, binds to DNA, and activates the transcription of proto-oncogenes. A CT-scan of the chest, abdomen and pelvis can be considered annually for the first 3 years for patients who are at high risk of recurrence (for example, those who had poorly differentiated tumors or venous or lymphatic invasion) and are candidates for curative surgery (with the aim to cure). Those with a more invasive tumor yet without node involvement (T3-4, N0, M0) have an average five-year survival rate of approximately 70%. Still, limitations to these studies exist, such as the inclusion of various disease stages in one study, inter- and intratrial variability of the chemotherapy regimens used, and lack of phase III data comparing neoadjuvant to adjuvant chemotherapy.
These genes are normally important for stem cell renewal and differentiation, but when inappropriately expressed at high levels, they can cause cancer.
As one example, the epigenetic alteration consisting of CpG island methylation of the DNA sequence encoding miR-137 reduces its expression.
This occurs in mucinous (colloid) adenocarcinoma, in which cells are poorly differentiated. A colonoscopy can be done after 1 year, except if it could not be done during the initial staging because of an obstructing mass, in which case it should be performed after 3 to 6 months.
Patients with tumors that lacked CTNNB1 expression (?-catenin), involved in Wnt signalling pathway, required more than 18 Metabolic equivalent (MET) hours per week, a measure of exercise, to observe a reduction in colorectal cancer mortality.
These heterogeneous factors make it difficult to offer firm recommendations about neoadjuvant chemotherapy. This subset analysis demonstrated that platinum-based regimens (8 studies) vs non–platinum-based regimens (6 studies) did improve survival following surgical resection.[7] Survival was improved by 4% at 2 years, with a 13% reduction in death. If the disease is showing symptoms and causing discomfort, u must see a doctor immediately.
This is a frequent early epigenetic event in colorectal carcinogenesis, occurring in 81% of colon cancers and in 14% of the normal appearing colonic mucosa adjacent to the cancers. If a villous polyp, a polyp >1 centimeter or high grade dysplasia is found, it can be repeated after 3 years, then every 5 years.
The mechanism of how exercise benefits survival may be involved in immune surveillance and inflammation pathways. Other matters of contention include the role of postoperative radiation and the concern for increased postoperative complications, especially when a right pneumonectomy is being considered after neoadjuvant chemotherapy.
In clinical studies, a pro-inflammatory response was found in patients with stage II-III colorectal cancer who underwent 2 weeks of moderate exercise after completing their primary therapy. To clarify these issues, well-structured phase III trials comparing adjuvant to neoadjuvant chemotherapy are needed. A significant decrease in 8-oxo-dG was found in the urine of patients who underwent 2 weeks of moderate exercise after primary therapy.

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